Ketamine for Depression Treatment
The only psychedelic or psychedelic-adjacent compound with a genuine, FDA- and EMA-approved registration for treatment-resistant depression — intranasal esketamine (Spravato) — alongside the still-unregistered but widely used off-label intravenous ketamine infusion offered at specialized clinics. A fast, unusual mechanism of action comes paired with real risks: dissociation during administration, abuse potential, and documented, serious bladder toxicity with chronic, non-medical misuse.
Number of studies
3
Safety
Requires caution
Time to effects
The antidepressant effect can be noticeable within hours to 24 hours after the first administration, though in most patients it's short-lived after a single dose and requires a series of repeated administrations within a supervised protocol to maintain the effect during the maintenance phase.
Monthly cost
W fazie indukcyjnej (2 podania tygodniowo) koszt miesięczny może sięgać kilku tysięcy złotych, zależnie od placówki i formy leczenia
Price in Poland
Jedna sesja dożylnego wlewu ketaminy w prywatnej klinice w Polsce: ok. 800–2000 zł; esketamina (Spravato) w ramach prywatnej opieki psychiatrycznej bywa droższa ze względu na koszt samego leku i wymóg certyfikowanej placówki
Who it's for
Koszt jest zmienny i zależy od placówki, formy leczenia oraz tego, czy terapia odbywa się w ramach NFZ (ograniczona dostępność) czy w sektorze prywatnym — ceny mają charakter orientacyjny.
Indicative prices for the Polish market — we don't point to specific retailers; the real price depends on the manufacturer, form and place of purchase.
Table of contents
TL;DR
The only psychedelic or psychedelic-adjacent compound with a genuine, FDA- and EMA-approved registration for treatment-resistant depression — intranasal esketamine (Spravato) — alongside the still-unregistered but widely used off-label intravenous ketamine infusion offered at specialized clinics. A fast, unusual mechanism of action comes paired with real risks: dissociation during administration, abuse potential, and documented, serious bladder toxicity with chronic, non-medical misuse.
- →Esketamine (Spravato) is a genuinely FDA- and EMA-approved drug for treatment-resistant depression — not an experimental, unregistered therapy
- →Unusually fast onset of antidepressant action — an effect sometimes visible within hours, not weeks as with classic SSRIs/SNRIs
- →Documented efficacy in reducing acute suicidal ideation under clinically supervised conditions, with real value in crisis situations
| Substance | Ketamine (racemic) / esketamine (S-enantiomer) — an NMDA receptor antagonist |
|---|---|
| Esketamine (Spravato) status | Approved by the FDA (3/5/2019) and EMA (12/18/2019) for treatment-resistant depression |
| IV ketamine status | Used off-label for depression treatment — registered only as an anesthetic |
| Evidence level | Strong for esketamine in registration trials; moderate for off-label IV ketamine |
| Administration | Exclusively at a certified medical facility, under supervision, with a minimum 2-hour observation period after dosing |
| Interactions | Yes — CNS-acting drugs, substances with abuse potential |
| Legal status | Prescription drug, controlled substance — not for self-administration |
Understand
Overview
Ketamine has been a known anesthetic drug for decades, used since the 1970s for general anesthesia and analgesia, especially in emergency and veterinary medicine, thanks to an unusually good hemodynamic safety profile compared to other anesthetics. The discovery of its rapid, though short-lived, antidepressant effect — the first controlled trial was published back in 2000 — opened an entirely new direction in depression pharmacotherapy, distinct from all antidepressant classes used until then, which are based on modulating monoaminergic systems (serotonin, norepinephrine, dopamine).
What sets ketamine apart from psilocybin or MDMA, discussed in other entries in our knowledge base, is its genuine, approved regulatory status. Intranasal esketamine (the S-enantiomer of ketamine, sold under the brand name Spravato) received approval from the US Food and Drug Administration (FDA) on March 5, 2019, for treatment-resistant depression in adults, used in combination with an oral antidepressant. The European Medicines Agency (EMA) issued a positive opinion in October 2019, with formal marketing authorization across the European Union following on December 18, 2019, for the same indication. This makes esketamine, unlike psilocybin therapy or MDMA, a legally available, registered prescription drug — though still administered exclusively in certified facilities, under the direct supervision of medical staff.
