PE-22-28
PE-22-28 is the seven-amino-acid sequence GVSWGLR, derived from the sortilin propeptide and studied as a shortened spadin analogue. Its TREK-1 and antidepressant claims come from cells and mice. The often-repeated 23-hour duration belongs to modified G/A or biotinylated analogues, not the base peptide.
seven-residue sortilin-propeptide fragment
- Sequence GVSWGLR
- Also called a shortened spadin or mini-spadin analogue
- TREK-1 inhibition shown in vitro
- No human administration study identified
Which molecule is PE-22-28?
Base PE-22-28 is GVSWGLR. G/A-PE-22-28 replaces the first glycine with alanine, and biotinylated G/A-PE-22-28 adds another modification. These forms cannot share duration or potency claims by default.
Does PE-22-28 last 23 hours?
That number came from a mouse behavioral figure for a high-dose biotinylated G/A analogue. The base GVSWGLR peptide was not shown to have a 23-hour human half-life or effect.
Primary paper · cells and mice
Cell and animal study
Djillani A et al. Frontiers in Pharmacology, 2017.
PE-22-28 inhibited human TREK-1 channels in a transfected-cell assay and changed forced-swim, novelty-suppressed-feeding, neurogenesis, and synaptogenesis measures in mice or mouse cells. Figure-level data assign the 14-to-23-hour half-time effects to G/A-PE-22-28 and biotinylated G/A analogues, not unmodified PE-22-28.
- Participants / model
- Transfected HEK cells, mouse neurons, and mice
- Treatment
- PE-22-28 plus multiple modified analogues
- Follow-up
- Acute or four-day mouse experiments
- Study design
- In-vitro channel assays and animal behavioral studies
Primary paper · cells and mice
Cell and animal study
Djillani A et al. Frontiers in Pharmacology, 2017.
PE-22-28 inhibited human TREK-1 channels in a transfected-cell assay and changed forced-swim, novelty-suppressed-feeding, neurogenesis, and synaptogenesis measures in mice or mouse cells. Figure-level data assign the 14-to-23-hour half-time effects to G/A-PE-22-28 and biotinylated G/A analogues, not unmodified PE-22-28.
- Participants / model
- Transfected HEK cells, mouse neurons, and mice
- Treatment
- PE-22-28 plus multiple modified analogues
- Follow-up
- Acute or four-day mouse experiments
- Study design
- In-vitro channel assays and animal behavioral studies
US11220527 · analogue claims
Patent
US Patent 11,220,527.
The patent describes PE-22-28-related sequences and focuses development claims on modified analogues, including the glycine-to-alanine form. A patent is applicant-written and does not establish human efficacy or safety.
- Study design
- Patent disclosure
Used for analogue identity and development context only.
Read the original sourceHas PE-22-28 treated depression in people?
No administered-human trial was identified. The depression claim rests on mouse behavioral models and cell assays, not clinical symptom remission, function, relapse prevention, or comparative treatment evidence.
PubMed and registry · no human trial
Registry and literature record
PubMed and ClinicalTrials.gov.
The cited PubMed and ClinicalTrials.gov records contain no registered human intervention trial or administered-human publication under PE-22-28, GVSWGLR, mini-spadin, or the listed analogues.
Read the original sourcePrimary paper · cells and mice
Cell and animal study
Djillani A et al. Frontiers in Pharmacology, 2017.
PE-22-28 inhibited human TREK-1 channels in a transfected-cell assay and changed forced-swim, novelty-suppressed-feeding, neurogenesis, and synaptogenesis measures in mice or mouse cells. Figure-level data assign the 14-to-23-hour half-time effects to G/A-PE-22-28 and biotinylated G/A analogues, not unmodified PE-22-28.
- Participants / model
- Transfected HEK cells, mouse neurons, and mice
- Treatment
- PE-22-28 plus multiple modified analogues
- Follow-up
- Acute or four-day mouse experiments
- Study design
- In-vitro channel assays and animal behavioral studies
What does the research actually show?
PE-22-28 blocked TREK-1 currents in a transfected-cell assay and changed several mouse behavioral and neural-plasticity measures. The cited studies do not show an antidepressant effect in people.
Forced-swim immobility and novelty-suppressed feeding are experimental readouts. Neither is a diagnosis of depression or a validated substitute for a clinical outcome.
Primary paper · cells and mice
Cell and animal study
Djillani A et al. Frontiers in Pharmacology, 2017.
PE-22-28 inhibited human TREK-1 channels in a transfected-cell assay and changed forced-swim, novelty-suppressed-feeding, neurogenesis, and synaptogenesis measures in mice or mouse cells. Figure-level data assign the 14-to-23-hour half-time effects to G/A-PE-22-28 and biotinylated G/A analogues, not unmodified PE-22-28.
