evidence·published September 15, 2026·every citation last verified September 15, 2026

does ketamine work for depression — what the trials actually show

an infusion clinic in a strip mall, a nasal spray with a two-hour observation period, an at-home lozenge from a telehealth company. all three are “ketamine for depression”, and the ads say it works in hours. nobody hands you the trials.

here they are. how big the effect is and how sure the reviewers are, whether the generic infusion and the branded spray are the same thing, how long it lasts, what the licensing trials found including the one that failed, what the critics say in their own words, what it does to suicidal thoughts, how it compares with ect in three studies that disagree, and what the safety literature knows and does not. fourteen sources, funding and patents printed where the record states them. the regulatory half, what is and is not approved and the compounded-ketamine warning, is on its own page.

two drugs, in one paragraph

racemic ketamine is the generic anaesthetic, usually given as an intravenous infusion of 0.5 mg per kilogram over about 40 minutes in the trials; every psychiatric use of it is off-label. esketamine is one of its two mirror-image halves, formulated as a nasal spray, taken through the fda process by janssen and approved on 5 march 2019 under a risk evaluation and mitigation strategy that requires a certified setting and observation^[14]. the trials below are mostly of one or the other, and the pooled reviews keep them apart, which turns out to matter.

the whole trial base: 64 studies, 5,299 people

the 2021 cochrane review pooled 64 randomised trials of glutamate-modulating drugs for unipolar depression, 31 of them ketamine and 9 esketamine. most ketamine trials gave a single intravenous dose; every esketamine trial used repeated intranasal dosing, usually twice a week for four weeks^[1]. against placebo at 24 hours, ketamine roughly quadrupled the odds of response or remission (odds ratio 3.94, 95% confidence interval 1.54 to 10.10, 7 studies, 185 people) and lowered depression scores by a large margin (standardised mean difference −0.87), and the reviewers graded both findings very low certainty^[1]. against midazolam, the active placebo that mimics ketamine's sedation, remission at 24 hours was higher (odds ratio 2.21, interval 0.67 to 7.32, low certainty) and response was uncertain^[1].

esketamine's numbers are smaller and better established: remission at 24 hours odds ratio 2.74 (1.71 to 4.40, 5 studies, 894 people, moderate certainty), depression scores −0.31 (moderate certainty), response odds ratio 2.11 (low certainty)^[1]. read those two paragraphs together. the generic drug has the bigger effect and the weaker evidence; the branded one has the smaller effect and the stronger evidence, because a company ran large trials of it. certainty and size are different things, and a clinic quoting one without the other is telling you half.

racemic versus esketamine, and dose

a 2023 meta-regression across 49 randomised trials and 3,299 people compared the two formulations directly. immediately after a first dose, high-dose racemic ketamine had the largest effect (standardised mean difference −0.73) and high-dose esketamine −0.48. during repeated dosing, racemic ketamine's effect stayed significantly above control at both doses; esketamine's did not (−0.15 low dose, −0.22 high dose, intervals crossing zero). at follow-up after the last dose, racemic ketamine's effect was still significant (−0.65) and esketamine's was not (−0.33, −0.96 to 0.31)^[2]. higher doses beat lower doses for both. the authors' own summary: effects were “numerically greater for racemic ketamine than esketamine”^[2]. this is a comparison across trials, not a head-to-head randomisation, and heterogeneity was high in places.

how long it lasts

a single infusion is measured in days. pooled patient-level data from 17 randomised trials, 809 people, put the effect at about 24 hours at a standardised 0.58 and at about seven days at 0.38^[3]. with repeated dosing, the racemic effect persisted in the pooled trials and the esketamine effect did not clearly outlast the dosing^[2].

the clearest maintenance number is esketamine's own withdrawal trial. 297 people who had reached stable remission or response on esketamine plus an antidepressant were randomised to keep the spray or switch to placebo spray. among the stable remitters, 26.7% relapsed on continued esketamine versus 45.3% on placebo, number needed to treat 6; among stable responders, 25.8% versus 57.6%^[7]. in the hospital trial of ketamine against ect, 70% of the ketamine remitters and 63% of the ect remitters had relapsed within twelve months, with a median of about two months in remission^[9]. real-world series, with no control arm, report about 45% responding and 30% remitting, with the effect not declining across repeated treatments and the most treatment-resistant remitting less often^[11].

