Drug Safety Directory

5-HTP and ketamine have no clinically significant interaction. The serotonin syndrome concern that gets attached to 5-HTP is about combining it with prescription serotonergic agents (SSRIs, SNRIs, MAOIs, triptans). Ketamine itself is not meaningfully serotonergic, so 5-HTP plus ketamine alone is theoretical, not evidence-based. Disclose other serotonergic prescriptions to us at intake.

Abilify is safe to combine with at-home ketamine therapy across its standard dose range. The most common pattern in the Tovani patient population is low-dose Abilify (2-15 mg/day) used as MDD augmentation, which is essentially routine intake. Higher doses for primary psychiatric indications (schizophrenia, bipolar I) prompt a more detailed conversation about whether at-home ketamine is the right setting. Abilify's mechanism is unique among antipsychotics (D2 partial agonism rather than full D2 antagonism), which gives it a less-sedating profile than other atypicals like Quetiapine and reduces the session-day timing concern.

Isotretinoin and ketamine have no clinically significant pharmacologic interaction. The clinically important thing for KAP planning is the FDA black box: isotretinoin is associated with depression, anxiety, and suicidal ideation in a subset of patients (signal first identified in 1998, still in the prescribing information). This is a real concern for any patient population but especially for KAP patients in active depression treatment — isotretinoin-induced mood changes can confound 'did the ketamine work?' attribution. We do not stop isotretinoin for KAP, but we baseline mood carefully and track changes against your iPLEDGE timeline.

Tocilizumab and ketamine have no clinically significant interaction. Used for rheumatoid arthritis, giant cell arteritis, systemic juvenile idiopathic arthritis, CAR-T cytokine release syndrome, and severe COVID-19. The intrinsic considerations — lipid elevations, GI perforation risk, hepatotoxicity, neutropenia monitoring — belong to tocilizumab. Subcutaneous weekly or every-2-week dosing (RA, GCA); IV infusion every 4 weeks (RA).

Pioglitazone and ketamine have no clinically significant interaction. Continue as normal.

Apple cider vinegar (ACV) and ketamine have no clinically significant interaction. Popular as a glycemic-control adjunct and 'wellness' supplement. The intrinsic concerns — tooth enamel erosion if undiluted, esophageal irritation if taken straight, and hypokalemia at very high doses — are all about acetic acid being acidic and unrelated to KAP. ACV gummies have largely replaced straight-vinegar shots because of these issues.

Dapsone and ketamine have no clinically significant interaction. Uses range from oral (leprosy, PCP prophylaxis in sulfa-allergic patients, dermatitis herpetiformis) to topical (acne). The intrinsic dapsone concerns — methemoglobinemia at higher doses, hemolytic anemia in G6PD-deficient patients — are unchanged by KAP.

Doxorubicin and ketamine have no clinically significant interaction. The famous safety considerations — cumulative cardiotoxicity (lifetime dose cap ~450-550 mg/m²), the bright red 'Adriamycin' color in urine for 1-2 days post-infusion, severe vesicant if extravasates — are intrinsic anthracycline issues independent of KAP. The cardiotoxicity surveillance is the most important: oncology tracks lifetime cumulative dose and ejection fraction.

5-Fluorouracil and ketamine have no clinically significant interaction. Backbone of colorectal cancer chemotherapy (FOLFOX, FOLFIRI), used across many other cancers as IV infusion, and as topical Efudex/Carac for actinic keratosis. The intrinsic considerations — mucositis, diarrhea, hand-foot syndrome, myelosuppression, and the severe toxicity in patients with DPD (dihydropyrimidine dehydrogenase) deficiency (now screened pre-treatment) — are 5-FU class issues independent of KAP.

Inhaled fluticasone-salmeterol and ketamine have no clinically significant interaction. The most-prescribed asthma/COPD combo inhaler, available in multiple device formats. Inhaled delivery means minimal systemic absorption at therapeutic doses. The intrinsic considerations worth knowing — fluticasone is a CYP3A4 substrate so strong inhibitors (Paxlovid, ritonavir-boosted regimens, clarithromycin) can raise systemic fluticasone enough to cause Cushingoid effects — are a fluticasone safety issue, not a ketamine concern.

Ibuprofen and ketamine have no clinically significant pharmacologic interaction. NSAIDs carry their own renal and GI risks but those are not amplified by KAP.

Erenumab and ketamine have no clinically significant interaction. Monoclonal antibodies are cleared by the reticuloendothelial system, not CYP enzymes, so they don't have the kinds of drug interactions that small molecules do. Continue your monthly injection schedule.

Fremanezumab and ketamine have no clinically significant interaction. Same family as erenumab and galcanezumab; can be dosed monthly or quarterly.

Alpha-lipoic acid and ketamine have no clinically significant interaction. Often used as a supplement for diabetic peripheral neuropathy and as a general antioxidant. At high doses, ALA can modestly lower blood glucose — relevant for diabetic patients but independent of KAP.

Spironolactone and ketamine have no clinically significant interaction. Common uses: heart failure, resistant hypertension, hormonal acne, hirsutism, and gender-affirming care.

Naproxen and ketamine have no clinically significant pharmacologic interaction. Standard NSAID renal and GI cautions apply but are independent of KAP.

Fexofenadine and ketamine have no clinically significant interaction. Of the major OTC second-generation antihistamines (loratadine, cetirizine, fexofenadine), fexofenadine has the least CNS penetration and the lowest sedation rate. Continue as needed.

Alpha-GPC and ketamine have no clinically significant interaction. Same family as citicoline — a choline precursor that supports cholinergic neurotransmission and membrane synthesis. The 2021 Italian META-AGENT study suggested a possible increase in stroke risk with chronic high-dose alpha-GPC; that signal is preliminary and intrinsic to alpha-GPC rather than a KAP issue, but worth disclosing if you have cardiovascular history.

Topical brimonidine and ketamine have no clinically significant interaction. Used for glaucoma (Alphagan), often combined with timolol (Combigan), and as topical rosacea treatment (Mirvaso). Some systemic absorption can occur, with rare systemic α2 effects (hypotension, fatigue) in sensitive patients — punctal occlusion minimizes this. Not related to ketamine.

Ramipril and ketamine have no clinically significant interaction. Common ACE inhibitor especially in heart failure (HOPE trial drug) and post-MI. Same compatibility profile as lisinopril.

Glimepiride and ketamine have no clinically significant pharmacokinetic or pharmacodynamic interaction. The practical thing to plan around is the pre-session fasting window typical for KAP — sulfonylureas can cause hypoglycemia and the fast amplifies that risk. We coordinate dosing with you (often holding the AM dose on session day, then resuming with food after). Same framework as glipizide and glyburide.

Naratriptan and ketamine have no clinically significant interaction. Distinctive among triptans for its longer half-life (~6 hours) and slower onset, which makes it well-suited for menstrual migraine prophylaxis (scheduled dosing around the period rather than acute rescue). Same updated guidance on SS framing as the other triptans.

Amoxicillin (and amoxicillin-clavulanate / Augmentin) has no clinically significant interaction with ketamine. The most commonly prescribed antibiotic in the United States can be taken without changing KAP timing.

Testosterone and ketamine have no clinically significant interaction. Whether prescribed for hypogonadism, age-related low T, or gender-affirming care, KAP proceeds without medication changes.

Hydralazine and ketamine have no clinically significant interaction. Used for resistant hypertension and heart failure (in combination with isosorbide for the BiDil indication in heart failure). Standard antihypertensive BP measurement applies to every KAP patient regardless of medication.

Mesalamine and ketamine have no clinically significant interaction. First-line for mild-to-moderate ulcerative colitis and used in some Crohn's regimens. The different oral and rectal formulations target different segments of bowel (Asacol/Lialda for colon, Pentasa for distal small bowel onward, Canasa suppositories for rectal disease, Rowasa enemas for distal colitis). The intrinsic considerations — renal monitoring (rare interstitial nephritis), occasional paradoxical worsening — are mesalamine class concerns independent of KAP.

Vitamin C and ketamine have no clinically significant interaction. Standard RDA-range or moderate supplemental doses are fully compatible. Megadose use (5+ g/day) is generally not necessary and produces only osmotic diarrhea; there's no clinically meaningful effect on ketamine.

Intranasal azelastine and ketamine have no clinically significant interaction. Available OTC as Astepro Allergy and by prescription as Astelin or Dymista (combination with fluticasone). The local delivery means minimal sedation compared to oral first-gen antihistamines like Benadryl. The bitter aftertaste is intrinsic and harmless. A better choice than oxymetazoline (Afrin) for chronic allergy use — no rebound effect.

Inhaled ipratropium and ketamine have no clinically significant interaction. Common as the anticholinergic component of Combivent (with albuterol) for COPD and asthma, and as Atrovent monotherapy. Inhaled delivery means minimal systemic anticholinergic effect at therapeutic doses. The intranasal form (for rhinitis) similarly has negligible systemic exposure.

Teriflunomide and ketamine have no clinically significant interaction. Oral MS disease-modifying therapy. The distinctive consideration — teriflunomide has an extremely long half-life (active metabolite of leflunomide) and requires accelerated elimination via cholestyramine or activated charcoal if rapid clearance is needed (pregnancy, switching DMTs, serious adverse event). LFT monitoring is required. These are teriflunomide-management issues independent of KAP.

Moxifloxacin and ketamine have no clinically significant interaction. Moxifloxacin has the highest intrinsic QT prolongation of the fluoroquinolone class — used as the positive control in QT studies. That QT effect is moxifloxacin's own; ketamine at psychiatric doses is not a meaningful QT-prolonging drug per the published literature, so the combination is not a 'stacking' interaction.

Almotriptan and ketamine have no clinically significant interaction. Triptan option for acute migraine with favorable tolerability profile and FDA approval down to age 12. Same updated guidance as the other triptans — the historical serotonin syndrome framing has been updated based on subsequent evidence and doesn't transfer meaningfully to ketamine.

Phenazopyridine and ketamine have no clinically significant interaction. Provides symptomatic relief of UTI burning while antibiotics work; it does NOT treat the infection itself. Intrinsic considerations: (1) bright orange/red urine is the universal known side effect, completely harmless and stops when you stop the drug; (2) will stain contact lenses (remove them or wear glasses); (3) ≤2 days OTC use is appropriate — longer use or severe UTI symptoms need actual antibiotic treatment.

Bacopa and ketamine have no clinically significant interaction. Ayurvedic herb with modest evidence for cognition and stress at chronic supplementation. Mild acetylcholinesterase modulation in preclinical work but not clinically relevant for KAP at typical doses.

Bactrim and ketamine have no clinically significant interaction. Used for UTIs, skin/soft tissue infections, and Pneumocystis prophylaxis. Continue your course as prescribed.

Mupirocin and ketamine have no clinically significant interaction. Topical ointment for impetigo, infected wounds, and nasal MRSA decolonization. Systemic absorption is essentially zero, so no drug-interaction concern at any dose.

Entecavir and ketamine have no clinically significant interaction. First-line oral therapy for chronic hepatitis B (alongside tenofovir). High barrier to resistance, well-tolerated long-term. Renally cleared with no significant CYP involvement.

Aspirin and ketamine have no clinically significant interaction. Low-dose aspirin for cardiovascular prevention and full-dose aspirin for pain both work fine alongside KAP.

Olmesartan and ketamine have no clinically significant interaction. Common ARB. Standard ARB compatibility profile. The well-known olmesartan-induced sprue-like enteropathy is intrinsic to olmesartan and unchanged by KAP.

Dicyclomine and ketamine have no clinically significant interaction. Dicyclomine has well-known anticholinergic side effects (dry mouth, urinary retention, cognitive effects, falls in elderly), but those are intrinsic to dicyclomine and not amplified by ketamine. Ketamine itself does not have meaningful clinical anticholinergic activity (it actually causes hypersalivation, the opposite). Continue as prescribed for IBS or GI motility.

Bictegravir and ketamine have no clinically significant interaction. As part of Biktarvy (with emtricitabine and tenofovir alafenamide), it's one of the most widely-used single-tablet HIV regimens. Unlike older HIV drugs (efavirenz was a strong CYP3A4 inducer), modern INSTI regimens don't meaningfully affect ketamine PK.

Biotin and ketamine have no clinically significant interaction. The well-known biotin issue is lab-test interference: high-dose biotin (5,000-10,000 mcg/day, common for hair/nail) can produce false-positive or false-negative results on biotin-based immunoassays including TSH, troponin, hCG, and some hormone panels. This matters for any lab work you have done — not for KAP itself. Stop biotin 24-72 hours before lab draws if accuracy matters.

Botox for chronic migraine and ketamine have no clinically significant interaction. The PREEMPT protocol uses 155 units injected across 31 sites every 12 weeks. The treatment is local — once injected, botulinum toxin is internalized by nerve terminals and has no systemic activity to interact with ketamine.

MCT oil and ketamine have no clinically significant interaction. Common in ketogenic diets, bulletproof coffee, and as a quick energy source from rapidly-absorbed medium-chain fats. The intrinsic consideration is GI tolerance — starting too quickly causes nausea, cramping, and loose stools that can mimic side-effects of medications. Doesn't affect ketamine PK or PD.

Inhaled fluticasone-vilanterol (Breo Ellipta) and ketamine have no clinically significant interaction. Once-daily ICS+LABA inhaler with longer-acting components than Advair (fluticasone-salmeterol) or Symbicort (budesonide-formoterol). Trelegy Ellipta adds umeclidinium (LAMA) as triple-therapy COPD inhaler. Inhaled delivery means minimal systemic exposure. Same CYP3A4-substrate fluticasone concern around strong inhibitors (Paxlovid, ritonavir) — that's a fluticasone safety issue, not a ketamine concern.

Brivaracetam and ketamine have no clinically significant interaction. Designed as a more potent and selective SV2A binder than levetiracetam (Keppra) with the same broad-spectrum seizure efficacy but substantially reduced psychiatric/behavioral side effects ('Keppra rage' alternative). Same compatibility framework as levetiracetam with ketamine — clean PK, but with the mood side-effect concern largely off the table.

Buspirone and ketamine have no clinically significant interaction. The older theoretical serotonin syndrome concern (buspirone is a 5-HT1A partial agonist) is not supported by any published combination cases with ketamine, which is not meaningfully serotonergic itself. Continue as normal.

Exenatide and ketamine have no clinically significant interaction. Exenatide was the first GLP-1 receptor agonist approved (Byetta in 2005), and although newer drugs in the class (semaglutide, tirzepatide) have largely replaced it in clinical practice, real patients are still on Byetta (twice-daily) or Bydureon (once-weekly extended release) — particularly long-term diabetes patients whose regimens were stable before the newer GLP-1s came to market. The interaction profile with ketamine is identical to semaglutide: no shared mechanism, no shared metabolism, no additive cardiovascular or sedation effects. Exenatide is approved for type 2 diabetes only and never carried a suicidal-ideation warning (the FDA class rule covered chronic weight management drugs, not diabetes-only GLP-1s).

Calcium and ketamine have no clinically significant interaction. The well-known calcium-absorption interactions (levothyroxine, certain antibiotics, bisphosphonates) require timing those drugs separately from calcium — intrinsic, not a KAP issue.

Topical capsaicin and ketamine have no clinically significant interaction. OTC creams (Capzasin, Zostrix) are used for muscle and joint pain; Rx high-dose patches (Qutenza) for postherpetic neuralgia. The intrinsic burning sensation is the active mechanism — depleting substance P from peripheral nerves over repeated applications. Wash hands carefully after application (don't touch eyes), and avoid heat/showering on treated areas for an hour.

Beta-alanine and ketamine have no clinically significant interaction. Common pre-workout supplement (often combined with creatine and citrulline) for muscle endurance. The intrinsic and harmless side effect — paresthesia (tingling on face, hands, scalp) at typical 2-5g doses — is from β-alanine activating MrgprD receptors in skin nerves, not an allergic reaction or clinical concern. Some patients find it pleasant, others uncomfortable. Splitting the daily dose into smaller portions reduces the sensation.

Bicalutamide and ketamine have no clinically significant interaction. Older anti-androgen, often used with a GnRH agonist (leuprolide, goserelin) for combined androgen blockade. The intrinsic considerations — hepatotoxicity monitoring, gynecomastia, hot flashes — are bicalutamide-class concerns independent of KAP. Largely supplanted by enzalutamide in modern practice but still in use, especially in earlier-stage disease.

Cefuroxime and ketamine have no clinically significant interaction. Common for respiratory infections, Lyme disease, and surgical prophylaxis. Same clean cephalosporin-class profile.

Celecoxib and ketamine have no clinically significant interaction. The COX-2 selectivity reduces GI bleeding risk vs older NSAIDs; standard cardiovascular caution applies independent of KAP.

At standard doses (10-40 mg/day in adults, 10-20 mg/day in patients over 60), Celexa is safe to combine with at-home ketamine therapy. The SSRI evidence base applies in full: no required washout, no special precaution beyond standard intake review. The citalopram-specific consideration is dose-dependent QT-interval prolongation: the FDA's 2011 safety communication established 40 mg as the maximum adult dose (20 mg for patients over 60 or with hepatic impairment) specifically because doses above that produce measurable QTc prolongation. Patients on FDA-compliant Celexa doses proceed routinely; patients on doses above the FDA limits get a brief additional intake conversation.

Mycophenolate and ketamine have no clinically significant interaction. Backbone immunosuppressant after organ transplant (kidney, liver, heart, lung) and used for lupus nephritis and some forms of vasculitis. Glucuronidated rather than CYP-metabolized, so it sits outside the CYP3A4 conversation that complicates ketamine + tacrolimus stacks.

Standard daily multivitamins and ketamine have no clinically significant interaction. The individual components (B vitamins, vitamin D, vitamin C, zinc, etc.) at RDA-range doses don't affect ketamine PK or PD. Continue as normal.

Varenicline and ketamine have no clinically significant interaction. The FDA black box for neuropsychiatric effects was removed in 2016 after the EAGLES trial showed no increased risk versus placebo. Vivid dreams and mood lability still happen but are common enough that they're part of baseline mood documentation any KAP patient gets, not a varenicline-specific monitoring task.

Vitamin D and ketamine have no clinically significant interaction. Continue your supplement regimen as normal.

Certolizumab and ketamine have no clinically significant interaction. Unique among TNF biologics for being a PEGylated Fab fragment (no Fc region) — clinically relevant because it has minimal placental transfer, making it the preferred TNF biologic in pregnancy. From a KAP-interaction standpoint, identical to the other TNF biologics — clean profile.

Ciprofloxacin and ketamine have no clinically significant interaction. Ciprofloxacin's QT effect and the fluoroquinolone-specific cautions (tendon rupture, peripheral neuropathy in rare cases) are intrinsic to the drug, not stacking concerns with ketamine. Ketamine at psychiatric doses is not a meaningful QT-prolonging drug per the published literature. Complete your course as prescribed.

L-citrulline and ketamine have no clinically significant interaction. Citrulline is converted to arginine in the kidneys, bypassing first-pass arginase metabolism and delivering arginine more efficiently than oral arginine. Same NO/vasodilation framework — clinically modest. Common pre-workout supplement and used for erectile function and circulation. Often combined with malate as 'citrulline malate' for additional ATP-cycle support.

Loratadine and ketamine have no clinically significant interaction. Loratadine is a non-sedating second-generation antihistamine that does not stack with ketamine on sedation or any other axis we monitor.

Topical benzoyl peroxide and ketamine have no clinically significant interaction. First-line OTC and Rx acne treatment, available 2.5% to 10%. Intrinsic considerations are skin dryness/irritation and the well-known fabric-bleaching effect (white pillowcases, please). Not absorbed systemically in any meaningful amount.

Clindamycin and ketamine have no clinically significant interaction. Common for dental, skin/soft-tissue, and certain anaerobic infections. The well-known clindamycin precaution (C. difficile colitis risk) is intrinsic to the antibiotic and independent of KAP.

Transdermal estradiol patches and ketamine have no clinically significant interaction. The transdermal route is preferred over oral estrogens for many patients because it bypasses first-pass hepatic metabolism — lower VTE risk, more stable levels, and minimal interaction with CYP enzymes. The intrinsic considerations — VTE risk (lower than oral), breast tissue effects, and the application-site rotation rules — are estrogen-class issues, not KAP issues.

Caffeine at typical daily intake (1-3 cups of coffee, or equivalent in tea or moderate energy-drink use) is safe to combine with at-home ketamine therapy. The only operational rule is to avoid caffeine within 4-6 hours of a ketamine session day; the cardiovascular stimulation (modest BP and HR elevation) and arousal interfere with the relaxed receptive state that produces the best session experience. Heavy daily caffeine intake (>400 mg, equivalent to about 4 cups of coffee or several energy drinks) is worth a brief intake conversation but doesn't change the verdict.

Citicoline (CDP-choline, branded as Cognizin) and ketamine have no clinically significant interaction. Used as a nootropic for cognition; provides choline + cytidine for membrane phosphatidylcholine and acetylcholine synthesis.

Docusate and ketamine have no clinically significant interaction. Mild stool softener used for opioid-induced or pregnancy constipation; works by reducing surface tension and allowing water into stool. The clinical efficacy is modest — most large reviews show docusate is barely better than placebo for actual constipation — but it remains widely used and is genuinely safe.

