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PE-22-28 (Spadin Analog)
Also known as: Spadin Analog, TREK-1 Blocker
Confidence
Updated 2026-03-18
PE-22-28 is a synthetic heptapeptide derived from sortilin propeptide (spadin) that acts as a specific blocker of the TREK-1 potassium channel. TREK-1 deletion in mice produces an antidepressant-resistant phenotype, making TREK-1 blockade a novel antidepressant mechanism. PE-22-28 shows rapid-onset antidepressant-like effects in animal models within 4 days — compared to 2–4 weeks for SSRIs. It is an early-stage research compound.
Class
Nootropic / Antidepressant Peptide
Routes
Intranasal, Subcutaneous
Half-Life
Not established in humans. Short peptide — likely minutes in plasma. Intranasal delivery may extend functional CNS duration.
PE-22-28 selectively blocks TREK-1 (TWIK-related K+ channel 1), a two-pore domain potassium channel expressed in the brain that regulates neuronal excitability. TREK-1 blockade increases serotonergic neuron firing in the dorsal raphe nucleus, enhances hippocampal neurogenesis, and increases BDNF expression. This mimics the TREK-1 knockout phenotype (depression-resistant mice). The mechanism is distinct from SSRIs — it produces similar downstream effects but through a different upstream target, potentially explaining the faster onset.
Half-Life
Not established in humans. Short peptide — likely minutes in plasma. Intranasal delivery may extend functional CNS duration.
Bioavailability
Not established. Preclinical studies used IP injection and intranasal routes in rodents.
No approved indications. Research: depression (rapid-onset antidepressant), cognitive enhancement, neurogenesis.
Preclinical studies published in high-impact journals (PNAS, Molecular Psychiatry) demonstrate rapid-onset antidepressant effects in rodent forced swim and tail suspension tests within 4 days. Enhanced hippocampal neurogenesis and BDNF expression confirmed. Improved by Dr. Bhourde's group over the parent compound spadin for stability and selectivity. No human clinical data exists. Mechanism is scientifically compelling and represents a genuinely novel antidepressant target.
Human Studies
0
Animal Studies
12
No human safety data. Well-tolerated in rodent studies at research doses. TREK-1 channels are expressed in cardiac tissue — theoretical cardiac safety concern with systemic TREK-1 blockade (though knockout mice show no obvious cardiac phenotype). Completely unknown risk profile in humans.
Investigational. Preclinical only. No IND filed. Available from research peptide suppliers. Very early-stage compound.
Drug Interactions: Unknown. Theoretical interactions with potassium channel modulators, SSRIs, other antidepressants. Monitoring: No established parameters. Mood assessment if used in research context. Research Gaps: Zero human data. Cardiac safety of TREK-1 blockade. PK/PD in humans. Translation from rodent depression models to human depression. Stability and delivery optimization needed.
Intranasal (research context — NO validated human protocol)
Common Range
100–500 mcg/day (extrapolated from rodent studies — NOT validated)
Timing
Morning
Frequency
Daily
Cycling
Unknown
Important Note
NOT FDA-approved. NO human data. Preclinical research compound only. Doses are entirely speculative extrapolations. Extreme caution warranted.
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Disclaimer: This content is for educational and informational purposes only and does not constitute medical advice. Always consult with a licensed healthcare provider before starting, stopping, or modifying any peptide therapy. PeptideSupplierMatch does not prescribe, sell, or distribute peptides.
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