the licensing trials, as they read

esketamine was approved on short-term trials that compared spray plus a newly started antidepressant against placebo spray plus the same new antidepressant, in people who had not responded to at least two prior drugs. transform-2, the flexible-dose trial in 227 people at 39 centres, was positive: a difference of −4.0 points on the 60-point montgomery-åsberg scale at day 28 (95% confidence interval −7.31 to −0.64). dissociation, nausea, vertigo, altered taste and dizziness were all more common on esketamine, appearing shortly after dosing and resolving by about 90 minutes, and 7% stopped for adverse events versus 0.9% on placebo^[5].

transform-1, the fixed-dose trial in 346 people, missed its primary endpoint: the 84 mg arm's difference was −3.2 points (−6.88 to 0.45, P = .088), and under the pre-specified testing sequence the 56 mg arm could not be formally tested, although its nominal difference was −4.1. the authors wrote that the effect nevertheless “exceeded what has been considered clinically meaningful for approved antidepressants vs placebo”^[6]. the third leg was the withdrawal trial above^[7].

the case against, in its authors' words

two psychiatrists reviewed the same record and concluded: “Licensing trials did not establish efficacy: two trials were negative, one showed a statistically significant but clinically uncertain effect, and a flawed discontinuation trial was included, against Food and Drug Administration precedent. Safety signals - deaths, including suicides, and bladder damage - were minimised.”^[13]

you can check that against the trials on this page. the “statistically significant but clinically uncertain” trial is transform-2's four points^[5]; the negative one is transform-1^[6]; the discontinuation trial is sustain-1^[7], whose randomised-withdrawal design measures what happens when responders are taken off a drug, which can include withdrawal effects as well as relapse. the fda accepted that design. whether four points on a sixty-point scale is worth a certified clinic and two hours of observation twice a week is a judgement the trials cannot make for you.

suicidal thoughts

the best evidence is patient-level: ten of eleven controlled trials, restricted to the 167 participants who had suicidal ideation at baseline. a single intravenous dose reduced suicidal thoughts within one day and for up to a week, with effect sizes from 0.48 to 0.85 on clinician-rated and self-report scales, and the effect remained after adjusting for the change in depression^[4]. that is ideation for a week, in 167 people; not attempts, not deaths. the authors' closing line: “Additional research on ketamine's long-term safety and its efficacy in reducing suicide risk is needed before clinical implementation.”^[4] the fda's 2020 esketamine indication for depressive symptoms in people with acute suicidal ideation, and the fact that an effect on the ideation itself was not demonstrated in those trials, is on the regulatory page.

ketamine versus ect: three studies that disagree

outpatients, no psychosis. elekt-d randomised 403 people referred to ect clinics with treatment-resistant depression and no psychosis to ketamine twice a week or ect three times a week for three weeks. response was 55.4% on ketamine versus 41.2% on ect, a 14-point difference that met the non-inferiority test (P<0.001). ect was associated with a fall in delayed recall at three weeks (t-score change −9.7 versus −0.9) with gradual recovery during follow-up; patient-reported quality of life improved similarly in both^[8]. open-label, and the outcome was self-reported.

inpatients. ketect randomised 186 hospitalised patients aged 18 to 85 to thrice-weekly ketamine infusions or ect, up to twelve sessions. remission was 63% on ect versus 46% on ketamine (P = .026), both after a median of six sessions. serious and long-lasting adverse events, including persisting amnesia, were more common with ect; treatment-emergent adverse events led to more dropouts with ketamine^[9]. the meta-analysis of six inpatient trials, all in people eligible for ect, found the same direction: ect ahead by a standardised mean difference of −0.69, with no significant difference in cognition or serious adverse events^[10].

who it works for

the patient-level pooled analysis went looking for who benefits most across 33 candidate moderators and found no reliable patient-level predictor. two study-level moderators emerged: the effect against placebo was larger in trials that required a higher degree of prior treatment resistance to enter, at least two failed antidepressants, and in crossover designs^[3]. the first is worth holding onto. ketamine's evidence base was built on people for whom several drugs had failed, and that is the population the effect sizes describe. the first author of that analysis is named inventor on a provisional patent for ketamine combined with cognitive training^[3]; it is disclosed in the record and so it is here.