Alongside registered esketamine there's a second, far less regulated access route: intravenous infusion of racemic ketamine (containing both the R and S enantiomers), used off-label — that is, outside the formal registered indication of a drug itself approved as an anesthetic, not as an antidepressant — in hundreds of specialized, usually private clinics worldwide, including in Poland. Such an infusion doesn't go through the same rigorous phase 3 registration trials specific to the depression indication as Spravato did, though it draws on the same well-established evidence base for ketamine's rapid antidepressant effect as a substance, built from dozens of smaller academic studies.
Who can this realistically help? Primarily patients with treatment-resistant depression — defined as a lack of response to at least two prior, adequately delivered lines of pharmacological treatment — in whom the risk of chronic suffering, hospitalization and suicide is elevated. A second, distinct and especially important group is patients in acute suicidal crisis, where ketamine's speed of action (an effect sometimes visible within hours rather than weeks, as with classic SSRIs) has real, potentially life-saving clinical value in hospital settings.
It's important to understand, though, that ketamine — regardless of the route of administration — is not a drug for self-administered, chronic use without medical supervision. It's a controlled substance (a prescription drug in Poland, additionally subject to regulations on controlled substances in certain contexts), and its antidepressant effect after a single administration is usually short-lived, which forces repeated administrations within a supervised treatment protocol rather than a one-off, self-directed intervention.
It's also worth clearly distinguishing between controlled, medical use and recreational, uncontrolled ketamine misuse, discussed further in the risks section — this distinction is key to understanding why some of the most serious, well-documented complications (especially bladder toxicity) come almost exclusively from case reports of people using ketamine recreationally, at high doses and high frequency, rather than from the medical protocols used in depression treatment under physician supervision.
History of use
Ketamine was synthesized in 1962 by chemist Calvin Stevens at Parke-Davis laboratories, as a safer alternative to phencyclidine (PCP), an earlier anesthetic from the same class burdened with stronger and longer-lasting psychotomimetic effects. The FDA approved ketamine as a general anesthetic in 1970, and the drug quickly gained popularity in emergency and field medicine (including with the US military during the Vietnam War) due to its unusually good hemodynamic and respiratory safety profile compared to other general anesthetics. The first controlled trial of its rapid antidepressant action, conducted by John Krystal and Robert Berman's team at Yale University, was published in 2000, showing a significant reduction in depression symptoms within hours of a single infusion — an observation unusual enough against the backdrop of the depression-drug knowledge of that era that it was initially met with considerable skepticism. The following decade and a half of academic research confirmed the reproducibility of this effect, leading Janssen (part of Johnson & Johnson) to develop intranasal esketamine as a separate medicinal product, approved by the FDA and EMA in 2019.
Mechanism of action
Ketamine's mechanism of action is fundamentally different from all classic antidepressants. While SSRIs, SNRIs and tricyclic antidepressants work by modulating monoaminergic systems (serotonin, norepinephrine) and require weeks of regular use to produce a clinical effect, ketamine acts as an antagonist of the NMDA (N-methyl-D-aspartate) receptor — one of the main types of glutamatergic receptors in the brain, the main excitatory neurotransmitter in the central nervous system.
Blocking NMDA receptors on GABAergic (inhibitory) neurons paradoxically leads to a sudden, transient surge in glutamate release in the prefrontal cortex — a phenomenon sometimes described as a "glutamate surge." This sudden excess of glutamate in turn activates AMPA receptors (another type of glutamatergic receptor), triggering a signaling cascade involving the mTOR (mammalian target of rapamycin) pathway and increased production of brain-derived neurotrophic factor (BDNF) — a protein crucial for synaptic growth and remodeling.
This cascade leads to rapid synaptogenesis — the formation of new synaptic connections in the prefrontal cortex, documented in animal models within just a few hours of ketamine administration. It's precisely this rapid structural remodeling of synapses, rather than the gradual, progressive receptor adaptation characteristic of classic antidepressants, that is considered the main mechanism behind ketamine's unusually fast antidepressant effect — sometimes noticeable within hours of administration, unlike the 2-6 weeks needed for an SSRI effect.
Ketamine is a racemic mixture of two enantiomers: R-ketamine and S-ketamine (esketamine). Esketamine shows roughly 3-4 times stronger affinity for the NMDA receptor than R-ketamine, which was one of the pharmacological arguments behind developing and registering esketamine itself (Spravato) as a separate medicinal product, allowing a comparable clinical effect at a lower total substance dose. At the same time, the dissociative, "derealizing" sensations during administration — typical of the whole arylcyclohexylamine class, to which ketamine belongs — are also indirectly tied to NMDA receptor blockade in the cerebral cortex and are regarded as an inherent, though controlled, part of administration, requiring a monitored clinical setting for at least two hours after dosing.
