PE-22-28

Also known as PE 22-28, Spadin analog, Mini-spadin, TREK-1 blocker peptide

A shortened spadin analog that potently blocks the TREK-1 potassium channel, studied in animals as a fast-acting antidepressant and pro-neurogenic peptide.

Molecular weight~773.9 g/mol (sequence GVSWGLR)

Half-lifePlasma half-life is short, but the analog is reported to extend in-vivo activity versus spadin, with antidepressant action lasting up to ~23 hours (vs ~7 hours for spadin) in rodent studies.

CategoryCognitive & Mood

Typical use cases

✓ Mood/antidepressant research✓ Neurogenesis (research)✓ TREK-1 channel studies

Dosing guidelines

StartingNo established human dose; rodent studies use mg/kg subcutaneous or intranasal dosing. Community protocols cite small fixed amounts, which are extrapolations rather than validated doses.

MaintenanceUndefined in humans; rodent antidepressant/neurogenesis effects appear after short (~4-day) daily courses. Any steady human dose is speculative.

Max (studied)Unknown — no human safety ceiling established; higher doses are unsupported.

Titration

Typically flat-dosed in existing research; no validated titration scheme.

Reconstitution

An 8 mg vial is commonly reconstituted with ~1–2 mL bacteriostatic water for subcutaneous research use; intranasal preparation is also seen.

Injection sites

Subcutaneous (abdomen/flank) in typical research protocols; intranasal administration is also reported.

Storage & handling

Lyophilized: stable months cool/dark, longer frozen. Reconstituted: refrigerate (2–8 °C).

Side effects

Injection-site reaction (subcutaneous) Mild · Uncommon
Human side-effect profile unknown (no clinical data) Moderate · Rare

Research summary

PE-22-28 is a seven-residue analog corresponding to amino acids 22–28 of spadin, a peptide derived from the sortilin propeptide that inhibits the TREK-1 (two-pore-domain potassium) channel implicated in depression; the shortened analog shows far greater TREK-1 affinity than spadin with improved in-vivo stability. In rodent models it produces rapid antidepressant-like effects and induces hippocampal neurogenesis after only a few days of treatment. All current evidence is preclinical (cell and animal studies) with no human clinical trials, so efficacy and safety in people remain unknown. Educational only — not medical advice.

Key references

Djillani et al., Neuropharmacology (2017) — shortened spadin analogs (incl. PE-22-28) improve TREK-1 inhibition and antidepressant activity
Mazella et al., PLoS Biol. (2010) — spadin as a TREK-1 blocker with antidepressant properties

Related compounds

Selank → Semax → P21 →

Where to buy

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Educational reference only — not medical advice. Dosing figures are commonly-cited ranges, not prescriptions. Consult a qualified clinician.

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