safety: what is known and what is not

after acute dosing, psychiatric, psychotomimetic, cardiovascular, neurological and other side effects were reported more often on ketamine than placebo across 60 studies. the review's more important finding was about the literature itself: “a selective reporting bias with limited assessment of long-term use and safety and after repeated dosing, despite these being reported in other patient groups exposed to ketamine (eg, those with chronic pain) and in recreational users”^[12]. the licensing trials add the short-term profile: dissociation, nausea, vertigo, dizziness and headache, mostly resolving within about 90 minutes^[5],[6]. the bladder and dependence questions the critics raise^[13] come from those other populations, and the trials in depression were too short to answer them either way. every trial on this page was run in a monitored setting; the at-home telehealth market operates outside the conditions the evidence was generated under, which is the subject of the fda's 2023 warning on the regulatory page.

what to ask before you sign up

these are questions, not advice. they are the ones the trials make it reasonable to ask.

racemic infusion or esketamine spray, and at what dose? the pooled effects differ by formulation and dose^[2]
the response rate you quote: is it from randomised trials or from your own patients with no control arm?^[1],[11]
what is the plan after the induction course, given that roughly half of responders relapse within months without maintenance?^[7],[9]
how many antidepressants have i actually tried? the evidence is strongest in people with at least two failures^[3]
if i am unwell enough to be an inpatient, was ect discussed, and why is ketamine preferred for me?^[9],[10]
what monitoring is there for blood pressure, dissociation, bladder symptoms and dependence over repeated courses?^[12]

this is not medical advice. it is a summary of published research, it is not a diagnosis, and it is not a recommendation for or against any treatment — nobody here has met you. decisions about starting, changing or stopping a medication belong to you and a prescriber who knows your history. do not change a prescribed medication on the strength of a web page, this one included.

last verified September 15, 2026. if a source is updated, corrected or retracted, this page gets changed and re-dated.

how we verify

every study below was fetched live on the access date shown — from PubMed (NCBI E-utilities) or Europe PMC for journal articles, or from the issuing body itself for regulatory documents and guidelines — and its details were checked against that record rather than copied from another article.
every record was checked for retractions, expressions of concern and errata. nothing retracted is used, and corrections are disclosed on the source.
funding is read, never inferred. a study is marked independent, industry, mixed or none only where we could read the funding statement itself. otherwise it says unknown — we do not guess a funder from the journal, the authors or the topic.
numbers here are read from the paper. where a paper does not report a figure, we leave it out instead of estimating.
every source carries its own caveat, including the ones whose findings we like. the evidence tier scores the method, funding and venue — not whether the conclusion is big, current or settled.
we are not clinicians. this page reports published evidence. it cannot account for your history, your diagnoses or your medications.

find an error? tell us and we will fix it and re-date the page. our full scoring method is at how we score evidence.

sources

primary sources only — no news write-ups, no secondary summaries. each was fetched and checked on the access date shown.

