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Ketamine blocks NMDA receptors in the brain, rapidly increasing glutamate signaling. This triggers synaptic plasticity and neurogenesis, rebuilding neural connections degraded by depression and chronic stress. Unlike SSRIs, effects can appear within hours to days.
The only FDA-approved ketamine product (Spravato/esketamine) requires clinical administration. Compounded ketamine allows oral troches, sublingual drops, nasal sprays, and topical creams for at-home protocols at a fraction of the cost.
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Ketamine is a Schedule III controlled substance originally developed as a surgical anesthetic. At sub-anesthetic doses, it produces rapid antidepressant, anxiolytic, and analgesic effects that have made it one of the most significant psychiatric treatments in decades.
Unlike traditional antidepressants that target serotonin or dopamine, ketamine works on the glutamate system, triggering rapid synaptogenesis — growth of new neural connections. This is why patients with treatment-resistant depression sometimes experience relief within hours of a single dose.
Compounded ketamine is prescribed for treatment-resistant depression, PTSD, anxiety disorders, bipolar depression, chronic pain syndromes, CRPS, and fibromyalgia. At-home protocols using oral troches or sublingual drops are increasingly common and significantly more affordable than IV infusion series.
NMDA Receptor Antagonism
Ketamine blocks NMDA receptors — glutamate-gated ion channels critical for synaptic plasticity. This triggers a glutamate surge that activates AMPA receptors, stimulating release of BDNF (brain-derived neurotrophic factor).
Rapid Synaptogenesis
BDNF promotes rapid growth of new synaptic connections in the prefrontal cortex — the area most impaired by depression. This structural repair is why ketamine can produce antidepressant effects within hours, not weeks.
mTOR Pathway Activation
Ketamine activates the mTOR signaling pathway, which regulates protein synthesis needed for new synapse formation, contributing to sustained antidepressant effects.
Psychiatric: Treatment-resistant depression (TRD), major depressive disorder, bipolar depression, PTSD, anxiety disorders, OCD (off-label)
Chronic Pain: Complex regional pain syndrome (CRPS), fibromyalgia, neuropathic pain, refractory migraine, phantom limb pain
Other: Acute suicidal ideation, palliative care pain management
Alcohol use disorder (off-label research), eating disorders (emerging research), post-surgical pain management
Depression / PTSD (Troches): 100mg–400mg per troche, 1–3x per week per provider protocol
Depression (IV): 0.5mg/kg over 40 minutes; standard induction = 6 infusions over 2–3 weeks
Chronic Pain (IV): 0.1–0.5mg/kg/hr over 4–5 hours in specialized protocols
Nasal Spray: 50–100mg per actuation; dosing varies by protocol
All dosing must be supervised and tailored by a licensed provider experienced in ketamine therapy.
Start at the lowest effective dose. For at-home troches, most providers begin at 100mg and adjust based on response. Allow 48–72 hours between sessions initially. Avoid driving for 24 hours post-dose. Integration therapy following ketamine sessions is strongly recommended for psychiatric indications.
During administration (transient):
After effects:
With repeated use:
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