PE-22-28
A seven-amino acid fragment of the neuropeptide spadin, studied as a TREK-1 channel blocker with potential antidepressant-like effects in preclinical models.
Also referenced as: Spadin Analog, PE-22-28 Spadin
Also appears in: Other
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This name primarily lives in the research market and should not be read like an approved pharmaceutical product.
Primary research area: Neuroprotection. Also surfaces under Other for browsing and discovery.
Spadin Analog, PE-22-28 Spadin
No FDA label signal · 0 trials · 1 PubMed results
Current evidence for PE-22-28 is limited to laboratory or animal studies — there are no name-matched human trials with reported results. Any claims about effects in people are not yet backed by clinical data.
PE-22-28 has no clinical trials that name it and 1 PubMed-indexed publication and is not FDA-approved. Current evidence is preclinical or mechanistic.
Re-checked nightly against the registries — tracked since 2026-07-09. No band changes yet.
Grades evidence strength, not efficacy or safety. Research-use context; not medical advice. Graded 2026-10-18 from PubMed, ClinicalTrials.gov, ISRCTN, openFDA, Health Canada, and OpenAlex — computed deterministically and refreshed nightly, with a retraction check. How we grade →
What is PE-22-28?
PE-22-28 is a synthetic heptapeptide derived from the sortilin propeptide (PE), corresponding to residues 22–28. It acts as a blocker of the TREK-1 potassium channel, a mechanism that has shown antidepressant-like effects in animal models. The parent compound spadin (a 17-amino acid fragment) was first identified by Mazella et al. at the Institut de Pharmacologie Moléculaire et Cellulaire (IPMC) in France.
How it works
- TREK-1 blockade — TREK-1 is a two-pore-domain potassium channel (K2P) expressed widely in the brain. TREK-1 knockout mice exhibit a depression-resistant phenotype (Heurteaux et al., EMBO Journal, 2006)
- Spadin mechanism — Spadin and its fragment PE-22-28 block TREK-1, mimicking the effect of gene deletion. This is proposed to increase serotonergic and noradrenergic neurotransmission (Mazella et al., Nature Medicine, 2010)
- Faster onset — In rodent forced swim and tail suspension tests, spadin showed antidepressant effects within 4 days, compared to 2–3 weeks for SSRIs (Mazella et al., Nature Medicine, 2010)
Research status
Published evidence is preclinical:
- Mazella et al. (2010) identified spadin as an endogenous TREK-1 blocker with rapid antidepressant-like effects in mice (Nature Medicine, 16(4):471–479)
- Devader et al. (2015) optimized shorter spadin analogs including PE-22-28 and showed maintained TREK-1 inhibition with improved stability (Journal of Medicinal Chemistry, 58(1):161–171)
- Veyssiere et al. (2015) demonstrated that spadin analogs increase hippocampal neurogenesis in mice (Neuropharmacology, 91:74–82)
No human clinical trials have been published for PE-22-28 or spadin as of mid-2025.
Key considerations
- The TREK-1 mechanism is well-published and the Nature Medicine foundational paper is widely cited
- PE-22-28 is the shorter, more stable analog preferred by research vendors over full-length spadin
- All efficacy data comes from rodent behavioral models of depression — human translation is unproven
- Available from research vendors as lyophilized powder (typically 10mg vials)