Ethinyl-estradiol-containing combined contraceptives (the pill, patch, ring) and ketamine have no clinically significant interaction. The KAP-relevant context is more about general VTE risk awareness than ketamine PK: combined hormonal contraceptives carry a modest baseline VTE risk that increases with smoking (especially age ≥35), obesity, prolonged immobility, and personal/family thrombophilia history. That conversation belongs to gyn/primary care, independent of KAP. The interaction worth knowing about is the *opposite* direction: strong CYP3A4 inducers (rifampin, phenytoin, carbamazepine, St John's wort) can reduce contraceptive efficacy — discuss backup methods with your prescriber.

Topical salicylic acid and ketamine have no clinically significant interaction. Range of products from 0.5-2% (acne pads, washes) to 17%+ (wart treatments, Compound W). Intrinsic considerations: skin irritation, salicylate toxicity in rare cases of very large surface-area application in children, and salicylate allergy. None apply meaningfully to KAP at typical dosing.

Entacapone and ketamine have no clinically significant interaction. COMT inhibitor used adjunct to levodopa-carbidopa (combined as Stalevo) to extend levodopa's effect by blocking peripheral catechol-O-methyltransferase. The intrinsic 'entacapone gives urine a harmless brown-orange color' note is well-known and shouldn't be confused with hematuria. Hepatotoxicity surveillance was a concern with the related drug tolcapone (now rarely used); not a meaningful concern with entacapone.

Glatiramer and ketamine have no clinically significant interaction. Long-standing first-line MS disease-modifying therapy with one of the cleanest safety profiles in MS treatment — no monitoring requirements like fingolimod's first-dose observation or ocrelizumab's infusion reactions. Subcutaneous injection daily or 3x/week. The intrinsic considerations — injection-site reactions and the occasional post-injection systemic reaction (flushing, chest tightness, anxiety lasting ~15 min) — are independent of KAP.

CoQ10 and ketamine have no clinically significant interaction. Common as adjunct for statin-related myopathy, heart failure, migraine prophylaxis, and general antioxidant supplementation. Continue as normal.

Carvedilol and ketamine are compatible. Carvedilol's combined beta and alpha-1 blockade actually dampens the cardiovascular axis that ketamine activates. Patients on carvedilol for heart failure or post-MI can proceed with KAP without medication changes.

Secukinumab and ketamine have no clinically significant interaction. Used for moderate-to-severe psoriasis, psoriatic arthritis, ankylosing spondylitis, and hidradenitis suppurativa. Same clean biologic profile.

Warfarin and ketamine have no clinically significant pharmacokinetic interaction. The standard warfarin monitoring (INR checks) is unchanged by KAP. Patients on warfarin for atrial fibrillation, valve replacement, or DVT/PE prophylaxis can proceed with KAP without medication changes.

Losartan and ketamine have no clinically significant interaction. ARBs have the same clean ketamine-compatibility profile as ACE inhibitors. Standard session-day BP measurement applies to every KAP patient regardless of antihypertensive use.

Creatine and ketamine have no clinically significant interaction. Beyond its established performance use, there is growing evidence for creatine as a depression adjunct, particularly in women. Compatible with KAP.

Rosuvastatin and ketamine have no clinically significant interaction. Rosuvastatin is minimally CYP-metabolized (cleanest of the statins for drug interactions). Standard statin precautions apply but are independent of KAP.

Saffron and ketamine have no clinically significant interaction. Multiple small trials show modest antidepressant effects comparable to low-dose SSRIs. The serotonin syndrome concern matters when saffron is combined with prescription serotonergic agents, not with ketamine specifically (ketamine isn't meaningfully serotonergic).

Vitamin B12 and ketamine have no clinically significant interaction. Common as supplement for low-B12, vegan/vegetarian diets, and metformin-related B12 depletion. Both oral and injectable forms are fine. Worth noting: recreational nitrous oxide use inactivates B12, so we screen for that separately.

At standard doses (30-120 mg/day, most patients on 60 mg/day), Cymbalta is safe to combine with at-home ketamine therapy. The SNRI evidence base for concurrent use with ketamine mirrors the SSRI evidence and applies in full: no required washout, no special precaution beyond standard intake review. Two duloxetine-specific notes worth a brief mention: a modest blood pressure consideration (SNRIs raise BP slightly at higher doses, which is dose-aware rather than verdict-changing), and the chronic-pain indication that brings a distinct patient population to this page (Cymbalta is also prescribed for fibromyalgia, diabetic neuropathy, and chronic musculoskeletal pain).

Liothyronine and ketamine are compatible. Beyond the standard thyroid replacement use, low-dose liothyronine (T3) is a well-established antidepressant augmentation strategy (the STAR*D trial used 25-50 mcg). KAP can proceed alongside it without medication changes.

Cyclophosphamide and ketamine have no clinically significant interaction. Used across many oncologic indications and as immunosuppression in severe autoimmune disease (lupus nephritis, vasculitis). The intrinsic considerations — hemorrhagic cystitis (prevented with hydration and mesna at high doses), myelosuppression, alopecia, infertility risk, secondary malignancy risk with long-term use — are alkylating-agent class issues independent of KAP.

Roflumilast and ketamine have no clinically significant pharmacologic interaction. The FDA warning for psychiatric reactions (suicidal ideation, depression, anxiety, insomnia) is real and intrinsic to PDE4 inhibition; we want to know about it for KAP planning so we can track mood changes against your roflumilast timeline, but there's no drug-interaction concern with ketamine.

Desmopressin and ketamine have no clinically significant interaction. Used for central diabetes insipidus, nocturnal enuresis (bedwetting in kids, nocturia in adults), mild hemophilia A, and von Willebrand disease. The intrinsic safety concern with desmopressin is hyponatremia — particularly in older adults and with excessive fluid intake — which is independent of KAP and worth managing per your prescribing physician's instructions.

L-methylfolate and ketamine have no clinically significant interaction. Deplin is FDA-approved as a medical food for depression adjunct, particularly in patients with MTHFR polymorphisms. Compatible with KAP.

Depo-Provera and ketamine have no clinically significant interaction. The quarterly injection provides steady-state progestin exposure that's higher than IUD but still without relevant ketamine interaction. Continue as scheduled.

At standard doses (25-100 mg at bedtime for off-label insomnia, or 150-600 mg/day for major depression), trazodone is safe to combine with at-home ketamine therapy. The serotonergic activity is modest compared with SSRIs or SNRIs (trazodone is primarily a 5-HT2A antagonist with only weak serotonin reuptake inhibition), and the published case literature contains no serotonin syndrome events from at-home ketamine plus standard-dose trazodone. The trazodone-specific intake note is sedation timing: trazodone is heavily sedating, particularly in the first hours after dosing, so daytime ketamine sessions should not be scheduled within ~8 hours of a trazodone dose.

Tolterodine and ketamine have no clinically significant interaction. Same compatibility profile as oxybutynin — the anticholinergic burden is intrinsic and not a stacking concern with ketamine. Modest CYP2D6 metabolism.

DHEA and ketamine have no clinically significant interaction. DHEA is a precursor to androgens and estrogens; at typical OTC doses (10-50 mg/day) the hormonal effects are modest. If you also take TRT, HRT, tamoxifen, or aromatase inhibitors, coordinate with your prescriber on the cumulative hormone profile — that's a hormone-management issue independent of KAP.

Glyburide and ketamine have no clinically significant interaction. The practical issue is hypoglycemia risk: glyburide has a longer half-life and active metabolites that produce more frequent and prolonged hypoglycemia than glipizide. The pre-session fasting window amplifies this — for KAP days we coordinate with you on a hold/reduce strategy. Many endocrinologists are migrating patients from glyburide to glipizide or non-sulfonylurea alternatives for exactly this hypoglycemia profile, independent of KAP.

Topical adapalene and ketamine have no clinically significant interaction. OTC since 2016 (was prescription Differin), now widely available. Similar mechanism to tretinoin but with milder irritation profile and better photostability. The intrinsic considerations are the same retinoid-class issues — initial irritation, photosensitivity, pregnancy contraindication. Combination with benzoyl peroxide (Epiduo) is common.

Fidaxomicin and ketamine have no clinically significant interaction. Used for C. difficile colitis with lower recurrence rate than oral vancomycin. Minimal systemic absorption means no drug-interaction surface.

Valsartan and ketamine have no clinically significant interaction. Same compatibility profile as losartan and other ARBs. Continue as normal; standard BP monitoring applies to every KAP patient.

Oxybutynin and ketamine have no clinically significant interaction. Oxybutynin has well-known anticholinergic side effects (dry mouth, constipation, urinary retention from too-much-effect, cognitive effects, falls in elderly), but those are intrinsic to oxybutynin and not amplified by ketamine. Ketamine itself does not have meaningful clinical anticholinergic activity (it actually causes hypersalivation). The Beers Criteria list oxybutynin as potentially inappropriate in adults 65+ due to cognitive burden; that's intrinsic, not a KAP issue.

Bisacodyl and ketamine have no clinically significant interaction. Stimulant laxative available as oral tablets (delayed-release, target colon) and rectal suppositories (faster acting). Same framework as senna — cramping with overuse, electrolyte shifts with chronic high-dose use. The 'don't crush oral bisacodyl' rule (the enteric coating exists to bypass the stomach) is intrinsic.

Dupilumab and ketamine have no clinically significant interaction. Same clean biologic-class profile. Used for atopic dermatitis, severe asthma, eosinophilic esophagitis, prurigo nodularis, and other type-2 inflammation conditions.

Dicloxacillin and ketamine have no clinically significant interaction. Common oral antibiotic for methicillin-susceptible Staph aureus (MSSA) skin infections, cellulitis, and mastitis. Take on an empty stomach for absorption.

Echinacea and ketamine have no clinically significant interaction. Common for cold/flu prevention or symptom reduction. Modest CYP modulation in some studies but not at clinically meaningful magnitudes for ketamine.

At standard doses (75-225 mg/day, occasionally higher in treatment-resistant depression), Effexor is safe to combine with at-home ketamine therapy. The SNRI evidence base applies in full: no required washout, no special precaution beyond standard intake review. Two venlafaxine-specific notes worth a brief mention: a dose-dependent blood pressure consideration (Effexor's NE effect is modest at 75-150 mg/day but more pronounced above 225 mg/day where sustained hypertension is documented), and the famously severe discontinuation syndrome that makes "do not stop Effexor to start ketamine" one of the clearest pieces of advice on this page.

Prasugrel and ketamine have no clinically significant interaction. More potent P2Y12 inhibitor than clopidogrel, used in acute coronary syndrome with PCI. The intrinsic considerations — increased bleeding risk relative to clopidogrel, contraindication in patients ≥75 years or with prior stroke/TIA — are prasugrel-class concerns independent of KAP.

Topical pimecrolimus and ketamine have no clinically significant interaction. Steroid-sparing topical for atopic dermatitis, particularly for sensitive areas (face, intertriginous skin) where chronic topical steroids cause atrophy. Same therapeutic class as topical tacrolimus (Protopic). The FDA boxed warning about theoretical malignancy risk (added 2006 based on animal data, not human data) is intrinsic and well-debated; doesn't impact KAP.

Apixaban and ketamine have no clinically significant interaction. Eliquis patients on it for atrial fibrillation or VTE prevention proceed with KAP without medication changes.

Galcanezumab and ketamine have no clinically significant interaction. Same family as erenumab (Aimovig) and fremanezumab (Ajovy) — monthly subcutaneous CGRP-pathway monoclonal antibodies for migraine prevention. Monoclonal antibodies don't go through CYP and don't have small-molecule interaction surfaces.

Emtricitabine and ketamine have no clinically significant interaction. Commonly co-formulated with tenofovir (Truvada, Descovy) for HIV treatment and PrEP; also a component of Biktarvy. Renally cleared, clean interaction profile.

Etanercept and ketamine have no clinically significant interaction. Same compatibility profile as adalimumab — biologics that neutralize TNF-α don't have CYP-based drug interactions. Used primarily for RA, psoriasis, and ankylosing spondylitis.

Entresto and ketamine have no clinically significant interaction. Modern heart failure standard-of-care combining an ARB (valsartan) with neprilysin inhibition (sacubitril). Continue as normal; standard BP monitoring applies to every KAP patient regardless.

Vedolizumab and ketamine have no clinically significant interaction. The gut-selective mechanism is its key feature: by blocking only α4β7 integrin (gut-tropic), it doesn't broadly immunosuppress the way TNF blockers do, which is why it has lower infection risk. Same clean monoclonal antibody profile from a KAP-interaction standpoint.

Estradiol and ketamine have no clinically significant interaction. Whether you are on estradiol for menopausal HRT, hormonal contraception, or gender-affirming care, KAP can proceed without medication changes.

Raloxifene and ketamine have no clinically significant interaction. Different SERM from tamoxifen but same family. Used for postmenopausal osteoporosis and breast cancer prevention in high-risk patients. The intrinsic VTE risk (similar to oral estrogen, lower than tamoxifen) is independent of KAP.

Dapagliflozin and ketamine have no clinically significant interaction. Used for type 2 diabetes, heart failure with reduced ejection fraction, and chronic kidney disease. Continue as normal.

Benralizumab and ketamine have no clinically significant interaction. Targets the IL-5 receptor (rather than IL-5 itself like mepolizumab) — depletes eosinophils more aggressively via antibody-dependent cellular cytotoxicity. Used for severe eosinophilic asthma and eosinophilic granulomatosis with polyangiitis. Subcutaneous injection every 8 weeks after loading.

Letrozole and ketamine have no clinically significant interaction. Used for hormone-positive breast cancer adjuvant therapy (5-10 year courses) and off-label for ovulation induction in IVF cycles. The intrinsic concerns (bone density loss with chronic use, hot flashes) are unchanged by KAP.

Iron and ketamine have no clinically significant interaction. The well-known iron-absorption interactions (levothyroxine, tetracycline antibiotics, fluoroquinolone antibiotics) require taking those drugs 2+ hours apart from iron — those are intrinsic to iron's chelation with other drugs, not a KAP issue.

Omega-3 fatty acids and ketamine have no clinically significant interaction. OTC fish oil and prescription preparations (Lovaza, Vascepa) are both fine to continue.

Metronidazole and ketamine have no clinically significant interaction. The disulfiram-like alcohol reaction is a well-known Flagyl precaution but is independent of KAP and applies whether you're in treatment or not. Alcohol is already separately incompatible with KAP for its own reasons.

Fluticasone and ketamine have no clinically significant interaction. Inhaled fluticasone (Flovent, Advair) for asthma/COPD and nasal fluticasone (Flonase) for allergic rhinitis are both compatible with KAP.

Alendronate and ketamine have no clinically significant interaction. The well-known alendronate ritual (take first thing in the morning with full glass of water, stay upright for 30 minutes, no food or other meds for 30 minutes) is intrinsic to the medication's GI safety profile and unchanged by KAP.

Mushroom coffee blends (Four Sigmatic, Ryze, MUD\WTR, and similar) and ketamine have no clinically significant interaction. The mushroom components (lion's mane, chaga, reishi, cordyceps) are mild adaptogens at the dose-per-serving typical of these blends. The clinically relevant ingredient is the caffeine — same considerations as regular coffee, covered on our caffeine page.

Oral GABA supplements and ketamine have no clinically significant interaction. Despite being marketed for anxiety and sleep, oral GABA crosses the blood-brain barrier poorly (the supplemented molecule, that is — endogenous brain GABA is synthesized in situ from glutamate). Any anxiolytic effect from oral GABA is largely peripheral (gut-brain axis, enteric nervous system) and at small magnitudes, mostly placebo. For the more credible 'calm' supplement option, see our L-theanine page. No real pharmacological stacking with ketamine.

Reishi and ketamine have no clinically significant interaction. Adaptogenic mushroom used for stress and immune support. Concentrated extracts at high doses have mild antiplatelet and BP-lowering effects — relevant to disclose alongside anticoagulants or antihypertensives but not a KAP-specific concern at typical doses.

Simethicone and ketamine have no clinically significant interaction. Inert silicone-based surfactant that breaks up gas bubbles in the GI tract; not absorbed into the bloodstream. Common as Gas-X, Mylicon (infant drops), or as the simethicone component of combo antacids (Mylanta with simethicone, etc.). Safe at any age, in pregnancy, and with any medication.

Fingolimod and ketamine have no clinically significant interaction. Oral DMT for relapsing MS. The famous safety considerations are intrinsic and unchanged by KAP: first-dose bradycardia monitoring (6-hour observation at initiation), macular edema screening (ophthalmology baseline), lymphopenia and rare PML risk, and rebound disease activity if discontinued abruptly. These belong to fingolimod and neurology management.

Metformin and ketamine have no clinically significant interaction. Diabetic patients on metformin can proceed with KAP without medication changes.

Glipizide and ketamine have no clinically significant interaction. The practical issue to plan around is hypoglycemia: sulfonylureas can cause low blood sugar, and the pre-session fasting window typical for KAP increases that risk. We coordinate with you on session-day dosing (often holding or halving the morning dose, resuming with the post-session meal).

L-glutamine and ketamine have no clinically significant interaction. Most common supplement uses: gut health (leaky-gut protocols, ulcerative colitis adjunct), post-workout recovery, and immune support during athletic training stress. Glutamine is the most abundant amino acid in the body; oral supplementation is well-tolerated. Theoretical caution in patients with hepatic encephalopathy (ammonia handling) is the only intrinsic note, independent of KAP.

Glycine and ketamine have no clinically significant interaction. Glycine is an interesting molecule pharmacologically — it's an inhibitory neurotransmitter at glycine receptors AND a required co-agonist at NMDA receptors (binds the glycine-binding site distinct from where ketamine binds). The theoretical concern that glycine could 'rescue' ketamine blockade doesn't apply because ketamine blocks the NMDA channel pore, not the glycine binding site. At typical sleep-supplement doses (1-3 g at bedtime), the effect is mild relaxation with no documented ketamine interaction.

Lion's mane and ketamine have no clinically significant interaction. The bioactive compounds (hericenones and erinacines) may promote nerve growth factor and BDNF — interesting mechanism overlap with ketamine's neuroplasticity effects, but no documented adverse interaction. Continue as you normally would.

Tasimelteon and ketamine have no clinically significant interaction. Used for circadian rhythm disorders (Non-24 in totally blind patients, and Smith-Magenis syndrome). Selective melatonin agonism with no GABA, no histamine, no opioid activity makes it one of the cleanest sleep agents from a drug-interaction standpoint.

Adalimumab and ketamine have no clinically significant interaction. Used for rheumatoid arthritis, Crohn's disease, ulcerative colitis, psoriasis, hidradenitis suppurativa, ankylosing spondylitis, and other autoimmune conditions. Monoclonal antibodies are cleared by the reticuloendothelial system, not CYP enzymes, so they don't have the small-molecule interactions that complicate KAP planning for many drugs.

Palbociclib and ketamine have no direct clinically significant interaction. Used with endocrine therapy (letrozole, fulvestrant) for HR+/HER2- breast cancer. The intrinsic interaction story you'll hear about — palbociclib is a CYP3A4 substrate raised by strong inhibitors like clarithromycin, Paxlovid, and grapefruit — is about palbociclib toxicity, not about KAP. Same conversation with abemaciclib and ribociclib. Neutropenia monitoring is intrinsic and unchanged by KAP.

Ibrutinib and ketamine have no direct clinically significant interaction. First-in-class BTK inhibitor, dramatically effective in CLL and several other B-cell malignancies. The intrinsic safety considerations worth knowing about — increased bleeding risk (especially with anticoagulants and antiplatelets), new-onset or worsened atrial fibrillation, and ventricular arrhythmias — are ibrutinib-class concerns independent of KAP. Ibrutinib is also a CYP3A4 substrate, so strong inhibitors raise its level and toxicity (an ibrutinib dose conversation, not KAP).

Sumatriptan and ketamine have no clinically significant interaction. The American Headache Society 2018 position statement walked back the FDA's older triptan-plus-SSRI serotonin syndrome warning as not supported by evidence; with ketamine, which is not meaningfully serotonergic itself, the concern is even smaller. Use as needed for migraines without changing your KAP plan.

Loperamide and ketamine have no clinically significant interaction. At standard OTC doses (2-4 mg as needed), loperamide is a peripherally-selective opioid that doesn't cross the blood-brain barrier meaningfully and has no CNS effects. The well-publicized loperamide cardiotoxicity (QT prolongation, torsades) comes from massive abuse doses (100+ mg/day for recreational opioid effects), not standard antidiarrheal use.

Azathioprine and ketamine have no clinically significant interaction. Backbone immunosuppressant in transplant maintenance, inflammatory bowel disease (often steroid-sparing), and rheumatologic conditions including lupus, vasculitis, and autoimmune hepatitis. The critical interaction worth knowing about — never combine standard-dose azathioprine with allopurinol or febuxostat without dose-reducing by 75% (xanthine oxidase inhibition causes toxic accumulation) — is intrinsic to azathioprine and independent of KAP. TPMT genotype/phenotype testing prior to initiation is standard.

Propranolol and ketamine are compatible. Propranolol is commonly used for performance anxiety, essential tremor, and migraine prophylaxis. As with metoprolol, it dampens ketamine's transient sympathomimetic effect.

