Shortened spadin-derived research peptide · Fact sheet
PE-22-28
Also known as PE 22–28
PE-22-28 is a shortened spadin-derived peptide investigated for TREK-1 channel effects and depression-like behavior in mice. It is not an established human antidepressant or a verified neurogenesis regimen.
What is PE-22-28?
The seven-amino-acid peptide derives from work on spadin, a sortilin-related peptide.
Spadin, PE-22-28 and chemically modified analogs are distinct interventions.
Benefits & claims
Interest centers on brain function and sleep. Biological activity does not itself establish a clinical treatment.
What the evidence supports
- PE-22-28 inhibited TREK-1 channels in laboratory assays.
- Mouse behavioral and synaptic-marker effects generated a development hypothesis.
- Forced-swim or feeding-test changes cannot establish antidepressant efficacy or rapid human neurogenesis.
Research areas
- Experimental tissue and cellular responses
- Formulation-specific outcomes
Dosage & frequency
No established human regimenThe reviewed sources do not establish a human treatment amount or frequency for PE-22-28. Animal and laboratory exposures are not human regimens.
How to read these amounts
An approved regimen belongs to a specific product, indication, and population. A study regimen describes what researchers tested; it does not establish a prescription or a safe self-use protocol. Products, routes, and formulations are not interchangeable. A prescriber uses the full label and individual clinical circumstances.
Personal accounts may describe amounts, schedules and outcomes beyond clinical research. They do not establish a regimen. Read the reported experiences
Formulations, interactions & practical context
- Identity and pharmacology
- The seven-amino-acid peptide derives from work on spadin, a sortilin-related peptide.
Formulation differences
- Spadin, PE-22-28 and chemically modified analogs are distinct interventions.
Interactions & precautions
- The reviewed sources do not establish a comprehensive human interaction profile for this exact substance or combination.
What is still unresolved
- Controlled human clinical outcomes for the exact substance
- Human exposure, pharmacokinetics and repeated-use safety
- Independent replication and formulation equivalence
Side effects & risks
- Human neurologic, cardiac, immune and interaction risks are not characterized adequately.
- Longer activity of an analog in mice does not establish a safer or more effective human product.
This is a summary of the cited evidence, not a complete product label. A lack of human safety data does not establish safety.
Clinical research
Mostly animal or lab researchThe direct PE-22-28 study used receptor assays, cultured mouse neurons and mouse behavioral models. Related spadin studies supply mechanism context rather than human efficacy.
Studies
Direct shortened-spadin analog study, including PE-22-28.
Original spadin/TREK-1 rodent work; related molecule.
Spadin channel-selectivity experiment; not human PE-22-28 evidence.
Personal experiences
Reports describe what someone noticed. They cannot establish cause, typical results, or how often a side effect happens. Amounts and schedules describe the individual account, not an effective or safe dose. Product identity and strength may be unverified, and missing details are left explicit.
No attributable personal accounts were found in the sources reviewed.
Approval status
PE-22-28 has no FDA-approved therapeutic product. The cited experiments or cosmetic uses do not establish an approved human treatment.
Preclinical evidence; no FDA-approved product
Approval covers the labeled product, use and population. A trial phase does not establish success; a stopped program is not ongoing research.
- Shortened Spadin Analogs Display Better TREK-1 Inhibition, In Vivo Stability and Antidepressant Activity.
- Spadin, a sortilin-derived peptide, targeting rodent TREK-1 channels: a new concept in the antidepressant drug design.
- Spadin Selectively Antagonizes Arachidonic Acid Activation of TREK-1 Channels.
Open questions
- Controlled human clinical outcomes for the exact substance
- Human exposure, pharmacokinetics and repeated-use safety
- Independent replication and formulation equivalence
Summary
Forced-swim or feeding-test changes cannot establish antidepressant efficacy or rapid human neurogenesis.
Sources
Medical evidence and regulatory sources are listed here. Personal reports are linked separately in the experiences section.
- pubmedShortened Spadin Analogs Display Better TREK-1 Inhibition, In Vivo Stability and Antidepressant Activity.
Direct shortened-spadin analog study, including PE-22-28.
- pubmedSpadin, a sortilin-derived peptide, targeting rodent TREK-1 channels: a new concept in the antidepressant drug design.
Original spadin/TREK-1 rodent work; related molecule.
- pubmedSpadin Selectively Antagonizes Arachidonic Acid Activation of TREK-1 Channels.
Spadin channel-selectivity experiment; not human PE-22-28 evidence.