NMDA receptor blockade
Ketamine antagonizes NMDA receptors on GABAergic neurons, disinhibiting glutamate release.
Glutamate "surge"
A transient, sharp increase in glutamate release in the prefrontal cortex activates AMPA receptors.
mTOR and BDNF pathway activation
AMPA receptor stimulation triggers the mTOR cascade and increases BDNF production, a protein key to synaptic plasticity.
Rapid synaptogenesis
New synaptic connections form in the prefrontal cortex within hours of administration — the basis of the fast antidepressant effect.
Dissociative effects
NMDA receptor blockade in the cortex simultaneously produces ketamine's typical dissociative sensations, requiring monitored administration.
Evidence: strong — based on 3 studies in this database.
Benefits
Common myths
MythKetamine used to treat depression is the same, uncontrolled substance sometimes misused recreationally in clubs.
FactChemically it's the same substance (or its enantiomer), but the context, dose, frequency and supervision are fundamentally different. Documented bladder toxicity and other serious complications come mainly from case reports of people using ketamine recreationally, at high doses and very frequently — not from medical protocols used in depression treatment under physician supervision.
MythEsketamine (Spravato) is still an experimental, unapproved drug.
FactEsketamine was formally approved by the US FDA in March 2019 and by the European EMA in December 2019 for treatment-resistant depression in adults, combined with an oral antidepressant — it's a registered prescription drug, not an experimental therapy.
MythSince ketamine works quickly, one session is enough to permanently cure depression.
FactThe antidepressant effect after a single administration is usually short-lived — lasting days to about a week. Maintaining the effect long-term requires a series of repeated administrations within a structured protocol (induction and maintenance phases), supervised by a psychiatrist, not a one-off intervention.
Forms & variants
Ketamine for Depression Treatment comes in several forms that differ in bioavailability and use case — the form you pick genuinely matters for how effective the supplementation is.
Intranasal esketamine (Spravato)
An FDA- and EMA-registered drug, the S-enantiomer of ketamine with stronger NMDA receptor affinity, administered under a restrictive distribution program at certified facilities.
Best for: Patients with a formal diagnosis of treatment-resistant depression, eligible for treatment with a registered drug combined with an oral antidepressant
Intravenous ketamine (racemic, off-label)
A racemic mixture of both enantiomers, given by infusion, used outside the formal registered indication of a drug approved as an anesthetic.
Best for: Patients treated at specialized ketamine clinics, often when esketamine is unavailable, too expensive, or contraindicated
Intramuscular or oral ketamine
Less commonly used forms, mainly in research contexts or where IV infusion isn't available — less well studied than the IV and intranasal forms for depression.
Best for: A research niche or facilities without IV capability — not a treatment standard
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Practice
Frequently asked questions
Esketamine was approved by the European Medicines Agency (EMA) on December 18, 2019, covering the entire European Union, including Poland. Availability in clinical practice, however, depends on the specific facility's certification and reimbursement conditions, which are worth verifying directly with the treating physician or facility, as they can change.
Esketamine (Spravato) is the S-enantiomer of ketamine, registered as a standalone medicinal product after going through phase 3 registration trials specifically for the treatment-resistant depression indication. IV ketamine used at clinics is usually a racemic mixture, given outside the formal registered indication of a drug approved as an anesthetic — it draws on a broad academic evidence base for ketamine's antidepressant action as a substance, but hasn't gone through the same registration process for that specific psychiatric indication.
Ketamine has documented abuse potential and can lead to psychological dependence, which is one reason it's administered exclusively at certified facilities, under direct supervision, rather than for self-administration at home. The risk in a controlled, supervised medical protocol is much lower than with uncontrolled, frequent, self-directed use, but it isn't zero and requires regular assessment by the treating physician.
It's a set of urinary tract symptoms — strong urgency, frequency, pain, and in severe cases blood in the urine and damage to bladder structure — first documented in the medical literature in 2007 (Shahani et al., Urology) based on a series of nine people regularly using ketamine recreationally. The phenomenon is strongly associated with chronic, high-dose misuse, and is far less often described in the context of controlled medical protocols for depression treatment, though it's worth knowing about as a real, documented risk of long-term, uncontrolled use of this substance.
Ketamine's antidepressant effect can be noticeable within hours to 24 hours of administration, radically faster than the 2-6 weeks typically needed for an SSRI or SNRI effect. This speed has particular clinical value in acute suicidal crisis, though the effect after a single administration is usually short-lived and requires repeated sessions to maintain the benefit.
