Skip to content
Specimen Atlas of Research Peptides81 plates · MIT
← CataloguePlate 55 of 81
55Plate 55Reviewed 2026-04-27

PE 22-28

TREK-1 Antagonist

also known as mini-spadin, shortened spadin, spadin fragment

Seven-amino-acid fragment of spadin (PE 12-28), a sortilin-derived peptide that selectively blocks TREK-1 potassium channels. Demonstrates potent antidepressant-like activity in rodent models at sub-nanomolar concentrations (IC50 0.12 nM vs 40-60 nM for full spadin). Shorter sequence confers enhanced in vivo stability, blood-brain barrier penetration, and improved therapeutic window. Pre-clinical only — no human trials reported.

§ I

At a glance

TREK-1 IC50
0.12 nM
Peptide length
7 AA
Evidence stage
Animal
Route

IP · SQ · Once Daily (animal models)

§ II

Mechanism

Edit ↗

Primary target — TREK-1 two-pore-domain potassium channel [djillani-2017][ma-2020].

Pathway — TREK-1 channel blockade → Neuronal membrane depolarisation → Enhanced hippocampal excitability → Increased neuroplasticity.

Downstream effect — Antidepressant-like activity in forced swim test and tail suspension test; reduced A1-like reactive astrocyte activation; neuroprotection via NF-κB pathway modulation [djillani-2017][cong-2023][wu-2021].

Origin — Synthetic truncation of spadin (PE 12-28), itself derived from the sortilin propeptide C-terminus. Residues 22-28: Val-Val-Arg-Gly-Trp-Leu-Arg. [djillani-2017][mazella-2018].

Feedback intact — N/A — direct ion channel blockade; not receptor-mediated endocrine axis.

§ III

Dosage

Protocols described in the cited literature; not medical advice.

Edit ↗
ParameterValue
Animal dose (antidepressant)0.3–3 µg/kg IPEffective in forced swim test, tail suspension test, CUMS models.
Animal dose (neuroprotection)0.03 µg/kg IP [pietri-2019]Low-dose TREK-1 activation post-stroke for 7 days, then high-dose blockade.
FrequencyOnce dailySustained antidepressant effect over 7+ days.
Onset (animal)Within hours (acute); full effect 4–7 days
Duration (animal)7–28 days tested [qi-2018][pietri-2019]
Comparison to fluoxetinePE 22-28 outperforms fluoxetine in CUMS-sensitive rats by day 7Chronic administration shows superior long-term efficacy.
Human equivalent (extrapolated)Not established — no clinical trialsAllometric scaling from rodent data unavailable.
Evidence basisMultiple rodent RCTs; behavioral + electrophysiology endpoints [djillani-2017][qi-2018][wu-2021]
§ III · b

Reconstitution

A pure mass-to-volume utility. Enter what you have in the vial; the atlas computes the volume per dose. No prescription information.

Inputs
mg
mL
mcg
The calculator does pure mass-to-volume math. It does not recommend a dose. Refer to PE 22-28's cited literature for protocol specifics.
Volumetric outputFig. C — reconstitution math
Volume per dose
0.100mL
10.0 units on a U-100 insulin syringe
Concentration
2500
mcg per mL
Doses per vial
20
at this dose
§ V

Adverse events

Severities follow the FDA / CTCAE convention.

Edit ↗
Toxicity (animal)mild
No adverse effects reported at therapeutic doses
Cardiovascular (theoretical)moderate
TREK-1 expressed in cardiac tissue; arrhythmia risk unclear
Weight change
Not reported in animal studies
Neurologicalmild
No seizures or behavioral abnormalities noted
Long-term safety
Unknown — longest animal study 28 days
Absolute contraindications
  • Human use — no clinical safety data available
Relative contraindications
  • Cardiac arrhythmia or channelopathy (theoretical TREK-1 cardiac role)
§ VI

Administration

Edit ↗
  1. 01
    Animal protocol (IP)

    Dissolved in sterile saline or vehicle. Intraperitoneal injection, 0.3–3 µg/kg body weight. Once daily administration in rodent behavioral studies.

  2. 02
    Stability

    Shorter peptide length (7 AA) confers improved plasma stability vs 17-AA spadin. Exact storage conditions not detailed in published protocols. [djillani-2017]

  3. 03
    BBB penetration

    Enhanced CNS bioavailability vs full spadin, likely due to smaller size. Mechanism (passive diffusion vs active transport) not fully characterized.

  4. 04
    Human formulation

    Not established — peptide synthesis methods for research use only. No pharmaceutical-grade formulation available.

Appendix

Sources

34%

of 47 rendered claims carry a resolvable citation.

  1. [cong-2023]
    Cong 2023Blocking Two-Pore Domain Potassium Channel TREK-1 Inhibits the Activation of A1-Like Reactive Astrocyte Through the NF-κB Signaling Pathway in a Rat Model of Major Depressive Disorder.
    journal, 2023
  2. [djillani-2017]
    Djillani 2017Shortened Spadin Analogs Display Better TREK-1 Inhibition, In Vivo Stability and Antidepressant Activity.
    journal, 2017
  3. [ma-2020]
    Ma 2020Spadin Selectively Antagonizes Arachidonic Acid Activation of TREK-1 Channels.
    journal, 2020
  4. [mazella-2018]
    Mazella 2018The Involvement of Sortilin/NTSR3 in Depression as the Progenitor of Spadin and Its Role in the Membrane Expression of TREK-1.
    journal, 2018
  5. [nasr-2018]
    Nasr 2018Identification and characterization of two zebrafish Twik related potassium channels, Kcnk2a and Kcnk2b.
    journal, 2018
  6. [pietri-2019]
    Pietri 2019First evidence of protective effects on stroke recovery and post-stroke depression induced by sortilin-derived peptides.
    journal, 2019
  7. [qi-2018]
    Qi 2018Comparison of Therapeutic Effects of TREK1 Blockers and Fluoxetine on Chronic Unpredicted Mild Stress Sensitive Rats.
    journal, 2018
  8. [wu-2021]
    Wu 2021Genetic and pharmacological inhibition of two-pore domain potassium channel TREK-1 alters depression-related behaviors and neuronal plasticity in the hippocampus in mice.
    journal, 2021
Plate composed 2026-04-27 · maturity human-reviewed · schema v1 · Contributors: peptidesdb-core · 31 fields uncited — open contributions