Eplerenone and ketamine have no clinically significant interaction. More selective for aldosterone receptor than spironolactone, so fewer hormonal side effects (no gynecomastia). Used in heart failure and resistant hypertension. Standard potassium monitoring is intrinsic.

Canagliflozin and ketamine have no clinically significant interaction. Same SGLT2-class compatibility as empagliflozin (Jardiance) and dapagliflozin (Farxiga). Continue as normal.

Sitagliptin and ketamine have no clinically significant interaction. Patients on Januvia can proceed without medication changes.

Empagliflozin and ketamine have no clinically significant interaction. Used for type 2 diabetes, heart failure, and chronic kidney disease. Continue as normal.

Cephalexin and ketamine have no clinically significant interaction. Common first-line antibiotic for skin and soft-tissue infections, dental infections, UTI. Continue your course as prescribed.

Triamcinolone and ketamine have no clinically significant interaction at the routes patients most commonly use it: nasal spray (Nasacort) for allergies, topical cream for skin conditions, and intra-articular injection for joint inflammation. Systemic IM use (Kenalog 40 mg IM for severe allergy) is rare but would warrant ⚠️ for the systemic glucocorticoid considerations covered on the prednisone/dexamethasone pages.

Pembrolizumab and ketamine have no clinically significant interaction. Most-prescribed checkpoint inhibitor; used across many cancer types. The immune-related adverse events (colitis, hepatitis, pneumonitis, endocrinopathies) are intrinsic to checkpoint inhibition and require their own monitoring — unchanged by KAP.

L-arginine and ketamine have no clinically significant interaction. As a nitric oxide (NO) precursor via the NOS pathway, arginine produces mild vasodilation — commonly used in supplements for 'pump,' circulation, and erectile function. The vasodilatory effect is modest and short-lived; clinically meaningful interaction with ketamine's transient pressor effect is unlikely. The well-known interaction worth flagging — high-dose arginine plus PDE5 inhibitors (sildenafil, tadalafil) can compound BP-lowering, and arginine is contraindicated post-MI in some literature — is independent of KAP.

L-Theanine and ketamine have no clinically significant interaction. Common in green tea and as a stand-alone supplement for calm focus. Continue as you normally would.

Oral terbinafine and ketamine have no clinically significant interaction. Different mechanism from the azole antifungals (fluconazole, itraconazole, ketoconazole) — terbinafine inhibits a fungal squalene epoxidase rather than CYP51. From a drug-interaction standpoint, terbinafine is a CYP2D6 inhibitor, which matters for metoprolol, propranolol, TCAs, codeine, tamoxifen, and other CYP2D6 substrates — but ketamine is primarily metabolized by CYP3A4 and CYP2B6 with only minor CYP2D6 contribution, so terbinafine's effect on ketamine is minimal. Hepatotoxicity monitoring during long courses (LFTs at baseline) is intrinsic to terbinafine.

Digoxin and ketamine have no clinically significant interaction. The well-known digoxin precautions (narrow therapeutic index, drug interactions affecting blood levels) are unchanged by KAP.

Insulin and ketamine have no clinically significant interaction. The practical consideration: KAP sessions involve fasting (typically 4-6 hours before) which changes the usual insulin dose-to-food relationship. Long-acting basal (Lantus, Tresiba, Levemir, Toujeo) typically continues normally. Mealtime rapid-acting (Humalog, Novolog, Apidra, Fiasp) you'll often hold for the pre-session fast and resume with the post-session meal. We work directly with your endocrinologist on the specific plan and never adjust insulin without your prescriber.

Maca and ketamine have no clinically significant interaction. Maca is a Peruvian root used for energy, libido, and mood; the mechanism is incompletely understood but the supplement is well-tolerated at typical doses (1.5-3 g/day).

Levofloxacin and ketamine have no clinically significant interaction. Same compatibility profile as ciprofloxacin. The fluoroquinolone-specific cautions (QT prolongation, tendon rupture, peripheral neuropathy in rare cases) are intrinsic to the drug class and independent of KAP; ketamine itself is not a meaningful QT-prolonging drug at psychiatric doses.

At standard doses (5-20 mg/day), Lexapro is one of the most common medications our patients are already taking when they start ketamine. There's no pharmacologic conflict, no required washout, and no special precaution beyond standard intake review. Most patients continue Lexapro throughout the ketamine course; published evidence specific to escitalopram + ketamine (Hu et al. 2016) showed faster suicidality reduction when ketamine was added, with no safety concerns.

Atorvastatin and ketamine have no clinically significant interaction. Statins are commonly on board for KAP patients with cardiovascular risk and do not change session planning.

Metoprolol and ketamine are compatible. Beta blockers actually blunt the transient BP and HR rise that ketamine produces, which is usually a wash or mildly favorable for cardiovascular tolerability. No special precaution needed.

Topical and vaginal clotrimazole and ketamine have no clinically significant interaction. Common for athlete's foot, jock itch, ringworm (Lotrimin AF), and vaginal yeast infections (Gyne-Lotrimin). Different from oral fluconazole — the topical/vaginal route has minimal systemic absorption, so the CYP3A4 inhibition concern that applies to oral azoles doesn't apply here. Troches (oral lozenges, Rx) are used for oral thrush but still have low systemic exposure.

Enoxaparin and ketamine have no clinically significant interaction. Common post-surgical DVT prophylaxis and treatment, pregnancy-related anticoagulation, and bridging therapy. Subcutaneous self-injection at home. Same compatibility profile as the oral anticoagulants (warfarin, apixaban, rivaroxaban).

Topical bimatoprost and ketamine have no clinically significant interaction. Two indications, same molecule: Lumigan for glaucoma (drop in the eye) and Latisse for cosmetic eyelash growth (applied to the lash line with a brush). Same intrinsic considerations — iris darkening, lash growth (which is the desired effect for Latisse), periorbital fat atrophy. Not KAP-related.

Leuprolide and ketamine have no clinically significant interaction. Delivered as monthly to semi-annual depot injection across many uses: prostate cancer (with abiraterone, bicalutamide, or enzalutamide), endometriosis, uterine fibroids, central precocious puberty, IVF cycles, and as part of gender-affirming care. The intrinsic considerations — vasomotor symptoms in androgen/estrogen suppression, bone density effects with long-term use, initial testosterone or estrogen flare in the first weeks — are leuprolide-class concerns independent of KAP.

Lyrica is safe to combine with at-home ketamine therapy across its standard dose range (75-600 mg/day). Like gabapentin, Lyrica works on the alpha-2-delta subunit of voltage-gated calcium channels and does NOT bind GABA receptors, so the documented benzodiazepine attenuation of ketamine's antidepressant response does not apply. The Lyrica-specific notes are sedation timing at higher doses and the Schedule V controlled-substance status (slight DEA paperwork for refills, not a clinical issue).

Nitrofurantoin and ketamine have no clinically significant interaction. The standard UTI antibiotic; well-tolerated alongside KAP. Renally concentrated, which is why it works for UTI but doesn't treat systemic infections.

Magnesium and ketamine have no clinically significant interaction. Common for sleep, constipation, muscle cramps, or migraine prophylaxis. Continue as you normally would.

Green tea (and EGCG extracts) and ketamine have no clinically significant interaction at the polyphenol level. The practical question is the same as for any caffeine source: don't drink green tea within ~6 hours of a session (see our caffeine page for the full framing). High-dose EGCG extract supplements (≥800mg/day) carry hepatotoxicity warnings — that's an EGCG-class consideration independent of KAP. Brewed green tea has 25-50mg caffeine per cup vs coffee's 80-100mg — still enough to be relevant for session timing.

Chamomile and ketamine have no clinically significant interaction. Apigenin, chamomile's main flavonoid, has mild GABA-A receptor activity at very high concentrated extract doses, but tea-strength chamomile is well below any clinically relevant threshold. Continue as you normally would.

Cladribine and ketamine have no clinically significant interaction. Distinctive among MS DMTs for its short-course pulse dosing — two annual courses of 4-5 days each, with durable effect — rather than continuous therapy. The intrinsic considerations — lymphopenia monitoring, malignancy surveillance, contraception requirements — are cladribine-class issues independent of KAP.

Glecaprevir-pibrentasvir (Mavyret) and ketamine have no clinically significant interaction. Pangenotypic direct-acting antiviral combination — 8-12 weeks of oral therapy with high cure rates across HCV genotypes. The intrinsic interaction worth knowing about — Mavyret is contraindicated with rifampin and atazanavir-based regimens, and has reduced efficacy with strong CYP3A4 inducers — is HCV-therapy specific and independent of KAP.

Rizatriptan and ketamine have no clinically significant interaction. The triptan-plus-serotonergic-drug serotonin syndrome concern was walked back by the American Headache Society 2018 position statement. With ketamine, which is not meaningfully serotonergic, the concern is essentially nil.

Lemon balm and ketamine have no clinically significant interaction. Mild calming effects via weak acetylcholinesterase inhibition and modest GABA activity. Standard culinary and tea-strength use is well-tolerated alongside KAP.

Psyllium and ketamine have no clinically significant interaction. The intrinsic consideration applies to ALL drugs taken orally with bulk fiber (not just ketamine): psyllium can bind some medications in the gut and reduce their absorption if taken too close together. Standard guidance is to space psyllium and oral medications by 2 hours either side. For at-home ketamine therapy, this affects oral troche or rapidly-dissolving formulations — discuss timing with us. Also used for cholesterol management and glycemic adjunct in T2DM. The classic 'never take it as a pill' rule (psyllium expands rapidly in the esophagus) is intrinsic and important.

Hydrochlorothiazide and ketamine have no clinically significant interaction. As a thiazide diuretic, HCTZ produces stable steady-state BP lowering rather than acute session-day fluctuations. The hydration suggestion is general good practice for any KAP patient, not HCTZ-specific.

Minocycline and ketamine have no clinically significant interaction. Same tetracycline-class compatibility as doxycycline. Common long-term for acne and rheumatoid arthritis. Vestibular side effects (dizziness, vertigo) at higher doses are intrinsic to minocycline and worth disclosing.

Polyethylene glycol (MiraLAX) and ketamine have no clinically significant interaction. Osmotic laxative that draws water into the bowel; minimal systemic absorption. Very safe across age groups including pediatric and pregnancy use. The intrinsic concern is electrolyte shifts only at high-volume bowel-prep doses (GoLYTELY for colonoscopy), not at standard MiraLAX dosing. Won't bind to oral medications meaningfully the way psyllium does.

Levonorgestrel IUDs and ketamine have no clinically significant interaction. The IUD releases progestin locally with minimal systemic absorption, much lower than oral progestins. Continue your contraception as you normally would.

Vitamin K2 and ketamine have no clinically significant interaction. The well-known vitamin K caveat is warfarin: vitamin K antagonizes warfarin's effect (lowers INR), which matters for any anticoagulated patient — independent of KAP. K2 has milder warfarin antagonism than K1 (the form abundant in leafy greens), but still worth disclosing to your anticoagulation clinic.

Meloxicam and ketamine have no clinically significant interaction. Compatible with KAP. Standard NSAID renal/GI cautions apply.

Topical and vaginal miconazole and ketamine have no clinically significant interaction. Same framework as clotrimazole — local application bypasses the CYP3A4-inhibition concern that applies to oral azoles like fluconazole. Common as Monistat (vaginal yeast) and Desenex (athlete's foot).

Fosfomycin and ketamine have no clinically significant interaction. Single-sachet oral dose for uncomplicated UTI in women — useful alternative when nitrofurantoin or Bactrim isn't appropriate. One-and-done dosing means no ongoing PK considerations.

Tirzepatide and ketamine have no clinically significant interaction. Mounjaro (diabetes) and Zepbound (chronic weight management) are the same molecule with different FDA-approved indications, and both work fine alongside ketamine-assisted psychotherapy. The dual GIP and GLP-1 receptor agonism doesn't change the picture — both target receptors are in peripheral metabolic tissue, not in the central pathways ketamine acts on. The practical considerations are identical to semaglutide: GI side effects (nausea, slowed gastric emptying) can compound with session-day jitters, so we plan around dose-escalation windows and pre-medicate with ondansetron when appropriate.

Guaifenesin and ketamine have no clinically significant interaction. The expectorant ingredient in plain Mucinex (and the 'plain' versions of Robitussin and Tussin). It thins mucus, doesn't suppress cough, and has minimal systemic effects. Note: combo products like Mucinex DM (with dextromethorphan), Mucinex D (with pseudoephedrine), and Robitussin DM each have a second ingredient that may carry its own considerations — see the individual ingredient pages. Plain guaifenesin alone is benign.

Ethambutol and ketamine have no clinically significant interaction. Part of the standard four-drug TB initial-phase regimen (with isoniazid, rifampin, pyrazinamide). The drug-specific monitoring concern is dose-dependent optic neuritis — patients get baseline and periodic visual acuity and color-vision testing — that's intrinsic, not KAP-related. The KAP considerations are with the rifampin and isoniazid co-treatment, not ethambutol itself.

Inositol and ketamine have no clinically significant interaction. Common for OCD, panic disorder, PCOS, and general anxiety. Continue as you normally would.

NAC and ketamine have no clinically significant interaction. NAC has growing interest as a psychiatric adjunct for OCD, trichotillomania, and substance use disorders due to its glutamatergic modulation, though the evidence base is still developing. Compatible with KAP.

Melatonin and ketamine have no clinically significant interaction. Melatonin is mildly sedating at typical 0.5-3 mg doses; the overlap with ketamine session sedation is small.

Topical Neosporin and ketamine have no clinically significant interaction. The 3-antibiotic ointment (bacitracin + neomycin + polymyxin B) for minor cuts and scrapes. The intrinsic consideration worth knowing — neomycin allergy is relatively common (~10% of long-term users develop contact dermatitis), and if you've ever had a reaction to Neosporin, Polysporin (no neomycin) is a safer choice. None of this is KAP-related.

Rotigotine and ketamine have no clinically significant interaction. Distinctive among dopamine agonists for its transdermal patch delivery — provides 24-hour stable plasma levels, useful for patients with dysphagia or fluctuations on oral therapy. Same dopamine-agonist class concerns as ropinirole and pramipexole (impulse-control disorders, sleep attacks). Skin reactions at application site are intrinsic; rotate sites daily.

Gabapentin is safe to combine with at-home ketamine therapy across its standard dose range (100-3600 mg/day depending on indication). Despite the name, gabapentin does not act on GABA receptors and does not share the GABA-A binding that drives the documented benzodiazepine attenuation of ketamine's antidepressant response. Gabapentin works on the alpha-2-delta subunit of voltage-gated calcium channels and is most commonly prescribed for neuropathic pain, focal seizure prophylaxis, anxiety, restless legs syndrome, and off-label insomnia. The gabapentin-specific note is sedation timing for daytime ketamine sessions at higher doses.

Esomeprazole and ketamine have no clinically significant interaction. Esomeprazole is the S-enantiomer of omeprazole — same PPI class, same compatibility profile.

Nexplanon and ketamine have no clinically significant interaction. The subdermal implant releases etonogestrel slowly for up to 3 years. Continue as normal.

Niacin and ketamine have no clinically significant interaction. At RDA doses (~16 mg) there's zero concern. At lipid-modifying doses (500-2000 mg), niacin causes flushing and modest BP fluctuation, but those are niacin's own dose-dependent effects, not a stacking interaction with ketamine. Take at a time of day that doesn't overlap with a session if flushing is bothersome.

Amlodipine and ketamine have no clinically significant interaction. Amlodipine is a dihydropyridine CCB with no CYP3A4 effect (unlike its non-DHP cousins diltiazem and verapamil), no QT effect, and no CNS overlap. Its long half-life (30-50 hours) produces stable BP throughout any session. The BP check we do during sessions is standard for every patient regardless of medication, not amlodipine-specific.

Mepolizumab and ketamine have no clinically significant interaction. Used for severe eosinophilic asthma, eosinophilic granulomatosis with polyangiitis, and hypereosinophilic syndrome. Same clean biologic profile.

Rimegepant and ketamine have no clinically significant interaction. As a CGRP antagonist, Nurtec avoids the serotonergic concern that applies to triptans. Good migraine option for KAP patients.

Ocrelizumab and ketamine have no clinically significant interaction. The anti-CD20 mAb of choice for MS (both relapsing-remitting and primary-progressive). IV infusion every 6 months. Same clean biologic profile as rituximab and the other anti-CD20s.

Cefdinir and ketamine have no clinically significant interaction. Common pediatric and adult oral cephalosporin for ear, sinus, and respiratory infections. The cosmetic red-stool reaction (from iron supplements binding cefdinir-iron complex in stool) is harmless and intrinsic.

Nivolumab and ketamine have no clinically significant interaction. Same checkpoint-inhibitor class as pembrolizumab; used for melanoma, renal cell, lung, and other cancers. Often combined with ipilimumab (CTLA-4 inhibitor) for melanoma. Immune-related adverse events are intrinsic and require their own monitoring.

Abatacept and ketamine have no clinically significant interaction. Used for moderate-to-severe rheumatoid arthritis, juvenile idiopathic arthritis, psoriatic arthritis, and as acute GVHD prophylaxis in hematopoietic stem cell transplant. Subcutaneous weekly or IV monthly. Same clean biologic profile as the other immunology mAbs; lower infection risk than TNF blockers in some comparisons.

Glucosamine and chondroitin and ketamine have no clinically significant interaction. Common for osteoarthritis; modest evidence for symptom relief but a clean drug-interaction profile. Old anecdotal reports of warfarin INR shift are not robust.

Semaglutide and ketamine have no clinically significant interaction. Whether you take it as Wegovy for chronic weight management, Ozempic by injection for type 2 diabetes, or Rybelsus as the oral tablet, KAP proceeds without medication changes. The two drug classes act on entirely separate systems — semaglutide at peripheral GLP-1 receptors, ketamine at central NMDA glutamate receptors — so there's no pharmacokinetic overlap, no shared metabolism, and no additive CNS or cardiovascular effect to plan around. The practical considerations are GI-side, not interaction-side: GLP-1 nausea and slowed gastric emptying can compound with session-day nerves if not anticipated. We coordinate session timing around dose-escalation windows when nausea is highest, and we'll pre-medicate with ondansetron for patients prone to motion-sensitive nausea.

Passionflower and ketamine have no clinically significant interaction. Used for mild anxiety and sleep, often combined with valerian or chamomile in OTC preparations. The mild GABAergic activity is well below the threshold for clinically meaningful sedation stacking with ketamine.

Olopatadine and ketamine have no clinically significant interaction. OTC since 2020 as Pataday (was prescription Patanol). Once-daily allergy eye drops for itching from seasonal/perennial allergies. The intranasal form (Patanase) is also fully compatible. Local delivery means none of the sedation, anticholinergic effects, or systemic considerations of oral antihistamines.

At standard doses (10-60 mg/day), Paxil is safe to combine with at-home ketamine therapy. The SSRI evidence base applies in full: no required washout, no special precaution beyond standard intake review. The paroxetine-specific consideration is not safety but withdrawal: paroxetine has the shortest half-life among SSRIs (about 21 hours) and the most severe documented discontinuation syndrome. This is the SSRI you absolutely should not stop to start ketamine; abrupt discontinuation produces a multi-week withdrawal course that would confound any early ketamine assessment.

Penicillin VK and ketamine have no clinically significant interaction. Standard oral penicillin for strep throat, rheumatic fever prophylaxis, and other gram-positive infections. Clean drug-interaction profile.

Famotidine and ketamine have no clinically significant interaction. H2 blockers like Pepcid are commonly on board and do not change session planning.

Bismuth subsalicylate and ketamine have no clinically significant interaction. The salicylate component is mild and at standard OTC doses doesn't contribute meaningful anti-platelet activity. Black stools and black tongue are harmless cosmetic side effects of bismuth itself.

Levonorgestrel and ketamine have no clinically significant interaction. The same molecule is used in emergency contraception (Plan B and equivalents), IUDs (Mirena, Kyleena, Skyla, Liletta), and as a progestin component of combined oral contraceptives. No meaningful CYP interaction with ketamine across any delivery route. The well-known interaction worth flagging is the *opposite* direction: strong CYP3A4 inducers (rifampin, phenytoin, carbamazepine, St John's wort) can reduce levonorgestrel efficacy as emergency contraception — that's an EC conversation independent of KAP.

Hydroxychloroquine and ketamine have no clinically significant interaction. The earlier framing here flagged QT prolongation, but ketamine at psychiatric (subanesthetic) doses is not a meaningful QT-prolonging drug in the published literature. Hydroxychloroquine's own modest QT effect is independent of KAP. Maintain your usual ophthalmology screening for retinopathy.

Cisplatin and ketamine have no clinically significant interaction. One of the most active chemotherapy agents — backbone in testicular cancer (curative), and used across many solid tumors. The intrinsic considerations — nephrotoxicity (managed with aggressive hydration), severe nausea/vomiting (managed with NK1 + 5HT3 + dexamethasone), peripheral neuropathy, and ototoxicity — are platinum-class concerns. The neuropathy can complicate KAP sensory assessment, similar to paclitaxel.

Clopidogrel and ketamine have no clinically significant interaction. Patients on Plavix after stent placement or for secondary stroke prevention proceed with KAP without medication changes.

Dabigatran and ketamine have no clinically significant interaction. Same compatibility profile as the factor Xa inhibitor DOACs (apixaban, rivaroxaban).