Yes — in fact, the FDA- and EMA-approved regimen for esketamine specifically calls for its use in combination with a newly initiated oral antidepressant, not as monotherapy. The decision on the specific combination and dosing is always made by the treating psychiatrist, taking into account the patient's full treatment history.
No. Due to dissociative effects and sedation, the patient must remain under observation at the medical facility for at least 2 hours after administration, and should not drive or operate machinery on the day of administration until the effects have fully resolved — usually by the following day.
Dosage & timing
Typical dose
Esketamine (Spravato): starting dose of 56 mg intranasally on day 1, then 56 or 84 mg twice weekly for the first 4 weeks, later once weekly or every 2 weeks during the maintenance phase, always combined with an oral antidepressant. Off-label IV ketamine: typically 0.5 mg/kg body weight over a 40-minute infusion, given as a series of several sessions (e.g. 6 sessions over 2-3 weeks) in a clinical setting.
Form
Spravato — an intranasal spray containing esketamine, a prescription drug. Off-label IV ketamine — an infusion given exclusively in clinical settings by medical staff.
Every administration, regardless of form, requires at least 2 hours of patient observation at a certified facility due to the risk of dissociation, sedation and blood pressure elevation. This is not a drug for self-dosing at home.
Best times to take it
- Administration always at a medical facility, never self-administered at home, regardless of form (intranasal esketamine or IV ketamine)
- Minimum 2-hour observation period after administration due to the risk of dissociation, sedation and blood pressure elevation
- The esketamine induction phase (first 4 weeks, more frequent dosing) differs from the maintenance phase (less frequent dosing) — the schedule is set by the treating physician
- No driving or operating machinery on the day of administration, until dissociative effects have fully resolved
Safety
Side effects & contraindications
Possible side effects
Dissociation — a sense of detachment from one's body, surroundings or thoughts, occurring in most patients during and shortly after administration
Transient increase in blood pressure requiring monitoring, especially in patients with existing cardiovascular disease
Nausea, dizziness, drug-induced sedation in the hours following administration
Risk of misuse and psychological dependence, especially outside a controlled clinical setting
Bladder toxicity (ketamine cystitis) — documented mainly with chronic, high-dose, recreational misuse, far less often in controlled medical protocols
Potential cognitive and memory impairment with long-term, frequent, uncontrolled use
Rarely: psychotomimetic symptoms (delusions, perceptual disturbances) amplified in predisposed individuals
Contraindications
Unstable or poorly controlled cardiovascular disease, including aortic aneurysm and uncontrolled hypertension — due to ketamine's pressor effect
History of psychosis or schizophrenia-spectrum illness — risk of worsening psychotic symptoms
Elevated intracranial pressure
Pregnancy and breastfeeding
Current or past substance use disorder — requires particularly careful screening given ketamine's own abuse potential
Interactions
Benzodiazepines — may blunt ketamine's antidepressant efficacy in some studies, though data are inconsistent
Opioids and other drugs with respiratory-depressant effects — increased risk of excessive sedation with concurrent use
Other psychoactive substances with abuse potential — increased risk of interaction and cross-dependence
Blood-pressure-raising or sympathomimetic drugs — potentially additive pressor effect
Alcohol — should not be consumed around the session period due to additive sedative and dissociative effects
Is it worth taking?
Who it's for
- Patients with a formal diagnosis of treatment-resistant depression who have not responded to at least two prior lines of standard pharmacological treatment
- Patients in acute suicidal crisis, treated in hospital settings, where ketamine's speed of action has genuine clinical value
- Patients qualified by a psychiatrist for treatment at a certified facility, without cardiac or psychotic contraindications
Not for
- Unstable or poorly controlled cardiovascular disease, including aortic aneurysm and uncontrolled hypertension — due to ketamine's pressor effect
- History of psychosis or schizophrenia-spectrum illness — risk of worsening psychotic symptoms
- Elevated intracranial pressure
- Pregnancy and breastfeeding
- Current or past substance use disorder — requires particularly careful screening given ketamine's own abuse potential
Evidence
Worth knowing
Esketamine (Spravato) received FDA approval on March 5, 2019, and EMA approval on December 18, 2019, for treatment-resistant depression.
Ketamine's mechanism of action (NMDA receptor antagonism, rapid synaptogenesis) is fundamentally different from classic antidepressants that act on monoaminergic systems.
