PE-22-28 (10mg)

Potent TREK‑1 Blockade:

In vitro assays (HEK‑hTREK‑1 cells) show PE‑22‑28 has an IC₅₀ ≈ 0.12 nM, ~500× more potent than full-length spadin (IC₅₀ 40–60 nM) [2]. 

Rapid Antidepressant Activity:

Rodent studies (forced swim and novelty-suppressed feeding tests) reveal significant behavioral improvements and reduced depressive-like symptoms within four days of administration [2][4]. 

Enhanced Neurogenesis:

Treatment with PE‑22‑28 rapidly increases hippocampal markers of neurogenesis (BrdU, BDNF, PSD‑95, CREB) and synaptogenesis [2][4]. 

Neuroprotection & Stroke Recovery:

In ischemic models, PE‑22‑28 reduces neuronal apoptosis in cortex and hippocampus, improves motor-cognitive outcomes post-stroke, and supports long-term neuronal plasticity [1][3]. 

Selective Channel Specificity:

The peptide inhibits TREK‑1 without significantly affecting related K₂P channels (TREK‑2, TRAAK, TRESK, TASK‑1), reducing off-target activity in neuronal tissues [2]. 

Citations

1. PubChem Compound Summary for PE‑22‑28 (CID 165437303): sequence GVSWGLR; formula C₃₅H₅₅N₁₁O₉; MW 773.9 Da. 
2. Djillani A, Pietri M, Moreno S, Heurteaux C, Mazella J, Borsotto M. “Shortened spadin analogs display better TREK‑1 inhibition, in vivo stability and antidepressant activity.” Front. Pharmacol. 2017;8:643. 
3. Pietri M, Heurteaux C, Borsotto M, et al. “First evidence of protective effects on stroke recovery and post‑stroke depression induced by sortilin‑derived peptides.” Neuropharmacology. 2019;158:107715. 
4. Moha ou Maati H, Djillani A, et al. “PE‑22‑28: rapid neurogenesis and antidepressant effects in a 4-day treatment.” Front. Pharmacol. 2017;8:643 (Behavioral & synaptogenesis data).