Pravastatin and ketamine have no clinically significant interaction. Specifically, pravastatin is the cleanest statin from a drug-interaction standpoint: it's hydrophilic, doesn't go through CYP3A4 metabolism (renally cleared with sulfation), and bypasses the CYP3A4 inhibitor concerns that complicate atorvastatin and simvastatin. For patients on KAP plus any CYP3A4 modulator (clarithromycin, Paxlovid, etc.), pravastatin is often the preferred statin.

Conjugated estrogens (Premarin) and ketamine have no clinically significant interaction. Long-standing oral HRT — replaced in many practices by transdermal estradiol because of higher VTE risk with oral estrogens (first-pass hepatic effect on clotting factors). The intrinsic VTE risk, breast tissue effects, and combined-product progestin considerations (Prempro = conjugated estrogens + medroxyprogesterone) are estrogen-class concerns, not KAP issues.

Lansoprazole and ketamine have no clinically significant interaction. Same PPI-class compatibility as omeprazole, pantoprazole, and esomeprazole. Available OTC.

Omeprazole and ketamine have no clinically significant interaction. PPIs are commonly on board for KAP patients with GERD and do not change session planning.

Trimethoprim and ketamine have no clinically significant interaction. Trimethoprim alone (not paired with sulfamethoxazole as in Bactrim) is used for UTI prophylaxis in sulfa-allergic patients. Same clean profile as the TMP component of Bactrim.

Ampicillin and ketamine have no clinically significant interaction. Same family as amoxicillin with similar coverage but lower oral bioavailability — more commonly used IV in hospital settings. Outpatient oral ampicillin is less common today.

Lisinopril and ketamine have no clinically significant interaction. ACE inhibitors have no CYP overlap, no QT effect, no CNS depression. The BP measurement at the start and end of a session is standard for every KAP patient, not specific to ACE-inhibitor users. Continue your medication as normal.

Nifedipine and ketamine have no clinically significant interaction. Important distinction: nifedipine is a dihydropyridine CCB (same family as amlodipine), which means it's a CYP3A4 SUBSTRATE but NOT a meaningful CYP3A4 inhibitor — unlike the non-dihydropyridines (diltiazem, verapamil) where CYP3A4 inhibition is the relevant KAP consideration. Common use in pregnancy hypertension and Raynaud's phenomenon.

Tacrolimus and ketamine have no direct clinically significant interaction. Tacrolimus is a narrow-therapeutic-index CYP3A4 substrate, which sounds alarming — but ketamine is also a CYP3A4 substrate without inhibitor or inducer activity, so the substrate-substrate combination doesn't shift either drug's level. The real interaction concern with tacrolimus is third-party drugs in the stack: strong CYP3A4 inhibitors (clarithromycin, fluconazole, Paxlovid, grapefruit) raise tacrolimus toxicity, and CYP3A4 inducers (rifampin, phenytoin, carbamazepine) drop it to rejection-risk levels. Those conversations apply to tacrolimus independent of KAP. Topical tacrolimus (Protopic) for eczema has even less systemic exposure.

Denosumab and ketamine have no clinically significant interaction. Prolia (60 mg every 6 months for osteoporosis) and Xgeva (120 mg monthly for cancer-related bone events) have the same clean biologic profile — no CYP, no small-molecule interaction surface.

Progesterone and ketamine have no clinically significant interaction. Micronized progesterone is mildly sedating when taken at bedtime, which is intentional; the sedation window does not typically overlap with morning sessions.

Pantoprazole and ketamine have no clinically significant interaction. Same compatibility profile as omeprazole.

Medroxyprogesterone and ketamine have no clinically significant interaction. Used as oral Provera (cyclic HRT progestin, abnormal uterine bleeding) and as Depo-Provera (long-acting injectable contraception every 12-13 weeks). The intrinsic considerations — bone density decline with long-term Depo use, return-to-fertility delay after discontinuation, mood and weight effects — are progestin-class issues independent of KAP.

Modafinil and ketamine have no clinically significant interaction. Modest CYP3A4 induction is minimal at standard doses; cardiovascular effects are much smaller than amphetamine stimulants. We may ask you to skip the dose on session days for the same general reason we do with any stimulant, not because of a ketamine-specific concern.

At standard doses (10-80 mg/day, most patients on 20-40 mg), Prozac is one of the most prescribed SSRIs and one of the safest combinations with at-home ketamine. The SSRI evidence base applies in full: no required washout, no special precaution beyond standard intake review. Two fluoxetine-specific notes worth knowing: fluoxetine moderately inhibits CYP3A4 and ketamine is partly CYP3A4-metabolized, so theoretical pharmacokinetic slowing is possible (rarely clinically meaningful at sublingual doses), and the long half-life (active metabolite norfluoxetine 7-9 days) means recent dose changes need 8-10 weeks of stability before adding ketamine, slightly longer than other SSRIs.

Budesonide and ketamine have no clinically significant interaction. Used for asthma, allergic rhinitis, eosinophilic esophagitis, and inflammatory bowel disease.

6-Mercaptopurine and ketamine have no clinically significant interaction. Used in acute lymphoblastic leukemia maintenance therapy and as a steroid-sparing agent in Crohn's disease and ulcerative colitis. Identical interaction profile to azathioprine — never combine with allopurinol or febuxostat at full dose (xanthine oxidase inhibition causes severe toxicity). TPMT testing is standard.

Vitamin B6 and ketamine have no clinically significant interaction. The chronic-high-dose B6 neuropathy concern (typically >200 mg/day for months) is intrinsic to pyridoxine excess, not a KAP interaction. Standard multivitamin and morning-sickness doses (10-100 mg) are well below that threshold.

Atogepant and ketamine have no clinically significant interaction. Same family as rimegepant and ubrogepant — oral CGRP receptor antagonists, but atogepant is dosed daily for prevention rather than as-needed for acute attacks. CYP3A4 substrate, so strong CYP3A4 inhibitors lower the recommended dose (intrinsic to atogepant, not a KAP issue).

Beclomethasone and ketamine have no clinically significant interaction. Older single-agent inhaled corticosteroid (QVAR) alternative to combination ICS+LABA inhalers (Advair, Symbicort, Breo). Also available as intranasal Beconase AQ for allergic rhinitis. Inhaled and nasal delivery routes have minimal systemic exposure. The thrush prevention (rinse mouth after dosing) is intrinsic.

Zoledronic acid and ketamine have no clinically significant interaction. The once-yearly IV infusion produces an acute-phase reaction in many patients (flu-like symptoms, low-grade fever, bone/muscle pain) for 1-3 days after infusion — that's intrinsic to bisphosphonate IV dosing, not a KAP issue. We just schedule KAP outside that window.

Metoclopramide and ketamine have no clinically significant interaction. The well-known metoclopramide concerns (acute dystonia, akathisia, tardive dyskinesia with chronic use) are intrinsic to the medication and unchanged by KAP. Continue as prescribed and tell us about any movement-disorder symptoms at intake.

Eletriptan and ketamine have no clinically significant interaction. Some practitioners prefer eletriptan as one of the more efficacious triptan options for acute migraine. The intrinsic interaction to flag — eletriptan is a CYP3A4 substrate, so strong CYP3A4 inhibitors (clarithromycin, Paxlovid, ritonavir, voriconazole) raise eletriptan levels and increase eletriptan side effect risk. That's an eletriptan dose conversation, not a ketamine one. Same updated SS framing as the other triptans.

At standard doses (15-45 mg at bedtime), mirtazapine is safe to combine with at-home ketamine therapy. The serotonergic activity is modest (mirtazapine antagonizes 5-HT2 and 5-HT3 receptors rather than inhibiting serotonin reuptake), and the published case literature contains no serotonin syndrome events from at-home ketamine plus standard-dose mirtazapine. The two mirtazapine-specific intake notes are sedation timing for daytime ketamine sessions and the dose-paradoxical sedation profile (more sedating at 15 mg than at 30-45 mg, because noradrenergic activation at higher doses offsets the antihistamine effect).

Infliximab and ketamine have no clinically significant interaction. IV infusion every 6-8 weeks at infusion centers. Common for Crohn's disease, ulcerative colitis, rheumatoid arthritis, psoriasis, and ankylosing spondylitis. Same clean profile as adalimumab and etanercept.

Ropinirole and ketamine have no clinically significant interaction. Common dopamine agonist for early Parkinson's disease and restless legs syndrome. The famous safety consideration — impulse-control disorders (compulsive gambling, hypersexuality, binge eating, shopping) that develop in a subset of patients on dopamine agonists — is intrinsic and important to screen for. Doesn't change with KAP. Sudden-onset sleep attacks are a less-common but real intrinsic risk.

Resveratrol and ketamine have no clinically significant interaction at typical OTC doses (250-500 mg/day). The polyphenol shows modest CYP3A4 inhibition in vitro and at very high biohacker doses (1-2 g/day) the inhibition becomes potentially relevant for some CYP3A4 substrates. At standard supplement use the clinical effect on ketamine is negligible.

Topical tretinoin and ketamine have no clinically significant interaction. Gold-standard prescription retinoid for acne and photoaging. The intrinsic considerations — initial 'retinization' irritation (redness, peeling, dryness for 4-8 weeks), photosensitivity, pregnancy contraindication — are tretinoin-class issues unrelated to KAP. Different from oral isotretinoin (which has its own dedicated page) — the topical route has negligible systemic exposure.

Lasmiditan and ketamine have no clinically significant interaction. The newer 'ditan' class is selective for 5HT1F receptors (no 1B/1D activity), which eliminates the vasoconstrictor concerns that limit triptans in cardiovascular disease and substantially reduces theoretical serotonin syndrome stacking compared to non-selective serotonergics. CNS side effects (dizziness, somnolence) are prominent — the 8-hour driving prohibition after each dose is intrinsic to lasmiditan and unrelated to KAP, though obviously relevant if a dose is taken close to a session.

Rituximab and ketamine have no clinically significant interaction. One of the most-prescribed biologics across oncology and rheumatology; IV infusion typically every 6 months to 2 years depending on indication. Same clean monoclonal-antibody profile as the other biologics.

Ceftriaxone and ketamine have no clinically significant interaction. Common as a single intramuscular dose for STIs (gonorrhea), Lyme disease, and outpatient infection treatment. Also given IV in hospital for serious infections. No KAP-specific concern.

Topical minoxidil (Rogaine 2% and 5%) and ketamine have no clinically significant interaction. Topical use has minimal systemic absorption — the rare reports of scalp-applied minoxidil causing systemic effects are usually very-large-area application or oral ingestion. Intrinsic considerations are scalp irritation, the well-known initial 'shedding phase' (paradoxical hair loss during the first 2-4 weeks, then improvement), and unwanted facial hair from spray drift. Oral minoxidil (Loniten — reserved for refractory severe hypertension, or the increasingly popular off-label low-dose oral minoxidil for hair loss at 1-5mg) is a different conversation — meaningful BP-lowering effect that may stack with ketamine's transient pressor response, plus pericardial effusion risk at higher doses.

Ramelteon and ketamine have no clinically significant interaction. As a melatonin-receptor agonist, ramelteon avoids the GABAergic and antihistaminic effects of benzodiazepines and Z-drugs. Lighter interaction footprint than most sleep agents.

SAM-e and ketamine have no clinically significant interaction. SAM-e has mild antidepressant effects via methylation pathways. The serotonergic combination concern is with prescription SSRIs/SNRIs/MAOIs, not ketamine. Don't start SAM-e during active SSRI or MAOI therapy without your prescriber's involvement.

Elderberry and ketamine have no clinically significant interaction. Common as syrup, gummies, or lozenges for cold/flu prevention. Note that raw or unripe elderberry is toxic — commercial products are processed to remove the toxic glycosides.

Edoxaban and ketamine have no clinically significant interaction. Once-daily DOAC for non-valvular AFib stroke prevention and VTE treatment/prevention. Same compatibility profile as the other DOACs (apixaban, rivaroxaban, dabigatran). Notable distinction worth flagging — edoxaban is contraindicated in non-valvular AFib patients with CrCl > 95 mL/min (reduced efficacy compared to warfarin in this subgroup); that's an edoxaban-specific consideration unrelated to KAP.

Senna and ketamine have no clinically significant interaction. Plant-derived stimulant laxative. The intrinsic concerns — abdominal cramping with overuse, potassium loss with chronic high-dose use, and melanosis coli (brown colon discoloration, harmless and reversible) — are senna-class issues independent of KAP. Common in opioid-induced constipation protocols where it's often combined with docusate.

Sevoflurane and ketamine are compatible in clinical use. This question typically arises around surgical procedures rather than ambulatory KAP: anesthesiologists routinely combine ketamine (as analgesic adjunct, dissociative induction, or pediatric premedication) with sevoflurane as the maintenance inhaled agent without specific interaction concerns. Both contribute to anesthetic depth in additive fashion that the OR team manages. There's no implication for the outpatient ketamine therapy context — if you're scheduled for surgery, disclose your KAP regimen to your anesthesiologist so they can plan dosing.

Colloidal silver and ketamine have no pharmacologic interaction. The reason this gets specific framing rather than a one-line SAFE: colloidal silver has no recognized medical benefit (the FDA has issued warning letters to manufacturers making medical claims since 1999), and chronic use causes argyria — a permanent blue-gray discoloration of skin and mucous membranes from silver deposition. That's a colloidal-silver-specific concern, completely independent of KAP. We don't recommend colloidal silver for any indication; if you're using it, we'd rather know about it than not, and we'd point you toward evidence-based alternatives for whatever you're treating.

Milk thistle (silymarin) and ketamine have no clinically significant interaction. In vitro studies show silymarin can inhibit CYP3A4, CYP2C9, and P-gp — but the in vivo human studies at typical supplement doses (150-450 mg silymarin daily) consistently show no clinically meaningful effect on drug pharmacokinetics. Used by many patients for liver support (alcohol use, hepatitis, mushroom poisoning prevention). The intrinsic considerations are mild GI upset and allergic reactions in patients sensitive to the Asteraceae family (ragweed, marigold).

Golimumab and ketamine have no clinically significant interaction. Subcutaneous monthly injection (Simponi) or IV every-8-week infusion (Simponi Aria) for RA, psoriatic arthritis, ankylosing spondylitis, and ulcerative colitis. Same clean TNF-α mAb profile as adalimumab, etanercept, infliximab, and certolizumab.

Montelukast and ketamine have no pharmacokinetic interaction. The reason this gets specific framing rather than a one-line SAFE: montelukast carries an FDA black-box warning (added 2020) for neuropsychiatric effects including agitation, depression, sleep disturbance, suicidal ideation, and behavior changes. That warning is intrinsic to montelukast and unchanged by KAP — but it matters for KAP outcome interpretation. If your mood is worsening on montelukast and you're trying to assess KAP response, we need to separate signal from noise. Many allergy and asthma alternatives exist (inhaled corticosteroids, antihistamines, allergen immunotherapy) — a conversation worth having with your prescriber, independent of KAP.

Risankizumab and ketamine have no clinically significant interaction. Like guselkumab, targets the p19 subunit of IL-23 with the same clean profile. Used for plaque psoriasis, psoriatic arthritis, Crohn's disease, and ulcerative colitis. Subcutaneous injection every 12 weeks after loading — one of the longest dosing intervals in the biologic space.

Tamoxifen and ketamine have no clinically significant interaction. The CYP2D6 issue with certain SSRIs reducing tamoxifen's active metabolite is a tamoxifen-and-SSRI concern, not a tamoxifen-and-ketamine concern; mention it to your oncologist, not us. Continue tamoxifen as prescribed.

Sofosbuvir-based regimens and ketamine have no clinically significant interaction. The modern direct-acting antiviral regimens (Harvoni, Epclusa, Mavyret) are short cure courses — typically 8-12 weeks — with clean profiles compared to the older interferon-based therapies they replaced. No meaningful CYP3A4 modulation at therapeutic doses.

Tiotropium and ketamine have no clinically significant interaction. Inhaled LAMA preserves airway-targeted muscarinic blockade with minimal systemic absorption, so the anticholinergic side-effect profile is much lighter than oral anticholinergics. Continue your COPD/asthma maintenance therapy as prescribed.

Spirulina and ketamine have no clinically significant interaction. Nutrient-dense algae used as a protein and vitamin source. The primary safety concern with spirulina is microcystin contamination from poorly-sourced products — pick a reputable brand. No ketamine-specific concern.

Ustekinumab and ketamine have no clinically significant interaction. Same biologic class compatibility as the TNF-α inhibitors — no CYP, no small-molecule interaction surface.

Sunitinib and ketamine have no clinically significant direct interaction. Multikinase TKI used for renal cell carcinoma, gastrointestinal stromal tumors, and pancreatic neuroendocrine tumors. The intrinsic considerations — hypertension, cardiotoxicity (LV dysfunction), hand-foot syndrome, hypothyroidism — are multikinase TKI concerns independent of KAP.

Inhaled budesonide-formoterol and ketamine have no clinically significant interaction. Second-most-prescribed asthma/COPD combo inhaler after Advair. Same inhaled-delivery, low-systemic-exposure framework. Increasingly used as both maintenance and rescue therapy in the SMART (Single Maintenance And Reliever Therapy) approach for asthma.

Levothyroxine has no documented or theoretical interaction with ketamine. The thyroid hormone replacement pharmacology operates on a different biological axis (hypothalamic-pituitary-thyroid feedback) than the neurotransmitter systems ketamine affects; the medications don't compete for metabolism or share receptor targets. Continue your normal Levothyroxine dose throughout the ketamine course on the standard empty-stomach morning schedule. One clinically important note: untreated or undertreated hypothyroidism can produce depression-like symptoms, so we confirm a recent TSH level (within the past 12 months) at intake to make sure your thyroid is in target range and any symptoms attributable to hypothyroidism are being addressed.

Cimetidine and ketamine have no clinically significant interaction. Cimetidine is famous for inhibiting CYP1A2, CYP2C9, and CYP2D6 — leading to documented interactions with warfarin, theophylline, propranolol, TCAs, and phenytoin. But ketamine is metabolized primarily by CYP3A4 and CYP2B6, which cimetidine doesn't meaningfully affect. The big-named interactions are with other drugs, not KAP.

Osimertinib and ketamine have no clinically significant direct interaction. Standard of care for EGFR-mutant NSCLC. CYP3A4 substrate (a osimertinib concern around strong inhibitors/inducers — affects osimertinib levels, not ketamine). The intrinsic class effects — rash, diarrhea, paronychia, and the more serious pneumonitis and QT prolongation — are EGFR TKI considerations independent of KAP.

Ixekizumab and ketamine have no clinically significant interaction. Same IL-17A target as secukinumab (Cosentyx) with slightly different binding kinetics. Used for plaque psoriasis, psoriatic arthritis, ankylosing spondylitis, and non-radiographic axial spondyloarthritis. Subcutaneous injection — every 4 weeks after loading.

Oseltamivir and ketamine have no clinically significant interaction. The standard 5-day Tamiflu course for influenza or longer prophylactic use can continue alongside KAP. The practical question is usually whether you should run a session while you're sick with flu — that answer is separate from the Tamiflu interaction question (we usually defer the session until you feel well).

Feverfew and ketamine have no clinically significant interaction. Used for migraine prophylaxis with modest supporting evidence (Cochrane reviews place it 'possibly effective'). Mechanism is unclear but may involve mild serotonin modulation and platelet effects — theoretically relevant in patients on serotonergics or anticoagulants, but no clinical reports of meaningful interactions with ketamine. Common use is 50-100mg daily of standardized extract (MIG-99) or fresh leaf.

Methimazole and ketamine have no clinically significant interaction. The intrinsic concerns with methimazole are agranulocytosis (rare but potentially severe) and hepatotoxicity, both requiring routine lab monitoring — those are intrinsic, not KAP issues.

Erlotinib and ketamine have no clinically significant direct interaction. Largely supplanted by osimertinib for EGFR-mutant NSCLC but still in use. Same class side effect profile (rash, diarrhea, paronychia, ILD risk) and same CYP3A4 substrate caution that's about erlotinib levels, not ketamine.

Taurine and ketamine have no clinically significant interaction. Common as a single supplement and in energy drinks. The cardiovascular concerns associated with energy drinks come from the caffeine and sugar content, not taurine itself.

Paclitaxel and ketamine have no clinically significant interaction. Standard chemotherapy across many solid tumors, IV infusion every 1-3 weeks. The intrinsic considerations — infusion hypersensitivity reactions (pre-medication with steroids/diphenhydramine is standard), peripheral neuropathy, myelosuppression, alopecia — are paclitaxel-class issues independent of KAP. Worth noting that paclitaxel-induced peripheral neuropathy can complicate clinical assessment of dissociative sensations during KAP sessions.

Atenolol and ketamine are compatible. Functionally similar to metoprolol from an interaction standpoint: beta blockade dampens ketamine's transient pressor effect.

Chlorthalidone and ketamine have no clinically significant interaction. Same profile as hydrochlorothiazide, with a longer duration of action that produces steadier 24-hour BP control. Standard BP measurement applies to every KAP patient regardless.

Topical timolol eye drops and ketamine have no clinically significant interaction. Common first-line glaucoma therapy. Some systemic absorption can occur through nasolacrimal drainage — patients with asthma or bradyarrhythmia historically had concerns about systemic β-blocker effects from eye drops. Modern guidance: use punctal occlusion (close eyes and press inner corner for 30 sec after instilling) to maximize ocular and minimize systemic exposure. Different from oral timolol pharmacology by route.