- Participants / model
- Transfected HEK cells, mouse neurons, and mice
- Treatment
- PE-22-28 plus multiple modified analogues
- Follow-up
- Acute or four-day mouse experiments
- Study design
- In-vitro channel assays and animal behavioral studies
Follow-up paper · nonhuman evidence
Preclinical study
Borsotto M et al. 2019.
The follow-up publication is preclinical and does not report administered-human efficacy, pharmacokinetics, or safety.
- Participants / model
- Experimental nonhuman systems
- Treatment
- PE-22-28 research intervention
- Study design
- Preclinical study
What is known about human safety?
Human pharmacokinetics, cardiac electrophysiology, neurologic effects, suicidality, mania risk, interactions, immune reactions, pregnancy, and repeated exposure are not characterized for PE-22-28.
TREK-1 channels participate in neuronal excitability and other physiology. Cell selectivity assays do not establish whole-person safety, especially with psychoactive medicines or mood disorders.
PubMed and registry · no human trial
Registry and literature record
PubMed and ClinicalTrials.gov.
The cited PubMed and ClinicalTrials.gov records contain no registered human intervention trial or administered-human publication under PE-22-28, GVSWGLR, mini-spadin, or the listed analogues.
Read the original sourcePrimary paper · cells and mice
Cell and animal study
Djillani A et al. Frontiers in Pharmacology, 2017.
PE-22-28 inhibited human TREK-1 channels in a transfected-cell assay and changed forced-swim, novelty-suppressed-feeding, neurogenesis, and synaptogenesis measures in mice or mouse cells. Figure-level data assign the 14-to-23-hour half-time effects to G/A-PE-22-28 and biotinylated G/A analogues, not unmodified PE-22-28.
- Participants / model
- Transfected HEK cells, mouse neurons, and mice
- Treatment
- PE-22-28 plus multiple modified analogues
- Follow-up
- Acute or four-day mouse experiments
- Study design
- In-vitro channel assays and animal behavioral studies
Is PE-22-28 approved?
No FDA-approved PE-22-28 drug, prescribing label, or registered human trial was identified.
PubMed and registry · no human trial
Registry and literature record
PubMed and ClinicalTrials.gov.
The cited PubMed and ClinicalTrials.gov records contain no registered human intervention trial or administered-human publication under PE-22-28, GVSWGLR, mini-spadin, or the listed analogues.
Read the original sourceUS11220527 · analogue claims
Patent
US Patent 11,220,527.
The patent describes PE-22-28-related sequences and focuses development claims on modified analogues, including the glycine-to-alanine form. A patent is applicant-written and does not establish human efficacy or safety.
- Study design
- Patent disclosure
Used for analogue identity and development context only.
Read the original sourceStudies and sources
Primary paper · cells and mice
Cell and animal study
Djillani A et al. Frontiers in Pharmacology, 2017.
PE-22-28 inhibited human TREK-1 channels in a transfected-cell assay and changed forced-swim, novelty-suppressed-feeding, neurogenesis, and synaptogenesis measures in mice or mouse cells. Figure-level data assign the 14-to-23-hour half-time effects to G/A-PE-22-28 and biotinylated G/A analogues, not unmodified PE-22-28.
- Participants / model
- Transfected HEK cells, mouse neurons, and mice
- Treatment
- PE-22-28 plus multiple modified analogues
- Follow-up
- Acute or four-day mouse experiments
- Study design
- In-vitro channel assays and animal behavioral studies
Follow-up paper · nonhuman evidence
Preclinical study
Borsotto M et al. 2019.
The follow-up publication is preclinical and does not report administered-human efficacy, pharmacokinetics, or safety.
- Participants / model
- Experimental nonhuman systems
- Treatment
- PE-22-28 research intervention
- Study design
- Preclinical study
US11220527 · analogue claims
Patent
US Patent 11,220,527.
The patent describes PE-22-28-related sequences and focuses development claims on modified analogues, including the glycine-to-alanine form. A patent is applicant-written and does not establish human efficacy or safety.
- Study design
- Patent disclosure
Used for analogue identity and development context only.
Read the original sourcePubMed and registry · no human trial
Registry and literature record
PubMed and ClinicalTrials.gov.
The cited PubMed and ClinicalTrials.gov records contain no registered human intervention trial or administered-human publication under PE-22-28, GVSWGLR, mini-spadin, or the listed analogues.
Read the original sourceWhy is PE-22-28 in C tier?
The C grade reflects TREK-1 cell assays and direct mouse behavioral studies. No administered-human study establishes antidepressant efficacy, duration, or safety.