PE 22-28 — questions, answered plainly.

PE 22-28 is a shortened analog of spadin — a peptide derived from the propeptide of neurotensin receptor 3 / sortilin — designed by the Mazella / Borsotto group at IPMC-CNRS to inhibit the TREK-1 (KCNK2) two-pore-domain potassium channel.

No. PE 22-28 is preclinical only — no FDA, MHRA, or EMA approval exists, and no peer-reviewed human clinical trials are indexed on PubMed.

Djillani 2017 (Frontiers in Pharmacology, PMID 28955242) reports PE 22-28 inhibited TREK-1 currents in hTREK-1/HEK cells and showed antidepressant-like activity in mouse behavioural models with longer in vivo persistence than the parent spadin peptide. Borsotto 2015 (British Journal of Pharmacology, PMID 25263033) reviews the TREK-1 / TASK-3 antidepressant rationale that PE 22-28 was developed from.

Spadin is the parent peptide derived from the sortilin propeptide. PE 22-28 corresponds to a shortened, optimised analog described in Djillani 2017 with improved in vivo persistence compared with spadin.

TREK-1 (KCNK2) is a two-pore-domain potassium channel. Borsotto 2015 reviews the rodent evidence linking TREK-1 inhibition to antidepressant-like behavioural effects, which is the rationale for the spadin / PE 22-28 series.

All published primary evidence originates from the Mazella / Borsotto group at IPMC-CNRS — independent replication is limited. No controlled human trials are indexed on PubMed. Findings are model-specific and are not extrapolated to therapeutic use.