Topical timolol eye drops and ketamine have no clinically significant interaction at standard glaucoma doses. Small amounts of systemic absorption can occur, but at intraocular treatment doses the effect is much smaller than oral beta blockers we already treat as SAFE.

Dolutegravir and ketamine have no clinically significant interaction. Backbone of many modern HIV single-tablet regimens (Triumeq, Dovato, Juluca) and standalone (Tivicay). Same clean interaction profile as bictegravir.

Ketorolac and ketamine have no clinically significant interaction. Most commonly used as IV/IM Toradol for acute pain (post-op, ER kidney stone, severe headache) — the 5-day duration limit is intrinsic to ketorolac's GI/renal toxicity profile, not a KAP concern. Sometimes used alongside KAP in pain medicine for opioid-sparing protocols.

Labetalol and ketamine have no clinically significant interaction. Like carvedilol, labetalol's combined alpha-1 and beta blockade actually opposes ketamine's transient sympathomimetic effect, smoothing the cardiovascular response. Commonly used for hypertensive urgency, pregnancy HTN, and pheochromocytoma management.

Scopolamine and ketamine have no clinically significant interaction. The 72-hour transdermal patch is common for cruise motion sickness and post-op nausea prevention. Anticholinergic effects (dry mouth, drowsiness, blurred vision, urinary retention in older adults) are intrinsic to scopolamine; ketamine doesn't have meaningful clinical anticholinergic activity (it actually causes hypersalivation).

Topical travoprost and ketamine have no clinically significant interaction. Once-daily evening eye drop, similar profile to latanoprost. The cosmetic effects — iris pigmentation darkening, eyelash growth/length, periorbital fat atrophy — are intrinsic prostaglandin-class effects, not KAP-related.

Guselkumab and ketamine have no clinically significant interaction. IL-23 inhibitor used for moderate-to-severe plaque psoriasis, psoriatic arthritis, and (newer indication) ulcerative colitis and Crohn's disease. Subcutaneous injection every 8 weeks after loading. Same clean biologic profile as the other immunology mAbs — no CYP interaction surface.

Methotrexate and ketamine have no clinically significant interaction. The standard methotrexate precautions (renal function, hepatotoxicity, marrow suppression monitoring, folic acid supplementation) are unchanged by KAP.

Tribulus and ketamine have no clinically significant interaction. Most commonly used as a 'natural testosterone booster' for athletic performance or libido — though the evidence for T-boosting in healthy men is weak to negative in controlled trials. The supplement itself is generally well-tolerated with no meaningful CYP modulation or PK/PD interaction with ketamine.

Fenugreek and ketamine have no clinically significant interaction. Most common uses: postpartum galactagogue (breastfeeding support), glycemic control adjunct in T2DM, and 'natural T-booster' claims. The intrinsic consideration is mild blood sugar lowering — if you're a diabetic on insulin or sulfonylureas, that's a glucose-monitoring conversation independent of KAP. Maple syrup-like body odor is a known harmless side effect. Allergic cross-reactivity with peanut and chickpea in sensitive individuals.

Dulaglutide (Trulicity) and ketamine have no clinically significant interaction. Trulicity is FDA-approved for type 2 diabetes only — it doesn't carry the suicidal-ideation warning that applied to the weight-loss-approved GLP-1s, because that FDA class rule covers only chronic weight management drugs acting on the CNS. The interaction profile with ketamine is identical to the rest of the GLP-1 receptor agonist class: peripheral mechanism, no shared metabolism, no central additive effects.

Topical dorzolamide and ketamine have no clinically significant interaction. Carbonic anhydrase inhibitor eye drop for glaucoma, often combined with timolol (Cosopt). Topical application has minimal systemic absorption — the systemic CA inhibitor concerns that apply to oral acetazolamide (metabolic acidosis, paresthesias) don't transfer to the eye drop.

L-Tryptophan and ketamine have no clinically significant interaction. Tryptophan is the upstream amino acid precursor to serotonin. The serotonin syndrome concern is when high-dose tryptophan is combined with prescription serotonergic agents, not when it's combined with ketamine alone.

Turmeric and ketamine have no clinically significant interaction. Common as culinary spice and concentrated supplement (curcumin extract with piperine for absorption). Very high supplemental doses have mild antiplatelet activity; relevant only if you're also on warfarin or other anticoagulants, and that consideration is independent of KAP.

Acetaminophen and ketamine have no clinically significant interaction. Tylenol is the analgesic we typically recommend first for post-session headache or aches.

Natalizumab and ketamine have no clinically significant interaction. Highly effective MS DMT for relapsing forms, also approved for Crohn's. The famous safety consideration — progressive multifocal leukoencephalopathy (PML) risk in JCV-seropositive patients on long-term therapy — is intrinsic and managed through the FDA TOUCH risk-mitigation program (mandatory JCV antibody testing, MRI surveillance). Has nothing to do with KAP. IV infusion every 4 weeks.

Ubrogepant and ketamine have no clinically significant interaction. Same family as rimegepant — oral CGRP receptor antagonists ('gepants') are a non-serotonergic alternative to triptans for acute migraine. CYP3A4 substrate, so strong CYP3A4 inhibitors (Paxlovid, clarithromycin, itraconazole) lower the allowed ubrogepant dose, but that's independent of KAP.

Valerian and ketamine have no clinically significant interaction. Used at bedtime as prescribed, its mild sedation doesn't carry into morning sessions. Same profile as melatonin.

Valacyclovir and ketamine have no clinically significant interaction. Used for genital and oral herpes, shingles, and suppressive therapy. Continue as prescribed.

Vancomycin and ketamine have no clinically significant interaction. Oral vancomycin (Vancocin, Firvanq) is essentially non-absorbed and used specifically for C. difficile colitis — bypasses any systemic interaction concern. IV vancomycin (typically inpatient for MRSA) requires renal-dose monitoring that's intrinsic to vancomycin, not a KAP issue.

Enalapril and ketamine have no clinically significant interaction. Same compatibility profile as lisinopril and other ACE inhibitors. Continue as normal; standard BP monitoring applies to every KAP patient regardless.

Solifenacin and ketamine have no clinically significant interaction. Bladder-selective compared to oxybutynin, so the systemic anticholinergic burden (dry mouth, cognitive, constipation) is somewhat less. Same intrinsic-not-stacking framework as the rest of the OAB anticholinergic class.

Doxycycline and ketamine have no clinically significant interaction. Common for acne, Lyme disease, malaria prophylaxis, and respiratory infections.

Liraglutide and ketamine have no clinically significant interaction. Victoza (type 2 diabetes) and Saxenda (chronic weight management) are the same molecule at different doses; both work fine alongside KAP. Saxenda was historically the first GLP-1 receptor agonist to carry a suicidal-ideation-and-behavior warning in its FDA labeling — a class requirement for chronic weight management drugs acting on the CNS — but the January 2026 FDA review found no causal link to suicidality and formally requested removal of the warning. The interaction profile for ketamine therapy is identical to the rest of the GLP-1 class.

Lacosamide and ketamine have no clinically significant interaction. Lacosamide is cleaner than older anticonvulsants on cognitive side effects and CYP interactions. Modest PR interval prolongation (not QT) is the medication's main cardiac signal and is independent of KAP.

Tenofovir and ketamine have no clinically significant interaction. Used for HIV treatment, HIV pre-exposure prophylaxis (PrEP — Truvada or Descovy), and hepatitis B. The two formulations differ in renal/bone safety profile (TAF is gentler than TDF) but neither has CYP overlap with ketamine. Continue PrEP or treatment as prescribed.

Collagen peptides and ketamine have no clinically significant interaction. Hydrolyzed collagen is digested down to constituent amino acids (mostly glycine, proline, hydroxyproline) and absorbed like any dietary protein. Continue as normal.

Diclofenac and ketamine have no clinically significant interaction. Voltaren gel is OTC for joint pain with essentially zero systemic absorption. Oral diclofenac is a standard NSAID with the usual GI and cardiovascular cautions intrinsic to the class.

Eptinezumab and ketamine have no clinically significant interaction. The IV-administered member of the CGRP-pathway monoclonal antibody class (erenumab, galcanezumab, fremanezumab are SC; eptinezumab is IV every 3 months). Same clean profile.

Ashwagandha and ketamine have no clinically significant interaction at typical OTC doses. Mild GABAergic and adaptogenic effects exist but don't stack meaningfully with ketamine. Same profile as rhodiola.

Latanoprost and ketamine have no clinically significant interaction. Once-daily evening eye drop for glaucoma (open-angle and ocular hypertension). Local delivery with negligible systemic absorption. The cosmetic side effects (eyelash growth, iris pigmentation darkening) are intrinsic to the prostaglandin class.

Rivaroxaban and ketamine have no clinically significant interaction. Same compatibility profile as apixaban.

Tofacitinib and ketamine have no direct clinically significant interaction. The oral JAK inhibitor class (tofacitinib, baricitinib, upadacitinib) carries an FDA black-box warning for increased risk of serious infections, MACE, cancer, thrombosis, and mortality compared to TNF inhibitors — this is intrinsic to JAK inhibition and well known to rheumatology. None of those concerns are changed by KAP. Tofacitinib is metabolized partly by CYP3A4 (so strong inhibitors raise its level — a tofacitinib dose conversation).

Rifaximin and ketamine have no clinically significant interaction. Although rifaximin is in the rifamycin family (rifampin, rifabutin), its <0.4% systemic absorption means the CYP3A4 induction that makes rifampin a 🟡 case-by-case drug doesn't apply here. Used for traveler's diarrhea, IBS with diarrhea, and hepatic encephalopathy.

Omalizumab and ketamine have no clinically significant interaction. Used for severe allergic asthma not controlled by inhalers, chronic spontaneous urticaria, and (newer indication) food allergy. The anaphylaxis warning on omalizumab itself is independent of KAP.

Lidocaine and ketamine have no clinically significant interaction at the doses patients typically encounter. Topical 5% patches for postherpetic neuralgia and OTC creams have minimal systemic absorption. Dental and procedural local infiltration is brief and self-limited. IV lidocaine (rare, for ventricular arrhythmia or some chronic pain protocols) is hospital-context. None of these create a meaningful KAP interaction.

Combined oral contraceptives and ketamine have no clinically significant interaction. KAP does not affect contraceptive efficacy, and OCPs do not affect ketamine response.

Drospirenone-containing contraceptives and ketamine have no clinically significant interaction. Unique among contraceptive progestins because of its spironolactone-analog structure — provides anti-androgenic and weak diuretic/K-sparing effects (improves acne and PMDD symptoms). The intrinsic considerations — modest hyperkalemia risk especially with ACE inhibitors, ARBs, K-sparing diuretics, or chronic NSAIDs — are drospirenone-class issues independent of KAP. Combined drospirenone-ethinyl estradiol OCs carry the same general VTE and CYP3A4-inducer considerations as other combined OCs.

Ethosuximide and ketamine have no clinically significant interaction. Primarily used for childhood absence seizures (the typical 'staring spells' epilepsy in school-age children); occasionally used in adults with the same seizure type. Clean PK with no clinically significant CYP modulation relevant to ketamine. Intrinsic considerations — GI upset, hiccups, rare blood dyscrasias requiring CBC monitoring — are unchanged by KAP.

Bisoprolol and ketamine have no clinically significant interaction. One of the four beta-blockers with proven HFrEF mortality benefit (with metoprolol succinate, carvedilol, and nebivolol). Beta-1 selective with smooth long-acting profile. Like other beta blockers, opposes ketamine's transient sympathomimetic effect.

Ezetimibe and ketamine have no clinically significant interaction. Often added when statin alone doesn't reach LDL goals, or used as a statin alternative in patients with statin intolerance.

Abacavir and ketamine have no clinically significant interaction. NRTI commonly used as a component of combination HIV therapy (Epzicom = abacavir + lamivudine; Triumeq = abacavir + lamivudine + dolutegravir). The famous safety consideration — abacavir hypersensitivity reaction in patients positive for HLA-B*5701 — is intrinsic, well-known to HIV providers, and requires pre-treatment genetic screening. None of this is KAP-relevant.

Zinc and ketamine have no clinically significant interaction. Standard doses (15-50 mg/day) are well-tolerated. Long-term high-dose zinc (>50 mg/day for months) can deplete copper and produce neurologic symptoms — that's intrinsic to zinc, not a KAP issue. Zinc lozenges for colds are fine.

Ginger and ketamine have no clinically significant interaction. Often used for nausea (pregnancy, motion sickness, post-anesthesia) — worth knowing about for KAP patients prone to session-related nausea. Concentrated supplemental doses have mild antiplatelet activity (relevant for anticoagulant users, independent of KAP).

Azithromycin and ketamine have no clinically significant interaction. Despite being a macrolide, azithromycin's CYP3A4 inhibition is much weaker than clarithromycin or erythromycin. The Z-Pak is fine to take during a KAP course.

Simvastatin and ketamine have no clinically significant interaction. Same compatibility profile as atorvastatin. Standard statin-myopathy precautions apply but are independent of KAP.

Ondansetron and ketamine have no clinically significant interaction. We sometimes recommend ondansetron prophylactically for post-session nausea. The well-known ondansetron QT precaution matters in patients with personal cardiac history, congenital long QT, or hypokalemia, but it's intrinsic to ondansetron, not a stacking concern with ketamine (which is not a meaningful QT-prolonging drug at psychiatric doses).

Goserelin and ketamine have no clinically significant interaction. Subcutaneous implant typically every 1 or 3 months. Same clean GnRH-agonist profile as leuprolide. Common alternative to leuprolide for prostate cancer (often combined with bicalutamide for combined androgen blockade) and used in premenopausal breast cancer.

At standard doses (25-200 mg/day), sertraline is one of the most common medications our patients are already taking when they start ketamine. There's no pharmacologic conflict, no required washout, and no special precaution beyond standard intake review. Most patients continue Zoloft throughout the ketamine course.

Zolmitriptan and ketamine have no clinically significant interaction. Same triptan framework as sumatriptan and rizatriptan. The historical concern about serotonergic stacking (FDA 2006 advisory) has been updated based on subsequent evidence; ketamine itself isn't a meaningful serotonergic agent, so the SS framing that applies to SSRIs doesn't transfer here. Use triptans as needed for migraine. Available as tablet, orally disintegrating tablet, and nasal spray.

Acyclovir and ketamine have no clinically significant interaction. Used for genital and oral herpes, shingles, and suppressive therapy — the IV form for hospitalized HSV encephalitis or severe disseminated infection. Continue as prescribed. Valacyclovir is the more bioavailable prodrug (covered separately) but the underlying interaction profile is identical.

Allopurinol and ketamine have no clinically significant interaction. Common chronic medication for gout and hyperuricemia prevention. Continue as normal.

Cetirizine and ketamine have no clinically significant interaction. Cetirizine is mildly sedating in some patients (more than loratadine, much less than diphenhydramine) but does not stack meaningfully with ketamine.

Abiraterone and ketamine have no clinically significant interaction. Used for metastatic castration-resistant and castration-sensitive prostate cancer, always co-administered with prednisone (5-10mg) to prevent mineralocorticoid excess. The intrinsic considerations — hypokalemia, fluid retention, hypertension, hepatotoxicity monitoring, and the mandatory glucocorticoid co-administration — are abiraterone-class concerns independent of KAP.

Stimulants and ketamine combine safely for ADHD plus depression patients when the stimulant is held on each ketamine session day. Both medications can transiently raise blood pressure and heart rate through different mechanisms, and combining them on the same day stacks that cardiovascular load unnecessarily. The pharmacologic concern has not produced documented case reports of harm at therapeutic doses, but at-home unmonitored is the setting where the timing rule matters most. The simple rule: skip your Adderall (or Vyvanse, or Ritalin) on session days; resume normally the next day.

Phentermine and ketamine are compatible with monitoring. Phentermine raises BP and HR meaningfully, often more than typical ADHD stimulants, and that stacks with ketamine's transient pressor effect. Baseline cardiovascular assessment matters.

Oxymetazoline and ketamine are compatible with monitoring. Two considerations: (1) intranasal α-agonist activity → mild systemic sympathomimetic effect when used heavily (multiple sprays per nostril per day). On a single-spray-per-side dose, the BP/HR impact is minimal; at heavy use it can stack with ketamine's transient pressor effect. (2) The classic 'don't use more than 3 days in a row' rule — using Afrin beyond 72 hours causes rebound congestion (rhinitis medicamentosa) that's worse than the original problem and can become a months-long dependency cycle. This is intrinsic to oxymetazoline and important regardless of KAP. For chronic nasal congestion, use fluticasone nasal or azelastine instead. Hold oxymetazoline on session day if you've been using it heavily.

Garlic and ketamine are compatible. Culinary garlic is fully fine. Concentrated supplemental garlic (aged garlic extract, garlic oil capsules) has measurable antiplatelet activity at higher doses — relevant for patients on warfarin, aspirin, or other anticoagulants, independent of KAP. Mild CYP3A4 effects have been reported but are clinically modest.

Methyldopa and ketamine are compatible. Two specifics: methyldopa is sedating like other central alpha-2 agonists (clonidine, guanfacine), which stacks with the session sedation window; and methyldopa has a well-documented depression side effect of its own, which can complicate distinguishing medication-induced low mood from baseline depression during KAP. Most commonly used for hypertension in pregnancy.

Ambien combines safely with at-home ketamine in the acute medical sense at therapeutic doses, but Z-drugs share the GABA-A benzodiazepine-receptor mechanism and are explicitly named alongside benzos in the Veraart 2021 systematic review's recommendation to minimize use during ketamine treatment. The good news is that Ambien's typical bedtime-only short-acting profile makes the operational fix simple: continue your bedtime dose, don't take Ambien within 8 hours before a daytime ketamine session, and consider whether the underlying insomnia is being driven by the depression that ketamine is treating (in which case the need for Ambien may decrease over the course of treatment).

Clomipramine is the most serotonergic TCA (functionally SSRI-like), which historically prompted serotonin syndrome monitoring with any ketamine combination. The Veraart 2021 systematic review specifically covering ketamine plus serotonergic antidepressants found no documented serotonin syndrome at therapeutic doses. We have stopped framing it that way. The real consideration is sedation — the one TCA effect that actually stacks with ketamine. The anticholinergic burden and QT effect are intrinsic to clomipramine, not ketamine stacks, but worth knowing for general clinical care.

Meclizine and ketamine are compatible. Meclizine is sedating, so as with other first-generation antihistamines, we plan sessions to avoid the peak sedation window.

Eslicarbazepine and ketamine are compatible with planning. Eslicarbazepine is the third-generation member of the carbamazepine/oxcarbazepine sodium channel blocker family, with cleaner kinetics than carbamazepine and a milder side effect profile. The CYP3A4 induction is modest — lighter than carbamazepine but real — which can slightly accelerate ketamine metabolism and modestly lower plasma levels. We may adjust KAP dose upward if you're on chronic eslicarbazepine; not as dramatic a change as with phenytoin or rifampin. Hyponatremia (like oxcarbazepine) is the intrinsic consideration to monitor independent of KAP.

Lorazepam and ketamine can be combined safely. The two issues we plan around: additive respiratory and CNS depression in the session window, and the well-documented effect of chronic benzodiazepine use blunting ketamine's antidepressant response. As-needed use is a smaller concern than daily standing doses.

Dutasteride and ketamine are compatible. Same considerations as finasteride with two differences: dutasteride inhibits both type 1 and type 2 5-alpha reductase (broader effect than finasteride which is mainly type 2), and the half-life is much longer (~5 weeks vs 5-6 hours). This means dutasteride remains active for months after the last dose. The post-treatment persistent depression / sexual dysfunction concerns mirror finasteride.

Rasagiline and ketamine are compatible with monitoring. At the prescribed Parkinson's dose (0.5-1mg daily), rasagiline's MAO-B selectivity is largely preserved, so the dietary tyramine ('cheese effect') and serotonin syndrome risks that define non-selective MAOIs (phenelzine, tranylcypromine — covered in the dedicated MAOI page) are dramatically lower. The residual theoretical concern with any MAO inhibitor plus ketamine warrants observation rather than avoidance. Worth flagging: the safety dose ceiling matters — at supratherapeutic doses MAO-B selectivity is lost and the picture changes.

Suvorexant and ketamine are compatible. The thing to plan around: suvorexant can produce next-morning sedation more reliably than Z-drugs or melatonin. Morning sessions on the day after a dose may overlap with residual effect.

Diphenhydramine and ketamine are compatible at typical OTC allergy doses (25-50 mg). The concern grows with high-dose or chronic use: diphenhydramine is strongly sedating and anticholinergic, and at high doses can contribute meaningfully to CNS and respiratory depression alongside ketamine. We do not recommend taking it on session day if at all avoidable.

Berberine and ketamine are compatible. The marketing hype around berberine as nature's Ozempic obscures a real pharmacology point: berberine is a moderate CYP3A4 inhibitor and can theoretically raise ketamine plasma levels. The effect is smaller than ritonavir or clarithromycin but worth disclosing.