[1] Dean RL, Hurducas C, Hawton K, Spyridi S, Cowen PJ, Hollingsworth S, et al.. Ketamine and other glutamate receptor modulators for depression in adults with unipolar major depressive disorder. Cochrane Database of Systematic Reviews, 2021. doi:10.1002/14651858.CD011612.pub3. PMID 34510411.
cochrane systematic review of 64 randomised trials (31 of ketamine, 9 of esketamine) with GRADE certainty ratings · n = 5,299 · evidence tier: gold standard · funding: independent; Medical Research Council grant on the record. declarations we could read: one author holds an Oxford patent on ebselen for treatment-resistant depression; the rest of the declaration was truncated in the record · accessed September 15, 2026
the catch: the ketamine-versus-placebo estimates are graded VERY LOW certainty (small trials, single doses, mostly 24-hour outcomes); the esketamine-versus-placebo estimates are moderate certainty because the industry trials were larger. certainty and size are different things, and both are on the page.
[2] Nikolin S, Rodgers A, Schwaab A, Bahji A, Zarate C, Sackeim HA, Loo CK. Ketamine for the treatment of major depression: a systematic review and meta-analysis. eClinicalMedicine, 2023. doi:10.1016/j.eclinm.2023.102127. PMID 37593223.
systematic review and meta-regression of 49 randomised trials by formulation (racemic vs esketamine) and dose, at first dose, during repeated dosing and at follow-up (PROSPERO CRD42021221157) · n = 3,299 · evidence tier: strong · funding: none stated ("Funding: None"); one author declares doctoral funding from the Canadian Institutes of Health Research and teaching honoraria · accessed September 15, 2026
the catch: heterogeneity ran from 5.7% to 87.6% across comparisons; the racemic-versus-esketamine difference comes from meta-regression across trials, not from head-to-head randomisation.
[3] Price RB, Kissel N, Baumeister A, Rohac R, Woody ML, et al.. International pooled patient-level meta-analysis of ketamine infusion for depression: In search of clinical moderators. Molecular Psychiatry, 2022. doi:10.1038/s41380-022-01757-7. PMID 36071111.
individual patient-level meta-analysis of 17 of 25 eligible randomised trials of intravenous ketamine · n = 809 · evidence tier: strong · funding: unknown; the first author is named inventor on a provisional patent for ketamine combined with neurocognitive training, and a co-author is co-inventor on ketamine-related patents · accessed September 15, 2026
the catch: patient-level data were available for 17 of 25 trials, and moderator data for a median of 56% of participants; the two moderators found are study-level (how treatment-resistant the entry criteria were, and crossover design), not patient-level predictors.
[4] Wilkinson ST, Ballard ED, Bloch MH, Mathew SJ, Murrough JW, Feder A, et al.. The Effect of a Single Dose of Intravenous Ketamine on Suicidal Ideation: A Systematic Review and Individual Participant Data Meta-Analysis. American Journal of Psychiatry, 2018. doi:10.1176/appi.ajp.2017.17040472. PMID 28969441.
individual participant data meta-analysis of 10 of 11 comparison trials (saline or midazolam control), restricted to people with suicidal ideation at baseline · n = 167 · evidence tier: strong · funding: independent; NIMH and NIH intramural grants on the record · accessed September 15, 2026
the catch: suicidal ideation for up to one week after a single dose, in 167 people; not suicide attempts, not deaths, and not beyond a week. the authors say long-term safety and efficacy in reducing suicide risk need more research before clinical implementation.
[5] Popova V, Daly EJ, Trivedi M, Cooper K, Lane R, Lim P, et al.. Efficacy and Safety of Flexibly Dosed Esketamine Nasal Spray Combined With a Newly Initiated Oral Antidepressant in Treatment-Resistant Depression: A Randomized Double-Blind Active-Controlled Study (TRANSFORM-2). American Journal of Psychiatry, 2019. doi:10.1176/appi.ajp.2019.19020172. PMID 31109201.
phase 3 double-blind randomised trial at 39 outpatient centres; esketamine plus a new antidepressant versus placebo spray plus a new antidepressant, 28 days · n = 227 · evidence tier: strong · funding: industry; a Janssen licensing trial (the funding statement itself was not readable in the record we used, so this is read from the trial’s registration and authorship, and recorded as industry on that basis) · accessed September 15, 2026
the catch: the one positive licensing trial: a 4-point difference on a 60-point scale at day 28. 7% of the esketamine arm stopped for adverse events versus 0.9% on placebo, and the comparator arm also got a new antidepressant, so this is esketamine’s addition on top of a switch, not versus nothing.
read our summary of this study →
[6] Fedgchin M, Trivedi M, Daly EJ, Melkote R, Lane R, et al.. Efficacy and Safety of Fixed-Dose Esketamine Nasal Spray Combined With a New Oral Antidepressant in Treatment-Resistant Depression: Results of a Randomized, Double-Blind, Active-Controlled Study (TRANSFORM-1). International Journal of Neuropsychopharmacology, 2019. doi:10.1093/ijnp/pyz039. PMID 31290965.
phase 3 double-blind randomised trial, fixed doses of 56 or 84 mg twice weekly plus a new antidepressant versus placebo spray plus antidepressant, 4 weeks · n = 346 · evidence tier: strong · funding: industry; a Janssen licensing trial (recorded on the same basis as source 5) · accessed September 15, 2026
the catch: the primary endpoint was not met: the 84 mg arm’s difference was −3.2 points (95% CI −6.88 to 0.45, P = .088), and under the pre-specified testing sequence the 56 mg arm could not be formally tested. the authors call the effect clinically meaningful anyway; the page quotes both.
