PE-22-28: Research & Evidence
Early-Stage ResearchPublished research, clinical trial data, and evidence grading for PE-22-28 across studied indications.
Back to PE-22-28 overviewResearch Summary
PE-22-28 has zero human studies and zero clinical trials. All data comes from mouse and rat models where TREK-1 channel inhibition produced antidepressant-like behavioral effects and hippocampal neurogenesis. The original spadin peptide was discovered by Mazella et al. (2010, PMID: 20096941), and PE-22-28 was developed as a more stable analog by Djelloul et al. (2015, PMID: 26100954). The novel TREK-1 mechanism is scientifically interesting but entirely unvalidated in humans. No pharmaceutical company has pursued clinical development. There are no registered clinical trials and no path to FDA approval.
Evidence by Indication (2 indications)
| Indication | Tier | Trials | Summary |
|---|---|---|---|
| Depression | Tier D | 0 | Mouse behavioral models only; zero human studies |
| Neurogenesis | Tier D | 0 | Rodent hippocampal data only; no human confirmation |
Graded using our evidence tier methodology.
Higher score = larger gap between therapeutic potential and available clinical evidence.
Citations (2 sources)
- 1. Spadin, a sortilin-derived peptide, targeting rodent TREK-1 channels: a new concept in the antidepressant drug design Study
Mazella J, Petrault O, Lucas G, et al. (2010), PLoS Biology
- 2. PE 22-28, a novel spadin analog, shows antidepressant-like activity and modulates hippocampal neurogenesis Study
Djelloul M, Bhatt S, Bhatt R, et al. (2015), Neuropharmacology