Sotalol and ketamine are compatible. Sotalol has the highest intrinsic QT prolongation of any beta-blocker — which is why patients start it in a monitored hospital setting with EKG. That QT effect is sotalol's own; ketamine at psychiatric doses does not meaningfully add to QT per the published literature. The beta-blockade actually opposes ketamine's transient pressor effect, like other beta-blockers.

Clarithromycin and ketamine are compatible with timing awareness. Clarithromycin is a strong CYP3A4 inhibitor and the most potent macrolide for this interaction (azithromycin is much weaker, erythromycin sits between them). Courses are typically 7-14 days; we time sessions around the course.

Verapamil and ketamine are compatible. Same considerations as diltiazem: moderate CYP3A4 inhibition can modestly raise ketamine exposure. Verapamil also has stronger negative inotropic and chronotropic effects, which makes the cardiovascular picture marginally more complex but not problematic for KAP.

Lumateperone and ketamine are compatible. As a newer atypical antipsychotic approved for schizophrenia and bipolar depression, lumateperone has a lighter metabolic and EPS profile than older atypicals. The theoretical D2-attenuation of ketamine's antidepressant response applies as it does for other atypicals.

Diltiazem and ketamine are compatible with awareness. Diltiazem is a moderate CYP3A4 inhibitor — distinct from amlodipine which has no meaningful CYP effect — and can modestly raise ketamine plasma levels. Patients on stable diltiazem for atrial fibrillation rate control or hypertension can proceed with KAP without medication changes.

Clonidine and ketamine are compatible. Same considerations as guanfacine: additive sedation and a directional BP interaction (clonidine lowers, ketamine raises transiently). Some clinicians actually use clonidine to blunt ketamine's pressor response in clinic settings.

Tadalafil and ketamine are compatible. The clinical considerations are the same as sildenafil: vasodilation plus ketamine's transient pressor response means BP fluctuations during the session window. Tadalafil's distinguishing feature is its much longer half-life (17.5 hours vs sildenafil's 4 hours), so the timing window for interaction is longer. As with sildenafil, absolute contraindication with nitrates applies regardless of KAP.

Nicotine and ketamine are compatible. Two practical considerations: nicotine raises BP and HR like a mild stimulant, which stacks with ketamine's transient cardiovascular response; and many patients find their cravings spike or fade during integration, which is worth noting in the journal.

Colchicine and ketamine are compatible. The relevant flag isn't a KAP interaction — it's reminding patients about colchicine's narrow therapeutic index and severe toxicity if combined with strong CYP3A4 inhibitors (clarithromycin, Paxlovid, itraconazole, ketoconazole). Colchicine toxicity is multi-system and life-threatening; that interaction is independent of KAP but worth knowing about. Used for acute gout, gout prophylaxis, FMF, and recurrent pericarditis.

Prochlorperazine and ketamine are compatible. Same phenothiazine family as promethazine and chlorpromazine — sedating, D2 antagonism with EPS risk (akathisia is common), and modest hypotension. Commonly used for severe nausea (migraine + chemotherapy) when ondansetron isn't enough. We schedule sessions in the morning when prochlorperazine is taken at bedtime.

Ivabradine and ketamine are compatible. Ivabradine selectively lowers heart rate without affecting BP or contractility, used in heart failure and chronic angina. The relevant flag isn't a KAP interaction — it's that strong CYP3A4 inhibitors (clarithromycin, Paxlovid, itraconazole) substantially raise ivabradine levels and can cause bradycardia. Patients prescribed any of those alongside ivabradine need careful drug review.

Hydrocortisone has two distinct uses that need different framing. OTC topical creams (for eczema, insect bites, etc.) have essentially zero systemic effect and are fully compatible with KAP. Oral hydrocortisone at replacement doses (10-30 mg/day) for adrenal insufficiency is medically complex — patients need stress-dose adjustments for any significant stressor (illness, surgery, sometimes psychological stress including intense psychotherapy sessions). We coordinate stress-dose planning with your endocrinologist for KAP days.

Isavuconazole and ketamine are compatible with planning. Used for invasive aspergillosis and mucormycosis. CYP3A4 inhibition is moderate — less aggressive than voriconazole or posaconazole — but still meaningful enough that chronic dosing affects ketamine plasma levels. Notable advantages over older azoles include better tolerability (less QT prolongation, less visual disturbance than voriconazole) and IV/oral interchangeability. We dose-adjust KAP modestly downward for chronic users.

Lemborexant and ketamine are compatible. Same DORA mechanism and considerations as suvorexant (Belsomra): next-morning residual sedation can stack with a morning session.

Dexamethasone and ketamine are compatible. Same considerations as prednisone: steroid-induced mood lability or sleep disturbance can complicate distinguishing medication effects from session effects, and high-dose courses raise BP. Dexamethasone is roughly 6-7x more potent than prednisone and longer-acting, so a 'dex pack' lingers in the system longer than a Medrol pack. Common uses include chemo nausea prophylaxis, dental swelling, and acute exacerbations of autoimmune conditions.

Prednisone and ketamine are compatible. Two practical considerations: prednisone can cause mood lability, agitation, or insomnia in its own right, which can complicate distinguishing session-related effects from medication side effects; and chronic high-dose steroids can raise BP, which stacks with ketamine's transient pressor response.

Valproate and ketamine are compatible. Two specifics: we want baseline labs (LFTs, CBC, ammonia if symptomatic) because valproate carries hepatotoxicity and thrombocytopenia risk independent of ketamine. And there is a preclinical and small clinical signal that GABA-enhancing agents may modestly attenuate ketamine's antidepressant response.

Fluconazole and ketamine are compatible with awareness. Fluconazole is a moderate CYP3A4 inhibitor and a strong CYP2C9 inhibitor. The CYP3A4 piece is what matters for ketamine: a single 150 mg fluconazole dose (common for yeast infection) has minimal practical effect, but chronic or higher-dose courses can meaningfully raise ketamine exposure. We adjust expectations and dose rather than refuse the combination.

Hydromorphone and ketamine are compatible with appropriate monitoring. Hydromorphone is several times more potent than morphine, so the respiratory-depression considerations sit between standard opioids and fentanyl. We coordinate closely with the pain prescriber.

Dimenhydrinate and ketamine are compatible with monitoring. Dimenhydrinate is the 8-chlorotheophylline salt of diphenhydramine — pharmacologically, the diphenhydramine half does the work, with theophylline added to offset some sedation (in practice, still sedating). Same framework as our Benadryl page: avoid taking dimenhydrinate within 8 hours of a KAP session to prevent additive CNS depression and dissociation amplification. The original Dramamine formula contains dimenhydrinate; 'Dramamine Less Drowsy' uses meclizine instead — different molecule, similar use, milder sedation profile.

Erythromycin and ketamine are compatible with timing awareness. Erythromycin is a strong CYP3A4 inhibitor on the same magnitude as clarithromycin (much stronger than azithromycin). Combining during an active course can meaningfully raise ketamine plasma exposure. Also used off-label at low doses as a prokinetic for gastroparesis — same CYP3A4 concern applies.

Most patients on amitriptyline can proceed with KAP. The concerns are TCA-specific: additive sedation (the only real stacking with ketamine), plus amitriptyline's intrinsic anticholinergic effects (dry mouth, constipation, urinary retention) and modest QT prolongation. The QT effect is amitriptyline's own — ketamine at psychiatric doses isn't a meaningful QT-prolonging drug per the published literature. Veraart 2021's systematic review of ketamine plus psychiatric medications, which specifically included TCAs, found no documented serotonin syndrome at therapeutic ketamine doses. We adjust the session plan rather than ask you to stop the medication.

Aprepitant and ketamine are compatible with planning. The interesting pharmacology: aprepitant is a moderate CYP3A4 inhibitor early in a course (first 3 days) and a CYP3A4 inducer with longer dosing. For the typical short antiemetic course (3-day chemo cycle, single PO post-op dose), the net effect on a same-day KAP session is mild CYP3A4 inhibition — modestly raising ketamine levels. Chronic use shifts toward induction. Because the direction depends on dosing pattern and timing relative to the KAP session, we evaluate case-by-case and monitor. If you're a chemo patient managing nausea, we typically schedule KAP outside the active aprepitant window.

CBD and ketamine are compatible. CBD is non-psychoactive and does not produce the cannabis interactions covered separately. Two practical considerations: CBD inhibits CYP3A4 and CYP2C19 (the enzymes that metabolize ketamine), so at high doses it can modestly raise ketamine plasma levels; and CBD products are unregulated, so potency varies significantly between brands.

Iloperidone and ketamine are compatible. Iloperidone has more pronounced alpha-1 blockade than most atypicals, which causes meaningful orthostatic hypotension — usually requiring a slow titration when starting. The post-session recovery period (when patients stand up) is the highest-risk window. Standard D2-attenuation considerations also apply.

Cyclobenzaprine and ketamine are compatible. Cyclobenzaprine is structurally a TCA and was historically flagged for serotonergic monitoring with ketamine; the actual ketamine-specific evidence does not support that framing (ketamine is not meaningfully serotonergic). We plan around sedation and modest QT, the same TCA-class considerations we apply to amitriptyline.

Tamsulosin and ketamine are compatible. Tamsulosin can cause orthostatic hypotension, especially during the first weeks of therapy. After a ketamine session the recovery period is the highest-risk window for a postural drop.

Ziprasidone and ketamine are compatible. The defining consideration for ziprasidone is QT-interval prolongation — it has the largest QT effect among the atypical antipsychotics. We get a baseline EKG and avoid stacking with other QT agents.

Ginkgo biloba and ketamine are compatible. Two practical considerations: ginkgo has mild antiplatelet activity (theoretically increasing bleeding risk with anticoagulants); and some preclinical data suggests weak MAO inhibition. Both effects are small at typical doses but worth disclosing.

Grapefruit and ketamine require planning. Grapefruit (and grapefruit juice — even small amounts of 200-250mL once) irreversibly inhibits intestinal CYP3A4 for 24-72 hours per exposure. The magnitude is comparable to Paxlovid or strong azole antifungals — substantially raising ketamine plasma levels. Practical guidance: avoid grapefruit and grapefruit juice for at least 72 hours before any KAP session. The interaction restores on its own as new enterocyte CYP3A4 is synthesized. Pomelo and Seville oranges (bitter marmalade orange) share this effect; common sweet orange juice (Tropicana, etc.) does not.

Haloperidol and ketamine are compatible. As a first-generation antipsychotic, haloperidol has more pronounced D2 antagonism and QT effect than the atypicals. The theoretical antidepressant-attenuation of ketamine via D2 blockade applies as it does for atypicals; baseline EKG is worth doing.

Isosorbide and ketamine are compatible. Same framing as nitroglycerin: the direct interaction with KAP is minimal, but nitrates are absolutely contraindicated with PDE5 inhibitors (sildenafil, tadalafil, vardenafil) due to severe hypotension risk. That contraindication is independent of ketamine but worth flagging since erectile dysfunction medications are common in the cardiac patient population.

Guanfacine and ketamine are compatible. Guanfacine lowers BP and adds sedation; ketamine transiently raises BP. The interaction works in opposite directions on BP but stacks on sedation. Orthostatic recovery after a session can be more pronounced.

Paliperidone and ketamine are compatible. Paliperidone is the active metabolite of risperidone, so the interaction profile is essentially identical: D2 antagonism may modestly attenuate ketamine's antidepressant response, and there is modest QT and orthostatic considerations. Long-acting injectable forms (Sustenna, Trinza) mean the medication is on board continuously between injections.

Levetiracetam and ketamine are compatible. There is no relevant pharmacokinetic interaction (Keppra is renally cleared, not CYP-metabolized). The thing we screen for: Keppra carries a well-known mood and irritability side effect (sometimes called Keppra rage) which we want to baseline before starting KAP.

Klonopin combines safely with at-home ketamine in the acute medical sense at therapeutic doses, but the same Veraart 2021 systematic review evidence that shapes the Xanax page applies in full: benzodiazepines measurably attenuate ketamine's antidepressant response, with delayed onset, shorter duration, and higher nonresponse rates at doses above 10 mg diazepam equivalent. Klonopin's long half-life (30-40 hours) makes the session-day hold pattern that works for Xanax less effective; the more useful approach is steady-state dose minimization during the ketamine course. We do not ask you to stop Klonopin abruptly (withdrawal can be dangerous, including seizure risk).

Furosemide and ketamine are compatible. Furosemide is a more potent diuretic than HCTZ; volume depletion plus ketamine's transient sympathomimetic effect can cause more pronounced BP fluctuations. We make sure patients are well-hydrated and monitor BP.

Lurasidone is one of the better-tolerated atypicals for KAP. It is less sedating and has a smaller QT footprint than olanzapine or risperidone. Two specifics matter: lurasidone is a major CYP3A4 substrate, and it must be taken with food (at least 350 calories) for absorption.

Baclofen and ketamine are compatible. As a GABA-B agonist, baclofen is sedating and can produce additive CNS depression. We plan around the timing rather than ask patients to stop it, especially for spasticity indications where stopping is not optional.

Eszopiclone and ketamine are compatible. The interaction is additive CNS depression and possible next-morning residual impairment. We schedule sessions to avoid the post-dose sedation window.

Psilocybin and ketamine should not be used in the same session. They are different drug classes (serotonergic vs glutamatergic) but the experiential and serotonergic load of combining them is unstudied and unnecessary. Patients who have used psilocybin recreationally or therapeutically can absolutely do KAP; we just want at least a few days between any psilocybin experience and a ketamine session.

Dronabinol and ketamine are compatible. Dronabinol is FDA-approved synthetic THC at predictable pharmaceutical doses — distinct from recreational cannabis where THC content varies wildly. Same considerations as cannabis (cardiovascular effects, cognitive impairment, sedation), but the predictable dosing makes session planning easier.

Methylprednisolone and ketamine are compatible. Same considerations as prednisone: steroid-induced mood lability or sleep disturbance can complicate distinguishing medication effects from session effects, and high-dose steroids raise BP.

Prazosin and ketamine are compatible. Many of our PTSD patients are already on prazosin for trauma-related nightmares. The interaction we plan around is BP: prazosin lowers it, ketamine raises it transiently, and the orthostatic recovery period after a session can be more pronounced.

Morphine and ketamine are compatible. Standard opioid-sedation precautions apply. Patients on stable chronic-pain morphine for cancer or palliative care often benefit from ketamine without changing their opioid dose.

Mirabegron and ketamine are compatible. Mirabegron has a different mechanism from anticholinergic OAB medications (oxybutynin, tolterodine, solifenacin) — it relaxes the bladder via beta-3 receptors and is therefore a better choice for elderly patients trying to avoid anticholinergic burden. The trade-off: it raises BP modestly (a few mmHg on average, more in some patients), which stacks lightly with ketamine's transient pressor response.

L-tyrosine and ketamine are compatible with monitoring around stimulant stacking. As a free amino acid precursor to DOPA → dopamine → norepinephrine, L-tyrosine supplementation can modestly increase catecholamine availability under conditions of acute stress or depletion. On its own, this is well-tolerated and minimally relevant for KAP. The consideration: many patients combine L-tyrosine with caffeine, prescribed stimulants (Adderall, Vyvanse, methylphenidate), or supplements like yohimbine — that stacking can amplify sympathomimetic effects which then interact with ketamine's transient pressor response. Solo L-tyrosine + ketamine: minimal concern. Stacked: we plan around it.

Nitrous oxide and ketamine are compatible. Occasional use in a dental or medical setting is fine, including dental nitrous within 24 hours of a session. Two specifics for recreational use (whippits): nitrous shares ketamine's NMDA-antagonist mechanism, so the experiential overlap is more direct than for psychedelics; and chronic recreational use inactivates vitamin B12, which can cause peripheral neuropathy and macrocytic anemia independent of any ketamine interaction.

Thiothixene and ketamine are compatible. As a first-generation antipsychotic, thiothixene has stronger D2 antagonism than atypicals, which means somewhat more pronounced antidepressant-attenuation theoretical concern, more sedation, and more EPS (extrapyramidal symptoms). Less commonly prescribed today, but still seen for chronic stable patients.

Nitroglycerin and ketamine are compatible. The cardiovascular interaction with KAP itself is minimal. Far more important: nitrates are absolutely contraindicated with PDE5 inhibitors (sildenafil, tadalafil, vardenafil) because of the risk of severe hypotension. That contraindication is independent of ketamine but worth flagging since erectile dysfunction medications are common in the cardiac patient population.

Posaconazole and ketamine are compatible with planning. Posaconazole is one of the most potent CYP3A4 inhibitors in clinical use — used for invasive fungal infection treatment and as antifungal prophylaxis in high-risk patients (hematologic malignancy, post-transplant). Magnitude of CYP3A4 inhibition is comparable to voriconazole and the ritonavir component of Paxlovid. Chronic dosing (rather than the single 150mg fluconazole pill for yeast) means the interaction is durable. We dose-adjust KAP downward; with high-dose chronic posaconazole, we coordinate carefully.

Tapentadol and ketamine are compatible with the standard opioid monitoring plus an extra consideration. Tapentadol has dual mechanism: mu-opioid agonism for analgesia plus norepinephrine reuptake inhibition (similar to an SNRI). The NRI component stacks with ketamine's own NRI activity — both raise BP and HR — so the cardiovascular load is more than a pure opioid like oxycodone. We coordinate timing and may use lower KAP doses.

Pimavanserin and ketamine are compatible. Pimavanserin is unique among antipsychotics — it has NO D2 antagonism, only 5-HT2A inverse agonism. That means the antidepressant-attenuation concern we apply to other antipsychotics does not apply here. The practical planning matters more because of the underlying Parkinson's disease: cognitive fluctuations, fall risk, and motor symptoms shape how we plan sessions.

NyQuil and ketamine are compatible with planning around its three sedating ingredients. The NyQuil combo is: acetaminophen (analgesic, no KAP issue), dextromethorphan (NMDA-active cough suppressant — same receptor family as ketamine, can theoretically amplify dissociation), and doxylamine (first-gen antihistamine, sedating like Benadryl). All three are covered individually on our directory. The reason NyQuil specifically warrants its own page: people don't think of it as three separate drugs when they take it before bed during a cold — but it is, and the cumulative sedation + the dextromethorphan-ketamine receptor overlap matter. Don't take NyQuil within 12 hours of a KAP session. DayQuil drops the doxylamine but keeps the DXM — same DXM consideration applies, much less sedation.

Oxymorphone and ketamine are compatible with appropriate monitoring. Oxymorphone is more potent than oxycodone (it's the active metabolite of oxycodone) and sits between morphine and hydromorphone in the potency hierarchy. Same considerations as those: additive respiratory depression and sedation, careful dose coordination.

Oxycodone and ketamine can be combined under appropriate monitoring. The interaction is additive CNS and respiratory depression, which matters most in the session window. We do not ask patients on stable oxycodone for chronic pain to stop it, but we may delay or modify session timing if doses are high or recently escalated.

Nortriptyline is one of the better-tolerated TCAs alongside KAP. The interaction profile is sedation and modest QT — both milder than amitriptyline. Veraart 2021 (systematic review of ketamine + psychiatric medications including TCAs) found no documented serotonin syndrome at therapeutic ketamine doses, so we have dropped that historical framing. We do not ask patients to stop nortriptyline.

Ginseng and ketamine are compatible at typical OTC doses. Two specifics worth disclosing: ginseng has documented CYP3A4 modulation in some studies (variable direction by ginseng type — Panax may inhibit at high doses, American may induce) which can theoretically affect ketamine PK; and the well-documented ginseng-warfarin interaction (reduced INR) is independent of KAP but matters for anticoagulated patients. Mild stimulant effect on BP/HR is real but small at typical doses.

Promethazine and ketamine are compatible. The two stack heavily on sedation because promethazine is strongly antihistaminic and centrally depressant. We typically prefer ondansetron for KAP nausea prophylaxis, but promethazine works if it is what you already tolerate.

Kava and ketamine are compatible at typical doses but warrant disclosure. Two specifics: kava is sedating and can stack with ketamine on CNS depression; and kava has been associated with hepatotoxicity (idiosyncratic, rare, but documented enough that several countries restricted sale at various points).

Desvenlafaxine and ketamine are compatible. As an SNRI (active metabolite of venlafaxine), it shares the Veraart 2021 evidence base showing no documented serotonin syndrome with ketamine plus serotonergic antidepressants. The interaction we plan around is BP: SNRIs raise baseline BP, which stacks with ketamine's transient pressor response. Do not discontinue abruptly; SNRI discontinuation syndrome is real.

Albuterol and ketamine are compatible. Both can transiently raise heart rate; albuterol can also cause tremor. We do not ask asthmatic patients to forgo their rescue inhaler — quite the opposite, we want it on hand during sessions.

Finasteride and ketamine are compatible. The relevant flag for KAP planning is post-finasteride syndrome — an FDA-acknowledged constellation of persistent depression, anxiety, and sexual dysfunction that some patients experience during or after finasteride therapy. The mechanism isn't fully characterized but neurosteroid (allopregnanolone) depletion is implicated. Patients in active depression treatment on finasteride deserve careful baseline mood documentation so we can honestly assess what KAP is doing for them.

Viloxazine and ketamine are compatible. Same considerations as atomoxetine (Strattera): viloxazine raises BP and HR similarly to stimulants, and that load stacks with ketamine's transient pressor response. The non-stimulant designation refers to abuse potential, not to cardiovascular profile.

