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PE22-28

Cognitive

Also known as: Spadin Analog, Sortilin-derived peptide

Half-life: Hours; precise value species-dependent

Last reviewed:  ·  Published:

CognitiveNeuroprotection

Overview

PE22-28 is a seven-amino-acid peptide analog of Spadin, a naturally occurring peptide derived from the sortilin neurotrophin receptor that selectively inhibits the TREK-1 potassium channel. TREK-1 is a two-pore-domain potassium channel expressed prominently in serotonergic neurons of the dorsal raphe nucleus; its activation is associated with reduced serotonergic firing and depression-like behavior. Knockout of TREK-1 in mice produces a depression-resistant phenotype, validating the channel as a therapeutic target for antidepressant drug development.

Spadin and its analogs (including PE22-28) act as selective TREK-1 blockers and produce robust antidepressant-like effects in mouse behavioral models (forced swim test, novelty-suppressed feeding) within hours of administration — substantially faster than the weeks-long onset of conventional SSRIs. PE22-28 was specifically optimized for stability and potency relative to native Spadin, retaining the antidepressant activity while being amenable to standard peptide synthesis and chronic administration.

PE22-28 has not been clinically tested in humans. It is sold by research-peptide vendors and used in subjective self-experimentation by users seeking rapid-onset mood effects, but the human safety and efficacy data are essentially absent. The TREK-1 inhibition mechanism is interesting and theoretically promising, but extrapolating from rodent forced-swim assays to human clinical depression is well-known to be unreliable.

History

Spadin was characterized by Marc Borsotto's group at the Institut de Pharmacologie Moléculaire et Cellulaire in France in 2010, building on the discovery that TREK-1 knockout mice were resistant to depression-like behavior. PE22-28 was developed as a more stable analog optimized for chronic use. Despite a decade of preclinical work demonstrating antidepressant activity in mouse models, the compound has not advanced to human clinical trials, and its presence on the research-chemical market substantially predates any clinical validation.

Effects

  • Selective TREK-1 potassium channel inhibition
  • Fast-onset antidepressant-like effects in rodent models
  • Increased serotonergic neuron firing in dorsal raphe
  • Enhanced BDNF / TrkB signaling downstream
  • Anti-anxiety effects in some assays

Side Effects

  • Essentially uncharacterized in humans
  • Theoretical: TREK-1 inhibition off-target in heart, immune cells
  • Subjective reports of mood activation, occasional anxiety
  • Injection-site reactions
  • Sleep disturbance with late-day dosing

Tolerability

Animal tolerability studies of PE22-28 have reported good safety profiles, with no major adverse events at therapeutic doses. Human safety data is absent. TREK-1 is expressed outside the brain (notably in the heart and immune system) and chronic systemic inhibition may have effects that the brief rodent antidepressant assays don't capture. Self-experimentation outside a research protocol carries unquantified risks, particularly for users with cardiovascular conditions or on antidepressant medications.

Dosing Ranges

Antidepressant research (preclinical)

Dose Range

100-500 mcg/kg

Frequency

Daily SubQ or IP

Duration

Per protocol

Self-experimentation (no clinical guidance)

Dose Range

50-200 mcg

Frequency

Once or twice daily

Duration

2-4 weeks per cycle

Dosing information is for educational purposes only. Consult a healthcare professional before using any peptide.

Reconstitution

Preparation Details

Typical Vial Size

5 mg

Water Type

Bacteriostatic water (BAC water)

Mixing Volume

2 mL

Half-Life

Hours; precise value species-dependent

Molecular Weight

~830 Da

Store reconstituted vial refrigerated at 2-8°C. Use within 14-21 days. Subcutaneous or intranasal administration; intranasal may offer better CNS bioavailability.

Calculate PE22-28 dose

Where to buy PE22-28

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Disclosure: PinnyPeptide may earn a commission on purchases made through the links above, at no extra cost to you. We only list vendors we're willing to point our community at, but inclusion is not a clinical endorsement. Always verify each vendor's third-party testing and your local legal status before purchasing.

Regulatory Status

FDA Status

Not FDA approved.

Legal Status

Unregulated research chemical.

USA

Not approved

Research-only

EU

Not approved

Not authorized as medicinal product

UK

Not approved

Classified as research chemical

Australia

Not approved

TGA has not evaluated

Canada

Not approved

Not authorized for human use

Cited Studies

Spadin, a sortilin-derived peptide, targeting rodent TREK-1 channels: a new concept in the antidepressant drug design

Mazella J, Pétrault O, Lucas G, Deval E, Béraud-Dufour S, Gandin C, El-Yacoubi M, Widmann C, Guyon A, Chevet E, Taouji S, Conductier G, Corinus A, Coppola T, Gobbi G, Nahon JL, Heurteaux C, Borsotto M

PLOS Biology (2010)

Original characterization of Spadin demonstrating selective TREK-1 inhibition and fast-onset antidepressant activity in mouse behavioral models, establishing the pharmacological rationale for analogs like PE22-28.

View Study →

Antidepressant drug design: shortening of the active sequence of Spadin and conformational restrictions of TREK-1 blockers

Veyssière J, Moha ou Maati H, Mazella J, Gaudriault G, Moreno S, Heurteaux C, Borsotto M

European Journal of Pharmacology (2015)

Describes the optimization process by which shorter, more stable Spadin analogs (including the PE22-28 series) were developed, retaining antidepressant activity while improving drug-like properties.

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Deletion of the background potassium channel TREK-1 results in a depression-resistant phenotype

Heurteaux C, Lucas G, Guy N, El Yacoubi M, Thümmler S, Peng XD, Noble F, Blondeau N, Widmann C, Borsotto M, Gobbi G, Vaugeois JM, Debonnel G, Lazdunski M

Nature Neuroscience (2006)

Genetic validation of TREK-1 as an antidepressant target, demonstrating that mice lacking the channel show resistance to behavioral despair in standard depression assays.

View Study →

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