[7] Daly EJ, Trivedi MH, Janik A, Li H, Zhang Y, Li X, et al.. Efficacy of Esketamine Nasal Spray Plus Oral Antidepressant Treatment for Relapse Prevention in Patients With Treatment-Resistant Depression: A Randomized Clinical Trial (SUSTAIN-1). JAMA Psychiatry, 2019. doi:10.1001/jamapsychiatry.2019.1189. PMID 31166571.
phase 3 randomised withdrawal trial: 297 people already in stable remission or response on esketamine were randomised to continue or switch to placebo spray · n = 297 · evidence tier: strong · funding: industry; Janssen Research & Development · accessed September 15, 2026
the catch: a randomised-withdrawal design measures what happens when responders are taken off the drug, which can include withdrawal effects as well as relapse; the critics in source 13 argue this design should not have counted toward licensing, and the fda accepted it. both positions are on the page.
read our summary of this study →
[8] Anand A, Mathew SJ, Sanacora G, Murrough JW, Goes FS, Altinay M, et al.. Ketamine versus ECT for Nonpsychotic Treatment-Resistant Major Depression (ELEKT-D). New England Journal of Medicine, 2023. doi:10.1056/NEJMoa2302399. PMID 37224232.
open-label randomised non-inferiority trial at five sites, patients referred to ect clinics without psychosis; ketamine twice weekly versus ect three times weekly for three weeks, six months of follow-up · n = 403 · evidence tier: strong · funding: independent; Patient-Centered Outcomes Research Institute · accessed September 15, 2026
the catch: open-label, outpatient, no psychosis, and the outcome was self-reported; 38 people withdrew before treatment began. the population is why its answer differs from sources 9 and 10, and the page says so.
read our summary of this study →
[9] Ekstrand J, Fattah C, Persson M, Cheng T, Nordanskog P, et al.. Racemic Ketamine as an Alternative to Electroconvulsive Therapy for Unipolar Depression: A Randomized, Open-Label, Non-Inferiority Trial (KetECT). International Journal of Neuropsychopharmacology, 2022. doi:10.1093/ijnp/pyab088. PMID 35020871.
open-label randomised non-inferiority trial in 186 hospitalised patients with unipolar depression, ketamine infusions thrice weekly versus ect, up to 12 sessions, 12 months of follow-up for remitters · n = 186 · evidence tier: strong · funding: unknown (not stated in the abstract we read) · accessed September 15, 2026
the catch: inpatients aged 18 to 85, and the primary outcome was clinician-rated remission; ketamine was inferior here (46% versus 63%), which is the opposite direction from source 8, in a sicker population.
[10] Rhee TG, Shim SR, Forester BP, Nierenberg AA, McIntyre RS, Papakostas GI, Krystal JH, Sanacora G. Efficacy and Safety of Ketamine vs Electroconvulsive Therapy Among Patients With Major Depressive Episode: A Systematic Review and Meta-analysis. JAMA Psychiatry, 2022. doi:10.1001/jamapsychiatry.2022.3352. PMID 36260324.
systematic review and meta-analysis of six trials (five randomised) comparing ect with ketamine in inpatients eligible for ect · n = 340 · evidence tier: strong · funding: independent; NIH grants (NIA, NIMH, NCATS) listed on the record · accessed September 15, 2026
the catch: search closed april 2022, before source 8 was published; all six trials were inpatient.
[11] Alnefeesi Y, Chen-Li D, Krane E, Jawad MY, Rodrigues NB, et al.. Real-world effectiveness of ketamine in treatment-resistant depression: A systematic review & meta-analysis. Journal of Psychiatric Research, 2022. doi:10.1016/j.jpsychires.2022.04.037. PMID 35688035.
systematic review and meta-analysis of 79 real-world (non-randomised) studies of ketamine in treatment-resistant depression, with 32 meta-regressions · n = 2,665 · evidence tier: moderate · funding: unknown (not stated in the abstract we read) · accessed September 15, 2026
the catch: no control arms: these are the numbers clinics quote, and they measure the experience of being treated as well as the drug. cited for the response and remission rates people will be shown, beside the randomised numbers.
[12] Short B, Fong J, Galvez V, Shelker W, Loo CK. Side-effects associated with ketamine use in depression: a systematic review. The Lancet Psychiatry, 2018. doi:10.1016/S2215-0366(17)30272-9. PMID 28757132.
systematic review of 60 studies reporting safety after single and repeated ketamine doses in depression · evidence tier: strong · funding: unknown (not stated in the abstract we read) · accessed September 15, 2026
the catch: the review’s own finding is a selective reporting bias with limited assessment of long-term and repeated-dose safety; it is cited for what is not known as much as for what is.
[13] Horowitz MA, Moncrieff J. Are we repeating mistakes of the past? A review of the evidence for esketamine. British Journal of Psychiatry, 2021. doi:10.1192/bjp.2020.89. PMID 32456714.
critical review of the esketamine licensing evidence by two psychiatrists critical of the approval · evidence tier: contested · funding: unknown (not stated in the abstract we read) · accessed September 15, 2026
the catch: the published case against, quoted in its own words so the reader sees it. it is a review, not new data; its claims about the licensing trials can be checked against sources 5, 6 and 7 on this page, and the page does that.
[14] US Food and Drug Administration, Center for Drug Evaluation and Research. FDA approval letter, Spravato (esketamine) NDA 211243, with REMS history. Drugs@FDA approval letter, 2019.
the regulator’s approval record: original approval 5 march 2019 under a risk evaluation and mitigation strategy, later supplements · evidence tier: strong · funding: n/a (regulator) · accessed September 15, 2026
the catch: the regulatory story (which uses are approved, the REMS, the 2023 warning on compounded ketamine) has its own page on this site; this page cites the letter only to anchor the approval date and route.

