This page is provided for research and educational purposes only and does not provide medical advice, diagnosis, treatment recommendations, dosing instructions, or instructions for human use. Research findings should be interpreted within the population, model, formulation, route, outcomes, and study design reported by each cited source.
PE-22-28 (10 mg Vial)
PE-22-28 is a synthetic heptapeptide (sequence: GVSWGLR) derived from the sortilin propeptide, engineered as a potent and selective antagonist of TREK-1 potassium channels[4]. Preclinical studies demonstrate rapid antidepressant-like effects, enhanced neurogenesis, and neuroprotection with a favorable safety profile showing no cardiac or metabolic side effects[2][3].
Quick Reference
What is PE-22-28?
Research overview based on the cited scientific literature.
• Goal: Support rapid neuroplasticity, mood regulation, and neuroprotection through selective TREK-1 inhibition[2][4].
• Storage: Lyophilized frozen; reconstituted refrigerated; replace vials every 4 weeks.
Storage Instructions
Proper storage helps preserve research material integrity.
• Lyophilized material: Keep sealed, dry, protected from light and moisture, and follow the supplier’s product-specific storage documentation.
• Prepared solutions: Refrigerated stability depends on formulation, solvent, concentration, and handling conditions. Follow product-specific laboratory or supplier guidance rather than assuming a universal storage period.
• Handling: Minimize unnecessary exposure to heat, light, and moisture, and avoid repeated freeze–thaw cycles.
• Allow cold-stored vials to equilibrate appropriately before opening to reduce condensation.
How is PE-22-28 studied?
PE-22-28 functions as a potent and selective antagonist of TREK-1 (KCNK2) two-pore domain potassium channels[2]. By blocking TREK-1, it depolarizes neurons and enhances excitability, leading to increased firing of serotonergic neurons and elevated monoamine neurotransmission[2]. This mechanism produces rapid antidepressant-like effects in preclinical models—within 4 days, PE-22-28 significantly increases hippocampal neurogenesis and synaptogenesis markers, changes typically requiring weeks with conventional antidepressants[4]. The peptide also activates CaMKII/CREB pathways that promote neuronal survival and plasticity[6]. PE-22-28 represents a shortened, optimized analog of spadin with superior potency (IC50 ~0.12 nM versus 40–60 nM for spadin) and longer duration of action (~23 hours versus ~7 hours)[4]. Notably, research also demonstrates neuroprotective effects in stroke models through biphasic dosing that leverages both TREK-1 activation at ultra-low doses and inhibition at standard doses[5].
What does the research report about PE-22-28?
Observations from preclinical literature and mechanistic studies.
• Rapid Antidepressant Effects: Produces behavioral improvements within 4 days in rodent models; reduces immobility in forced swim tests and decreases latency to feed in novel environments[4].
• Enhanced Neuroplasticity: Increases hippocampal neurogenesis, synaptogenesis markers (PSD-95), dendritic spine density, and BDNF expression within days[4].
• Neuroprotection: In stroke models, preserves dopaminergic neurons, reduces motor deficits, and prevents post-stroke depressive behavior[5].
• Favorable Safety Profile: Shows high selectivity with no effects on hERG channels (cardiac safety), no impact on heart rate, blood pressure, glucose regulation, or pain perception in preclinical studies[3]. No TREK-1-related side effects or withdrawal observed[3].
• No Human Data: All evidence is from cell culture and animal studies; human safety and pharmacokinetics remain unestablished[1].
• Potential Mild Reactions: Subcutaneous administration may occasionally cause minor injection-site reactions (slight redness or tenderness).
Important Note
This content is provided for scientific research and educational purposes only. It does not provide medical advice, diagnosis, treatment, dosing, or administration instructions. The compounds discussed may be investigational and are not presented as approved for human use.
What are the limitations of the research on PE-22-28?
Evidence should be interpreted within the population, experimental model, formulation, route, outcome measures, and study design used in each cited source. Preclinical or early-stage findings do not establish clinical efficacy, safety, or approved human use. Where human evidence is available, results should not be generalized beyond the populations and conditions actually studied.