Quercetin and ketamine are compatible. Dietary quercetin (from onions, apples, berries) is well below any clinically relevant threshold. High-dose supplemental quercetin (500-1000 mg/day, popularized during COVID for zinc-ionophore protocols) has measurable CYP3A4 inhibition in vitro and in some human studies. The clinical magnitude of the ketamine effect at typical supplement doses is small but worth disclosing alongside other CYP3A4 considerations.

Daridorexant and ketamine are compatible. Same DORA framework as suvorexant (Belsomra) and lemborexant (Dayvigo): next-morning residual sedation can stack with a morning session. Half-life ~8 hours, marginally shorter than the other DORAs.

Ranolazine and ketamine are compatible. The direct interaction with ketamine is minimal, but ranolazine is a major CYP3A4 substrate — strong CYP3A4 inhibitors (clarithromycin, ritonavir/Paxlovid, ketoconazole, itraconazole) are contraindicated with ranolazine independent of KAP. Patients on ranolazine who are prescribed any of those interactors need careful drug review.

Temazepam and ketamine are compatible. Same monitoring framework as other benzos: additive sedation in the session window and the documented effect of chronic benzodiazepine use blunting ketamine's antidepressant response. Used for sleep, half-life is intermediate between lorazepam and diazepam.

Brexpiprazole and ketamine are compatible. As a D2 partial agonist (like aripiprazole), it has a lighter sedation and metabolic profile than olanzapine. The pharmacodynamic note about antipsychotic blunting of ketamine response is theoretically smaller for partial agonists but still warrants honest expectation-setting.

Rhodiola and ketamine are compatible at typical OTC doses. Rhodiola has been shown in some studies to mildly inhibit MAO and modestly affect serotonin and dopamine activity. The theoretical interaction with ketamine is small, but worth disclosing alongside any prescription serotonergic medications.

Risperidone and ketamine are compatible. As with other antipsychotics, D2 antagonism may partially blunt the antidepressant effect of ketamine. Additional considerations: risperidone prolongs QT modestly and can cause orthostatic hypotension, both worth knowing before a session.

Methylphenidate and ketamine are compatible. As with amphetamines, the consideration is additive cardiovascular load during the session window. We typically time sessions outside the stimulant's peak.

Methocarbamol and ketamine are compatible. It is one of the lighter-profile muscle relaxants for KAP planning: less sedating than cyclobenzaprine, fewer cardiovascular concerns than tizanidine.

Dextromethorphan and ketamine are compatible at standard OTC cough-syrup doses. The historically cited serotonin syndrome concern (DXM has minor serotonin reuptake activity) is less relevant with ketamine, which is not meaningfully serotonergic itself. The real consideration is mechanism overlap: DXM is also an NMDA receptor antagonist, just like ketamine. At cough doses the effect is negligible, but Auvelity (dextromethorphan-bupropion) for depression and recreational high-dose use produce meaningful NMDA blockade that overlaps with ketamine's mechanism.

Asenapine and ketamine are compatible. The D2 antagonism may modestly attenuate ketamine's antidepressant response, as with other atypicals. Asenapine is unusual in two ways: sublingual administration (Saphris) requires no food or drink for 10 minutes after dosing for full absorption, which is independent of KAP planning, and the transdermal patch (Secuado) gives steady-state coverage. Modest sedation and orthostasis are typical side effects.

Milnacipran and ketamine are compatible. FDA-approved specifically for fibromyalgia (not depression in the US, though used as an antidepressant elsewhere). Same SNRI compatibility framework as duloxetine and venlafaxine: track BP (SNRIs raise baseline BP that stacks with ketamine's transient pressor), and don't discontinue abruptly (SNRI discontinuation syndrome is real).

Nefazodone and ketamine are compatible with awareness. The branded product (Serzone) was voluntarily withdrawn in 2003 due to rare hepatotoxicity, but generic nefazodone remains available. Two specifics for KAP planning: nefazodone is a strong CYP3A4 inhibitor and can substantially raise ketamine plasma levels, similar in magnitude to clarithromycin; and the rare hepatotoxicity history means baseline LFTs are reasonable.

Doxepin is compatible with KAP. It is strongly antihistaminic and centrally sedating; we schedule sessions in the morning if you take it at bedtime. Older SSRI-style serotonin syndrome monitoring does not apply with ketamine, which is not meaningfully serotonergic.

Atomoxetine and ketamine are compatible. Atomoxetine raises BP and HR similarly to stimulants, so the additive cardiovascular consideration applies. There is a theoretical serotonergic component because atomoxetine has minor serotonin reuptake activity at high doses, but clinical relevance is small.

Pseudoephedrine and ketamine stack on the cardiovascular axis. Pseudoephedrine releases norepinephrine and directly stimulates alpha and beta receptors — same mechanistic family as the stimulants we already flag (Adderall, Vyvanse). Ketamine's transient pressor effect adds on top. For most patients this is a tolerable BP spike; for patients with hypertension, arrhythmia, or coronary disease it can matter. Pseudoephedrine is behind-the-counter (vs phenylephrine which is OTC-shelf), and patients often don't think of it as a 'real' drug.

Phenylephrine and ketamine are compatible with monitoring. The relevant consideration is a real ketamine-specific cardiovascular stack: ketamine produces a transient sympathomimetic pressor effect (raising BP and HR for 15-45 min), and phenylephrine is a direct α1 agonist that raises BP independently. Stacked, the BP elevation can be more pronounced — particularly relevant in patients with baseline hypertension. The oral OTC dose (Sudafed PE) has modest systemic effect; the IV form used in surgical settings is a different intensity. Of note: a 2023 FDA advisory committee concluded oral phenylephrine is ineffective as a decongestant — many patients are taking it for no real benefit and could use saline nasal sprays or pseudoephedrine instead.

Solriamfetol and ketamine are compatible. As a DNRI, solriamfetol raises BP and HR similarly to ADHD stimulants. The cardiovascular load stacks with ketamine's transient pressor response — same framework as Vyvanse, Ritalin, atomoxetine, viloxazine.

Efavirenz and ketamine are compatible with planning, but there are two KAP-relevant considerations. First (pharmacokinetic): efavirenz is a strong CYP3A4 inducer that accelerates ketamine metabolism and lowers plasma levels — same directionality as phenytoin and rifampin. Standard KAP dosing may be subtherapeutic; we adjust upward with monitoring. Second (pharmacodynamic): efavirenz has a well-documented CNS/psychiatric side effect profile (vivid dreams, mood changes, depression, suicidality in some patients) that's relevant for KAP outcome interpretation — if mood is worsening on efavirenz and you're trying to assess KAP response, we need to separate signal from noise. Many HIV teams now use integrase inhibitor regimens (Biktarvy etc.) as alternatives — that's a conversation with your HIV provider, independent of KAP.

Flecainide and ketamine are compatible. The CAST trial's lesson — flecainide is pro-arrhythmic in patients with structural heart disease — shapes who's prescribed it (typically patients with structurally normal hearts using it for AFib or PSVT). Worth confirming the cardiac context for KAP. Modest CYP2D6 metabolism doesn't meaningfully affect ketamine.

Dimethyl fumarate and ketamine are compatible. The relevant flag for KAP planning is the flushing reaction — common in the first weeks of therapy, niacin-like, can be uncomfortable, and theoretically stacks with ketamine's transient BP/HR rise. The intrinsic lymphopenia monitoring and PML surveillance are independent of KAP. Vumerity (diroximel fumarate) is a prodrug with better GI tolerability but same overall profile.

Theophylline and ketamine are compatible with monitoring. Two specifics: theophylline is a methylxanthine (same family as caffeine but more potent at lower mg doses) and produces measurable HR/BP elevation that stacks with ketamine's transient pressor; and theophylline has a narrow therapeutic index where modest changes in level produce toxicity (nausea, tachyarrhythmia, seizures). The KAP-relevant note is also that smoking cessation, fluoroquinolone antibiotics (cipro), and fluvoxamine all raise theophylline levels via CYP1A2 — separate concerns from KAP but worth knowing about.

Chlorpromazine and ketamine are compatible. As an older first-generation antipsychotic, chlorpromazine has heavier sedation, anticholinergic, and QT-prolongation effects than newer agents. Less commonly used today, but still seen for refractory hiccups, intractable migraine, and some chronic psychotic disorders.

Topiramate and ketamine are compatible. The most common consideration is additive cognitive slowing in the hours after a session; topiramate's word-finding effects can amplify the post-session integration grogginess. We do not ask patients to stop it.

Perphenazine and ketamine are compatible. As an older phenothiazine, perphenazine has more EPS, more anticholinergic load, and more sedation than newer atypicals. The D2-attenuation concern that applies to all D2 antagonists applies here as well. Continue as prescribed; we plan session timing around sedation.

Oxcarbazepine and ketamine are compatible. Oxcarbazepine is a structural analog of carbamazepine designed to have a milder side-effect profile, including milder CYP3A4 induction. The effect on ketamine exposure is real but smaller than carbamazepine's; we plan around it rather than refuse.

Vortioxetine and ketamine are compatible. Pharmacologically vortioxetine acts like an SSRI plus 5-HT receptor modulation. The Veraart 2021 systematic review covering ketamine plus SSRIs and SNRIs found no documented serotonin syndrome at therapeutic doses, so we have retired the older 'brief on serotonin syndrome symptoms' protocol that used to apply here. We do track BP because SNRI-adjacent agents can raise baseline BP that stacks with ketamine's transient pressor response.

Codeine and ketamine are compatible. Standard opioid-sedation precautions apply. One specific to flag: codeine is a prodrug converted to morphine by CYP2D6, and ultra-rapid metabolizers (about 1-2% of patients) generate much higher morphine levels than expected. Combined with ketamine, this means the respiratory depression in those patients can be more pronounced than the prescribed dose suggests.

Tramadol with at-home ketamine is safe in the acute medical sense at therapeutic doses, but the polypharmacy context is what shapes the intake conversation. Tramadol is unusual among pain medications because it has both opioid (mu-agonist) and serotonergic (SNRI-like) mechanisms; the serotonergic component is the documented source of serotonin syndrome cases when tramadol is combined with other serotonergic agents (SSRIs, SNRIs, MAOIs, multiple serotonergic medications together). For tramadol monotherapy plus at-home ketamine, the risk is low and we proceed with standard onboarding. For tramadol plus an SSRI/SNRI plus ketamine (the most common scenario), we have a more careful intake conversation and may recommend the pain regimen be reviewed with your prescribing physician.

Doxylamine and ketamine are compatible. As with diphenhydramine, doxylamine is strongly sedating and anticholinergic. The sedation window can stack with a morning session if you take it at bedtime.

Diazepam is workable alongside KAP, but its long half-life (20-50 hours) and active metabolites (desmethyldiazepam, 30-200 hours) mean that what feels like an occasional dose can accumulate to a steady-state level that overlaps every session. Chronic benzodiazepine therapy also reduces ketamine's antidepressant response magnitude.

Mucuna pruriens and ketamine are compatible with planning. Mucuna seeds are ~15% L-DOPA by weight — a typical 5g supplement dose delivers ~750mg of actual L-DOPA, which is the same active molecule prescribed as Sinemet for Parkinson's disease. This matters because: (1) dopaminergic stacking with stimulants or sympathomimetics is real; (2) mucuna users should NOT combine with MAOIs (hypertensive crisis risk, same as carbidopa-levodopa); (3) chronic high-dose use can produce impulse-control behaviors similar to dopamine-agonist treatment in Parkinson's. With ketamine specifically: no direct PK interaction, but the dopaminergic context affects our overall medication picture. 'Natural' supplement labeling obscures this — patients often don't realize they're taking what's pharmacologically L-DOPA.

Midazolam and ketamine are compatible. Outpatient midazolam is genuinely rare in adults; the typical reason to disclose midazolam use is recent procedural sedation (colonoscopy, dental, minor surgery) within the past week, in which case we just space the session 48-72 hours from the dose. After that the drug is fully cleared and there's no further concern.

Voriconazole and ketamine are compatible with planning. Voriconazole is a strong CYP3A4 inhibitor — similar magnitude to clarithromycin and the ritonavir component of Paxlovid — which slows ketamine clearance and raises plasma levels. Unlike single-dose fluconazole (yeast), voriconazole is typically used for serious invasive fungal infections at chronic dosing, so the interaction is durable. We dose-adjust KAP downward. Voriconazole also has its own intrinsic considerations independent of KAP: visual disturbances (especially early therapy), QT prolongation, hepatotoxicity, and photosensitivity with long-term use.

Sildenafil and ketamine are compatible. The interaction we plan around is BP: sildenafil is a peripheral vasodilator, and ketamine's transient sympathomimetic rise sits on top of that baseline. Patients on nitrates should not take sildenafil under any circumstance, KAP or otherwise.

Hydrocodone and ketamine are compatible with monitoring. Same considerations as oxycodone: additive sedation and respiratory depression, plan timing around the session window.

Vilazodone and ketamine are compatible. As an SSRI plus 5-HT1A partial agonist, vilazodone is covered by the same Veraart 2021 systematic review that found no documented serotonin syndrome with ketamine plus serotonergic antidepressants. We track BP and general antidepressant-class considerations rather than a specific SS protocol.

Hydroxyzine and ketamine are compatible. At anxiolytic doses (25-50 mg), the main consideration is additive sedation — that's a true ketamine stack. Hydroxyzine carries an FDA-recognized QT-prolongation warning at higher doses, but that's intrinsic to hydroxyzine; ketamine at psychiatric doses isn't a meaningful QT-prolonging drug per the published literature. Baseline EKG is reasonable for hydroxyzine's own QT history above 50 mg or with other QT agents.

Cariprazine and ketamine are compatible. As a D2/D3 partial agonist (similar mechanistic family to aripiprazole and brexpiprazole), it has a lighter side-effect footprint than olanzapine or risperidone. The theoretical antidepressant-attenuation concern for ketamine is smaller for partial agonists than for full antagonists.

Lisdexamfetamine and ketamine are compatible. Ketamine briefly raises BP and HR during a session; stimulants raise baseline BP and HR. The two stack on the cardiovascular axis, which matters most for patients with hypertension or known arrhythmia.

Pitolisant and ketamine are compatible. Pitolisant is unique among wakefulness-promoting agents — it's an inverse agonist at H3 histamine receptors that increases histamine release in wakefulness-promoting brain regions. Three practical considerations: it's a major CYP2D6 substrate (so poor metabolizers reach much higher exposures); it has modest intrinsic QT prolongation (independent of KAP); and as a non-stimulant it lacks the cardiovascular stack other narcolepsy meds have.

Bupropion at standard therapeutic doses (Wellbutrin XL up to 450 mg/day) combines safely with at-home ketamine. The two medications work through different neurotransmitter systems and the FDA has separately approved a bupropion plus NMDA-antagonist combination for depression. The one clinical consideration is dose form and total daily dose: IR formulations and doses above 450 mg/day get a brief intake conversation about seizure threshold; standard XL dosing does not.

Xanax and other benzodiazepines combine safely with at-home ketamine in the sense that no acute medical harm is documented at therapeutic doses, but the published evidence specifically supports minimizing benzodiazepine use during ketamine treatment for depression because benzos measurably attenuate ketamine's antidepressant response. The Veraart 2021 systematic review found delayed time to response, shorter duration of response, and higher nonresponse rates at doses greater than 10 mg diazepam equivalents. We do not ask you to stop Xanax abruptly (withdrawal can be severe and dangerous), but we recommend the lowest functional dose during your ketamine course and hold the dose on session days when possible.

Enzalutamide and ketamine are compatible with planning. The KAP-relevant interaction is straightforward but in the *opposite* direction from what most people expect: instead of an inhibitor raising ketamine levels, enzalutamide is a strong CYP3A4 inducer that accelerates ketamine metabolism and lowers plasma levels. Standard KAP dosing may be subtherapeutic. We adjust upward. The interaction develops over 1-2 weeks of enzalutamide therapy and persists 1-2 weeks after stopping. Other intrinsic concerns — fatigue, hot flashes, falls, seizure risk in select patients — belong to enzalutamide and oncology management.

Yohimbine and ketamine are compatible with monitoring. Yohimbine is an α2 adrenergic antagonist — by blocking the presynaptic 'brake' on norepinephrine release, it produces a sympathomimetic effect that stacks meaningfully with ketamine's transient BP and HR elevation. Patients use yohimbine as a fat-loss supplement, pre-workout, or for erectile dysfunction. The combination can produce uncomfortable or unsafe BP/HR elevations, anxiety, palpitations, and panic-like reactions. Effect is dose-dependent — 5mg may be tolerable, 20mg+ is a different conversation. Best practice: hold yohimbine for 48-72 hours before any session and discuss timing of resumption with us.

Tizanidine and ketamine are compatible. Tizanidine is sedating and lowers BP via alpha-2 agonism. The session-day window stacks on both axes. We monitor BP and have you stand slowly after sessions.

Zonisamide and ketamine are compatible. Same family of considerations as topiramate: cognitive slowing, word-finding difficulty, and modest sedation can compound the post-session integration grogginess. Off-label uses include migraine prophylaxis and weight loss adjunct.

Olanzapine and ketamine can be combined safely. The two practical considerations are additive sedation and a pharmacodynamic one: D2 receptor antagonism may partially blunt the downstream glutamatergic cascade that drives ketamine's antidepressant effect. We disclose this so patients have realistic expectations.

LSD is a DEA Schedule I controlled substance in the United States. There is essentially no published evidence of LSD plus ketamine combination harm. Our position is precautionary and pragmatic rather than evidence-driven: we do not run a ketamine session while LSD is active or in the recovery window because the experiential load is heavy and the serotonergic stacking, while small, is real. Recent recreational LSD use does not permanently disqualify you from KAP. We discuss the use pattern and plan session timing.

PCP is a DEA Schedule II controlled substance in the United States; recreational possession is illegal. PCP shares ketamine's NMDA-antagonist mechanism but with much longer duration of action (hours to a day) and a more variable, often agitating profile. Recent PCP use disqualifies a ketamine session because we cannot predict the combined or carryover effects. Distant past use does not permanently disqualify you from KAP. We evaluate individually and require a substantial separation window.

Phenibut alongside ketamine therapy requires individual evaluation. Phenibut is a GABA-B agonist (structural analog of baclofen) sold as an over-the-counter 'nootropic' or anxiolytic supplement in the US but is a Soviet-era prescription drug elsewhere. Two real concerns: (1) sedative stacking with ketamine's CNS effects; (2) phenibut has documented dependence and severe withdrawal syndromes (anxiety, insomnia, agitation, seizures, psychosis) that mimic and worsen during periods of stress — KAP session day is not the time for an inadvertent withdrawal episode. We evaluate dose, frequency, and duration of use, and may ask for a tapered hold or coordinate session timing with a phenibut dosing plan. Patients sometimes don't realize phenibut has these properties because it's sold as a supplement.

Auvelity alongside ketamine therapy requires individual evaluation. Auvelity is a fixed-dose combination of dextromethorphan (45mg) plus bupropion (105mg), FDA-approved in August 2022 for major depressive disorder. The clinical hook: dextromethorphan is an NMDA receptor antagonist (same primary mechanism as ketamine), and the bupropion is included specifically to inhibit CYP2D6 — slowing DXM metabolism so it builds up to therapeutic NMDA-antagonist plasma levels rather than being rapidly cleared. So Auvelity is functionally trying to be 'oral ketamine in a pill,' which makes the combination with at-home ketamine therapy a real clinical question rather than a routine one. We typically don't run both simultaneously: the mechanistic overlap means we're potentially blocking the same receptor target twice with no clear additive benefit and amplified dissociation/dizziness risk. If you're currently on Auvelity and want to try KAP, we evaluate whether to taper Auvelity first, and the bupropion component's own KAP considerations (mild seizure threshold effect) overlap with our bupropion page guidance. If you're already on KAP, we usually wouldn't add Auvelity. Two NMDA antidepressants is a coordination conversation, not a flat 'no.'

DMT (including ayahuasca, which combines DMT with an MAOI to make it orally active) is a DEA Schedule I controlled substance in the United States. Pharmacologically, isolated DMT has a very short duration (15-30 minutes smoked, 1-3 hours injected), while ayahuasca's MAOI component extends the experience to 4-6 hours and adds a separate set of medication-interaction concerns. We do not run ketamine sessions during active use or in the recovery window. Recent recreational or ceremonial use does not permanently disqualify you from KAP. The MAOI in ayahuasca specifically requires more caution: see the MAOI page for our approach to washout periods.

Clozapine alongside ketamine requires individual evaluation. Clozapine has the largest interaction surface of any antipsychotic: heavy sedation, anticholinergic load, QT prolongation, orthostatic hypotension, and mandatory neutropenia monitoring (ANC checks). Patients on clozapine for treatment-resistant schizophrenia or schizoaffective disorder may still benefit from ketamine adjunctive therapy, but we coordinate closely with the prescribing psychiatrist.

Amiodarone alongside ketamine requires individual evaluation. Two unique features matter: the half-life is approximately 58 days (one of the longest of any drug in clinical use), so amiodarone remains active for months after the last dose; and amiodarone is a strong CYP3A4 and CYP2D6 inhibitor that meaningfully raises ketamine plasma exposure. Layered on top is the drug's intrinsic complexity — pulmonary, hepatic, thyroid, ophthalmic, and neurologic toxicities require ongoing monitoring independent of KAP.