questions

Does ketamine actually work for depression?

In randomised trials, yes, quickly, with caveats about how sure we can be. The 2021 Cochrane review of 64 trials found ketamine roughly quadrupled the odds of response or remission at 24 hours versus placebo (odds ratio 3.94) but graded that evidence very low certainty, because the trials were small and mostly single-dose. Esketamine’s evidence is moderate certainty and smaller in size: odds of remission at 24 hours 2.74 versus placebo. Across 49 trials, the effect sizes were numerically larger for racemic ketamine than for esketamine and larger at higher doses.

How long does ketamine last for depression?

A single infusion’s effect is measured in days: in pooled patient-level data the effect was large at about 24 hours and about two-thirds as large at seven days. With repeated dosing the effect persisted for racemic ketamine in the pooled trials and did not clearly persist for esketamine after dosing stopped. The clearest maintenance number is from the esketamine withdrawal trial: among people in stable remission, 26.7% relapsed if they kept taking it versus 45.3% if they were switched to placebo. In the hospital ketamine-versus-ECT trial, 70% of ketamine remitters relapsed within twelve months.

Is esketamine (Spravato) proven to work?

One of its two short-term licensing trials was positive (a 4-point difference on a 60-point scale at day 28), one missed its primary endpoint (a 3.2-point difference, P = .088), and a randomised-withdrawal trial showed continuing it halved relapse among responders. The FDA approved it in March 2019 on that record. Two psychiatrists reviewing the same trials wrote that they “did not establish efficacy”. Both readings are on this page with the numbers they rest on.

Does ketamine help with suicidal thoughts?

In pooled patient-level data from ten trials, 167 people with suicidal ideation at baseline, a single intravenous dose reduced suicidal thoughts within a day and for up to a week, with moderate-to-large effect sizes, partly independent of the effect on mood. That is suicidal ideation for a week, not suicide attempts or deaths, and the authors said more research on long-term safety and suicide risk is needed before clinical implementation.

Is ketamine as good as ECT?

Three studies, three answers, and the difference is who was enrolled. In outpatients without psychosis referred to ECT clinics, ketamine was non-inferior and had more responders (55.4% versus 41.2%) with less memory loss. In hospitalised patients, ECT produced more remissions (63% versus 46%). A meta-analysis of six inpatient trials favoured ECT. So: for the sickest inpatients ECT has the edge in the trials that exist; for outpatients without psychosis ketamine held its own.

What are the side effects of ketamine for depression?

In the licensing trials, dissociation, nausea, vertigo, dizziness and headache were the most common, appearing shortly after dosing and mostly resolving within about 90 minutes; 7% of the esketamine arm stopped for adverse events versus 0.9% on placebo in the positive trial. The systematic review of safety found psychiatric, dissociative, cardiovascular and neurological effects more often on ketamine than placebo, and, more importantly, a selective reporting bias with little assessment of long-term or repeated-dose safety.

Who does ketamine work best for?

The pooled patient-level analysis of 17 trials found no reliable patient-level predictor. Two study-level ones emerged: the effect versus placebo was larger in trials that required a higher degree of treatment resistance to enter (at least two failed antidepressants), and in crossover designs. Real-world series report about 45% responding and 30% remitting, with the most treatment-resistant patients remitting less often.

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