Documented, serious bladder toxicity (ketamine cystitis) comes mainly from case reports of chronic, recreational misuse, not from controlled medical protocols.
Every ketamine or esketamine administration for depression treatment requires at least 2 hours of patient observation at a certified medical facility.
Studies
Esketamine combined with a newly initiated oral antidepressant showed a significantly greater reduction in depression symptoms compared to the oral antidepressant alone with intranasal placebo, in patients with treatment-resistant depression.
Popova V et al. (TRANSFORM-2), American Journal of Psychiatry, 2019
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)
Strong evidencePopova V, Daly EJ, Trivedi M, et al. · American Journal of Psychiatry · 2019
A randomized, double-blind, active-controlled phase 3 trial (one of the two TRANSFORM registration trials) showed that flexibly dosed intranasal esketamine combined with a newly initiated oral antidepressant produced a significantly greater reduction in depression symptoms (a 4.4-point MADRS difference at day 28) than the oral antidepressant alone with intranasal placebo in patients with treatment-resistant depression. This is the only one of the two main short-term TRANSFORM trials that reached statistical significance on the primary endpoint.
View studyEffect of Esketamine Nasal Spray on Time to Relapse in Treatment-Resistant Depression (TRANSFORM-1)
Moderate evidenceFedgchin M, Trivedi M, Daly EJ, et al. · International Journal of Neuropsychopharmacology · 2019
The second phase 3 registration trial (TRANSFORM-1) compared fixed doses of esketamine (56 mg or 84 mg) with intranasal placebo, each combined with a newly initiated oral antidepressant. The 84 mg dose did not reach statistical significance on the primary endpoint versus placebo, though the 56 mg dose showed a numerically favorable trend. The authors stressed the need for larger, longer trials — the result illustrates that not every esketamine registration trial produced an unambiguously positive outcome, despite the drug's eventual approval based on the overall research program.
View studyKetamine-Associated Ulcerative Cystitis: A New Clinical Entity
Moderate evidenceShahani R, Streutker C, Dickson B, Stewart RJ · Urology · 2007
The first published case series (9 patients, all daily recreational ketamine users) describing severe, cystoscopically and biopsy-confirmed ulcerative cystitis with sterile urine cultures. Discontinuing ketamine along with pharmacological treatment brought partial symptomatic relief. The paper established ketamine cystitis as a distinct clinical entity, associated mainly with chronic, high-dose substance misuse.
View studySources & bibliography
- Popova et al. 2019 (TRANSFORM-2) — American Journal of Psychiatry
- Fedgchin et al. 2019 (TRANSFORM-1) — International Journal of Neuropsychopharmacology
- Shahani et al. 2007 — Urology
- EMA — EPAR: Spravato
The PubMed identifiers in this knowledge base were checked against NCBI records (October 2026). If you spot an error in a source, please let us know via the contact form.
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About the authors of this entry
Author
dr Piotr ZielińskiEndocrinologist
Piotr has practiced endocrinology for more than fifteen years, mostly in male hormonal disorders and metabolic health. He joined VitMode as a scientific consultant because, as he jokes, he got tired of explaining the same testosterone questions at every appointment and decided to write the answers down properly, once. He reviews content on hormone therapy, supplement pharmacology and drug interactions, making sure articles never turn into encouragement to self-supplement in situations that genuinely need diagnostics and medical supervision. His professional motto — "evidence first, enthusiasm second" — has come up more than once with a patient who arrived with a supplement plan they found online.
297 publications on this site
Medical review
dr Katarzyna LewandowskaCardiologist
Katarzyna works as a cardiologist at a Warsaw teaching hospital and has spent years focused on cardiovascular prevention — trying, as she puts it, to convince people to change their habits before they end up on her ward, not after. She joined VitMode after a series of conversations with Anna at a lifestyle-medicine conference, where the two discovered they shared the same frustration: an internet full of contradictory claims about cholesterol, aspirin and heart supplements, with no clear signal of what's actually backed by research. She reviews content on cardiovascular health, lipid panels and pharmacological prevention, consistently distinguishing what helps a statistical population from what makes sense for a specific person. Off duty, she road-cycles — not for performance, but because, in her words, it's hard to write credibly about prevention without practicing it yourself.
61 publications on this site
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Comments (2)
- KW
Kasia W. 2 weeks ago
Very clearly explained, especially the interactions section — I hadn't seen it laid out this well anywhere else.
- MT
Marek T. a month ago
Are you planning to update this with the newest study from this year? I saw an interesting meta-analysis.