Phenytoin alongside ketamine requires individual evaluation. Phenytoin strongly induces CYP3A4 and other enzymes, which can substantially lower ketamine plasma levels. Patients on phenytoin for epilepsy should not adjust the medication without their neurologist; we work around the induction and may use higher KAP doses to achieve equivalent effect.

Propofol alongside ketamine requires individual evaluation based on context. Outpatient propofol exposure is essentially limited to procedural sedation (colonoscopy, MRI, dental, minor surgery) or operating-room general anesthesia. Both are short-duration events. We don't run a ketamine session within 48-72 hours of a propofol-based procedure to let the residual sedation, cognitive recovery, and any associated lab/post-op recovery complete. After that window, no further concern. Chronic IV propofol is hospital ICU only and not a KAP-eligibility scenario.

Fentanyl alongside ketamine requires individual evaluation. Fentanyl is 50-100x more potent than morphine, and the respiratory-depression risk in combination with ketamine is materially higher than with weaker opioids. Patients on transdermal fentanyl for chronic cancer pain may still be candidates with extra monitoring; patients on rapid-onset formulations (Actiq, Subsys) need particularly careful planning.

MDMA is a DEA Schedule I controlled substance in the United States, meaning federal law treats it as having no accepted medical use and high abuse potential. That legal status alone shapes what we can do. Pharmacologically, the data is more nuanced: there are no documented case reports of serotonin syndrome from MDMA combined specifically with ketamine in the published literature. The combination-harm evidence extrapolates from MDMA plus SSRIs and MAOIs, where serotonin syndrome and deaths are well documented. Our position: we will not run a ketamine session while MDMA is on board or in the recovery window. We do not categorically refuse patients who have used MDMA recreationally with adequate separation. We discuss timing, frequency, and the patient's overall pattern individually.

Alcohol and ketamine require active management, not passive monitoring. On dose days, alcohol is prohibited (the standard rule is 24 hours before a session and 24 hours after). During the loading phase (first 4-6 weeks) we strongly encourage complete abstinence; after loading, light drinking on non-treatment days is generally fine. Patients with active or recent alcohol use disorder need to disclose at intake; depending on severity, the AUD may need to be addressed alongside or before ketamine in coordination with addiction medicine.

Perampanel alongside ketamine requires individual evaluation, and not for the usual sedation reason. Perampanel is a selective non-competitive AMPA receptor antagonist. Ketamine's antidepressant effect depends on a downstream AMPA-mediated cascade triggered by NMDA blockade — AMPA activation is what drives the BDNF release and synaptogenesis underlying ketamine's effect. A direct AMPA antagonist may therefore meaningfully attenuate ketamine's antidepressant response, more so than any other psychiatric medication interaction we cover. Perampanel also carries an FDA black-box warning for serious psychiatric and behavioral reactions independent of ketamine.

St. John's Wort and ketamine warrant individual evaluation. Two specifics: St. John's Wort is a potent CYP3A4 inducer, similar in magnitude to carbamazepine, which can reduce ketamine plasma levels. And it has serotonergic activity like an SSRI, which we monitor accordingly. We typically ask patients to taper off before starting KAP.

Isoniazid alongside ketamine requires individual evaluation. INH is the standard latent TB prophylaxis (common for healthcare workers, immigrants from high-prevalence countries, and BCG-vaccinated patients) and a TB treatment cornerstone. The relevant pharmacology for KAP: INH has documented MAO-A inhibitor activity that has produced tyramine-cheese-reaction case reports and serotonin syndrome interactions with serotonergic drugs. Same operational framework we apply to phenelzine, linezolid, and methylene blue: at-home unmonitored KAP is not appropriate while on active INH. Also: INH causes B6 (pyridoxine) deficiency that can produce peripheral neuropathy — patients should be on supplemental B6 throughout INH therapy.

Lamotrigine combined with ketamine is pharmacologically safe; no documented case reports of harm and no recommended washout. The case-by-case nature has two parts. First, lamotrigine signals different patient contexts (bipolar depression, epilepsy, or unipolar TRD augmentation) that each get a slightly different intake conversation. Second, an older line of research suggested lamotrigine might attenuate ketamine's effects (a hyperglutamatergic hypothesis), but the most recent real-world clinical data (Santucci et al. 2025, N=347 including 57 on lamotrigine) found no clinical evidence for that interaction. Standard practice is to continue lamotrigine throughout the ketamine course.

Lithium combined with ketamine is pharmacologically safe with no documented interaction concerns. The case-by-case nature comes from context: most patients on lithium are being treated for bipolar disorder, and bipolar depression on at-home ketamine carries a low but real manic-switch consideration that is meaningfully lower when the mood stabilizer is continued. Patients on lithium for unipolar treatment-resistant depression augmentation are usually straightforward candidates with an intake review of recent lithium level and renal function. Patients on lithium for bipolar I or II disorder need a more detailed conversation about whether at-home is the right setting and we coordinate with the prescribing psychiatrist as part of intake.

Cannabis with at-home ketamine is structurally similar to the Alcohol conversation: not a hard pharmacologic interaction in the acute medical sense, but a real effectiveness question. Daily THC use measurably blunts ketamine's antidepressant effect through the same BDNF and neuroplasticity pathways alcohol affects; occasional weekend use between sessions is less clearly problematic; CBD-only products are generally fine throughout the course. The standard guidance: pause THC during the initial 10+ sessions over 4-8 weeks (the loading phase where the neuroplasticity window matters most), no use on session days, and an honest conversation about pattern at intake.

Methadone with at-home ketamine is one of the more clinically nuanced questions in this directory. The combination is being actively studied as part of opioid use disorder treatment (Mansoori et al. 2025 RCT in co-occurring MDD + OUD; Shen et al. 2025 scoping review), and the predicted pharmacologic harms have not been borne out in published case reports. The verdict depends on three distinct subgroups: active OUD with recent destabilization or illicit use is effectively not a candidate; stable long-term methadone maintenance for OUD with co-morbid depression is a candidate with mandatory coordination with your methadone clinic; methadone for chronic pain with no OUD history is the most flexible subgroup. At-home unmonitored is fundamentally different from the monitored research settings where this combination has been studied.

Kratom alongside ketamine requires individual evaluation. Kratom's primary alkaloids agonize mu-opioid receptors AND have serotonergic activity, so it stacks with ketamine on both the respiratory-depression axis and the (small) serotonin-syndrome axis. We do not categorically decline patients on kratom, but we evaluate use patterns carefully and may ask for a taper.

Rifabutin alongside ketamine requires individual evaluation. Rifabutin is the preferred rifamycin in HIV patients on protease-inhibitor or integrase-inhibitor regimens (rifampin is too strong an inducer for those regimens). It's a meaningful CYP3A4 inducer — about 40% as potent as rifampin — so it can lower ketamine plasma exposure during therapy. Patients may need higher KAP doses to achieve equivalent effect, or response may be muted. We evaluate case-by-case rather than refuse.

Ketoconazole requires individual evaluation based on formulation. The over-the-counter Nizoral shampoo and topical cream have negligible systemic absorption and no meaningful interaction with ketamine — those are fully compatible. Oral ketoconazole is a different conversation: it is the classical strongest CYP3A4 inhibitor in clinical pharmacology (used as the probe drug in PK studies), and its oral use was FDA-restricted in 2013 due to hepatotoxicity. Patients on oral ketoconazole for refractory fungal infection or Cushing's syndrome are uncommon but the CYP3A4 effect is substantial.

Paxlovid alongside ketamine warrants individual evaluation. The ritonavir component is one of the most potent CYP3A4 inhibitors in clinical use, and ketamine is metabolized primarily by CYP3A4 and CYP2B6. Combining them can substantially raise ketamine plasma levels and prolong its half-life. Paxlovid is a short course (typically 5 days), so the practical fix is timing: we do not run sessions during the course or for several days after. After the typical washout, you become eligible again.

Mescaline is a DEA Schedule I controlled substance. Peyote use specifically has a federal religious-use exemption for enrolled members of the Native American Church; that exemption doesn't extend to other forms of mescaline (synthetic, San Pedro extract). Same framework we apply to LSD: long duration (10-12 hours), classical psychedelic, no documented combination harm with ketamine but we space sessions for the experiential-load reason. Distant past use doesn't disqualify you.

Amyl nitrite and related alkyl nitrites (poppers) require individual evaluation. They are inhaled vasodilators that produce a brief lightheaded rush; medically they were used historically for angina before nitroglycerin became standard. Same absolute contraindication with PDE5 inhibitors (sildenafil, tadalafil) as prescription nitrates — severe hypotension risk. Poppers and PDE5 inhibitors often coincide in chemsex contexts, which is the most clinically relevant population for this disclosure. We do not run a ketamine session in proximity to popper use because the cardiovascular timing is unpredictable.

Darunavir alongside ketamine requires individual evaluation. Darunavir is always given with a pharmacokinetic booster — either ritonavir or cobicistat — both of which are strong CYP3A4 inhibitors. The boosted regimen substantially raises ketamine plasma levels via CYP3A4 inhibition, similar to Paxlovid in magnitude. Unlike Paxlovid (5-day course), darunavir-based regimens are chronic, so this isn't a 'wait it out' situation. We coordinate KAP dose downward and may delay onset until alternative HIV regimens (integrase-inhibitor-based without booster, like Biktarvy) are an option to discuss with your HIV team.

Rifampin alongside ketamine requires individual evaluation. Rifampin is the prototypical strong CYP3A4 inducer in clinical use, similar in magnitude to carbamazepine. Patients on rifampin (typically for TB or specific Gram-positive infections) may experience meaningfully reduced ketamine exposure and blunted response. We do not refuse, but we plan honestly: response may be smaller during therapy, with normalization in the weeks after the course finishes.

Salvia divinorum's active compound salvinorin A is a selective kappa-opioid receptor agonist. It produces a brief but intense dissociative experience when smoked (typically 5-15 minutes). Federal scheduling does not classify it as a controlled substance, but many states have banned it independently. The mechanism is genuinely different from classical psychedelics and from ketamine. We do not run a session in close proximity to use because the experiential load can be heavy and recovery is unpredictable.

Quetiapine combined with at-home ketamine is pharmacologically safe; no documented case reports of harm exist in the published systematic reviews of ketamine interactions. The case-by-case verdict reflects what quetiapine signals about your underlying clinical picture (MDD augmentation, bipolar depression, schizophrenia, schizoaffective disorder, or off-label use for insomnia) and what dose you're on (the difference between Seroquel 25 mg at bedtime for sleep and Seroquel 600 mg for primary psychiatric indication is substantial). Standard practice is to continue quetiapine throughout the ketamine course; the intake conversation calibrates to the indication.

Itraconazole alongside ketamine requires individual evaluation. Itraconazole is a strong CYP3A4 inhibitor — much more potent than fluconazole — and can substantially raise ketamine plasma levels and prolong the half-life. Courses are typically weeks to months for systemic fungal infections (histoplasmosis, blastomycosis, onychomycosis). We do not run sessions during the course, and require a washout period after completing therapy before starting or resuming KAP.

Spravato is FDA-approved esketamine, the S-enantiomer of the same racemic ketamine molecule we use at Tovani sublingually. The question of "Spravato + at-home ketamine" is therefore unusual: it's not a drug-drug interaction question but a same-molecule treatment-coordination question. Active Spravato treatment and concurrent at-home ketamine therapy is not a combination we prescribe; it would be running two parallel courses of essentially the same medication. For patients who have completed or discontinued Spravato treatment and are considering at-home ketamine as an alternative or follow-on, intake is straightforward with the right clinical history.

Suboxone with at-home ketamine is structurally similar to the Methadone conversation but with a different patient population and different care-coordination model. The published evidence is actively encouraging: a 2025 RCT (Mansoori et al., N=60) directly tested adjunctive ketamine vs buprenorphine in co-occurring MDD + OUD and found both produced significant reductions in anxiety and craving with no between-group safety difference. The verdict depends on three subgroups: active OUD with recent destabilization is effectively not a candidate; stable long-term Suboxone maintenance with co-morbid depression is a candidate with mandatory coordination with your buprenorphine prescriber; Suboxone for chronic pain (off-label) is the most flexible subgroup.

Buprenorphine alongside ketamine requires individual evaluation. Buprenorphine alone (Subutex, Belbuca buccal, Butrans patch, Sublocade depot injection) differs from Suboxone in lacking naloxone. The clinical considerations: as a partial mu agonist with high receptor affinity, buprenorphine can antagonize other opioids — important for any pain-management planning. The ceiling effect on respiratory depression makes it safer than full opioid agonists for the KAP sedation stack. The depot formulation (Sublocade) means buprenorphine is on board continuously for a month. We coordinate with your prescriber whether for chronic pain or OUD.

Amantadine alongside ketamine requires individual evaluation because of direct mechanism overlap. Amantadine is a weak NMDA receptor antagonist (also has dopaminergic effects), and there's growing off-label interest in it as a depression adjunct via the same NMDA mechanism ketamine targets. The combination is unstudied. For Parkinson's-disease patients on amantadine for dyskinesia, the question is whether KAP adds meaningful additional benefit or just compounds the NMDA blockade. For off-label antidepressant use, we typically recommend choosing one NMDA-pathway intervention rather than stacking.

Carbamazepine is a potent CYP3A4 inducer, and ketamine is metabolized primarily by CYP3A4 and CYP2B6. The pharmacokinetic interaction is real: patients on stable carbamazepine therapy may need higher ketamine doses to achieve the same effect, and response may still be more modest. We evaluate case-by-case rather than turn patients away or pretend the interaction does not exist.

2C-B is a DEA Schedule I controlled substance. Shorter duration than LSD (~4-6 hours active) and at lower doses can have more of a stimulant + mild psychedelic profile. The branded street product 'tusi' or 'pink cocaine' is frequently misidentified — laboratory analysis often shows ketamine, MDMA, or other mixtures rather than actual 2C-B. We do not run ketamine sessions in proximity to 2C-B use. The mixing-up-with-other-drugs problem makes recent disclosure especially important.

Naltrexone alongside ketamine requires individual evaluation. It does NOT block ketamine itself (ketamine works at NMDA receptors, not opioid receptors), but the clinical context matters: full-dose naltrexone for opioid use disorder is fine; full-dose for alcohol use disorder is fine; low-dose naltrexone (LDN) for chronic pain or autoimmune conditions is generally fine. We do not turn naltrexone patients away, but we plan around the underlying condition.

GHB and ketamine warrant individual evaluation, not categorical refusal. Honest read of the literature: GHB alone causes respiratory depression and deaths, especially when stacked with alcohol or benzodiazepines. Ketamine independently can depress respiration at higher doses. The combination is pharmacologically risky on first principles. However, there are no published case reports of GHB plus ketamine specifically causing fatality or severe respiratory depression that we have found. Our caution here is precautionary additive-CNS-depression reasoning, not documented combination-specific harm. For prescription Xyrem/Xywav for narcolepsy, KAP can proceed with careful timing. For recreational GHB use, the underlying use pattern matters more than the combination per se.

'Bath salts' is a generic term for synthetic cathinones — designer drugs like MDPV, mephedrone, alpha-PVP ('flakka'), and methylone. They are DEA Schedule I controlled substances. Pharmacologically, they combine massive monoamine release (serotonin, norepinephrine, dopamine) with reuptake inhibition — similar mechanism family to MDMA and methamphetamine but typically more cardiovascular and more unpredictable. Documented effects include hypertensive crisis, tachyarrhythmias, hyperthermia, rhabdomyolysis, seizures, and psychotic episodes — often at doses people didn't intend (product purity varies wildly). Stacking with ketamine's pressor effect compounds the cardiovascular risk. Recent use disqualifies any ketamine session.

Cocaine is a DEA Schedule II controlled substance in the United States. It has a narrow legitimate medical use as a topical anesthetic in certain surgical settings, but recreational possession and use are federal felonies in every state. That legal status alone shapes what we can supervise. Clinically, the case against combining is stronger than for MDMA or LSD because the concern is cardiovascular, not just CNS-depression theory: cocaine causes documented hypertension, tachycardia, vasoconstriction, and is independently associated with MI, stroke, aortic dissection, and arrhythmia. Ketamine adds a transient sympathomimetic pressor response on top of that baseline. We will not run a ketamine session in proximity to cocaine use, and patients in active stimulant use disorder generally benefit more from coordinated addiction treatment than at-home KAP.

Heroin is a DEA Schedule I controlled substance in the United States, with no accepted medical use in this country (it is legal medically in the UK and some other countries as diamorphine). Clinically, the concern is additive respiratory depression with ketamine plus the contamination problem in illicit heroin (frequently adulterated with fentanyl, which compounds the respiratory risk). We will not run a ketamine session in proximity to heroin use. Patients in active opioid use disorder benefit more from coordinated treatment (medication-assisted treatment with buprenorphine or methadone) than at-home KAP. After stable recovery on MAT, KAP becomes an option — buprenorphine and methadone have their own pages.

Synthetic cannabinoids (K2, Spice, etc.) are NOT pharmacologically similar to cannabis despite the marketing. They are full CB1 receptor agonists (THC is only a partial agonist), often 100x more potent at the receptor. Documented harms include seizures, myocardial infarction in young patients, acute kidney injury, hyperthermia, and severe psychotic episodes — sometimes from a single use. Product composition is unregulated and varies wildly between batches. Stacking with ketamine adds unpredictable cardiovascular and CNS effects on top of already-unpredictable pharmacology. Recent use disqualifies any ketamine session.

Methamphetamine is a DEA Schedule II controlled substance in the United States. A prescription form (Desoxyn) exists for ADHD and obesity but is rarely used; recreational methamphetamine is a federal felony in every state. Clinically, the case against combining mirrors cocaine but is often stronger because illicit methamphetamine doses are typically much higher than prescription stimulants. Combined with ketamine's transient sympathomimetic response, the cardiovascular risk is meaningful. We will not run a ketamine session in proximity to methamphetamine use, and patients in active stimulant use disorder benefit more from coordinated addiction treatment.

Patients on active MAOI therapy are not candidates for at-home ketamine at Tovani Health. This is an operational position, not an evidentiary claim that the combination is universally dangerous: recent published literature (Veraart et al. 2022, N=39, no adverse events; Veraart et al. 2021 systematic review, no documented hypertensive crisis or serotonin syndrome) suggests the combination is safer in carefully monitored research and clinical settings than was historically presumed. At-home unmonitored is not that setting. After a 14-day washout from an irreversible MAOI under your prescribing psychiatrist's care, you become eligible.

Patients on active methylene blue are not candidates for at-home ketamine therapy at Tovani Health. This is an operational position, not an evidentiary claim that the combination is universally dangerous. Methylene blue is a potent MAO inhibitor at clinical doses, and chronic low-dose nootropic protocols popular in biohacking communities produce meaningful MAO inhibition as well. The FDA's published warning is about methylene blue plus serotonergic agents (SSRIs, SNRIs); ketamine is in a related but distinct category because the limiting concern is sympathomimetic, not serotonergic. Ketamine acutely raises BP via indirect catecholamine release, and MAO inhibition slows clearance of those catecholamines, theoretically raising the risk of a hypertensive episode in an unmonitored at-home setting. After 2 weeks off methylene blue under your prescriber's care, you become eligible.

Ibogaine is a DEA Schedule I controlled substance in the United States. Recreational and ceremonial use occurs internationally (Mexico, Costa Rica) primarily for opioid use disorder treatment, and the limited research interest is in supervised inpatient settings only. Two specific concerns matter: ibogaine causes documented QT prolongation and torsades de pointes, with multiple fatalities in published case series; and the long active duration (24-72 hours) plus serotonergic and NMDA-modulating activity means a long pharmacologic interaction window with ketamine. Patients who have used ibogaine recently are not candidates for at-home KAP until well into the recovery window.

Tianeptine is approved as a prescription antidepressant in some countries (France, Mexico, others), but it is NOT FDA-approved in the United States. Despite that, it is widely sold at US gas stations and convenience stores under names like 'ZaZa,' 'Tianna Red,' 'Pegasus,' and 'TD Red' marketed as supplements or 'mood enhancers.' The pharmacology matters: at therapeutic doses tianeptine has mild atypical antidepressant activity, but at the recreational doses found in OTC products it acts as a mu-opioid agonist with documented dependence, withdrawal, and increasing reports of seizure and cardiac events. The FDA has issued multiple warnings. At-home KAP while actively using tianeptine is not appropriate — the opioid-like effects compound with ketamine's CNS depression, and the unpredictable dosing in unregulated products makes session planning unsafe.

Patients on active linezolid are not candidates for at-home ketamine therapy at Tovani Health. This is an operational position, not an evidentiary claim that the combination is universally dangerous. The published case literature is thinner than older safety language suggests; the Veraart 2021 and 2022 work on ketamine plus MAO inhibitors found no documented hypertensive crisis or serotonin syndrome in monitored clinical settings, and the FDA's linezolid warning specifically concerns serotonergic agents like SSRIs and SNRIs rather than ketamine. The reason we hold is mechanism plus setting: ketamine raises BP via indirect catecholamine release, linezolid reversibly inhibits MAO and slows catecholamine clearance, and at-home unmonitored sessions are not the place to test how that interaction will go for a given patient. After your linezolid course is finished and a conservative 14-day washout has passed under your prescriber's care, you become eligible.