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No. 033 · Mind · Nootropic Peptide

Spadin

Sortilin propeptide fragment PE 12–28

C Tier C · Animal data how tiers work →
  • Not FDA approved
  • WADA ✗ S0
Compare Cite
Fingerprint 18 residues
Spadin sequence fingerprint
  • Nonpolar 13
  • Polar 3
  • Positive charge 2

Each dot is a residue placed around the ring from N- to C-terminus; its distance from the centre reflects its chemistry.

01

Evidence

  1. D In vitro
  2. C Animal
  3. B Human pilot
  4. A RCT
  5. S Approved

TIER C — Evidence comes mostly from animal studies.

Evidence is limited to rodent studies (Mazella et al., PLoS Biol 2010, and follow-ups); no published human studies.

Tiers rate the strength of published evidence — not effectiveness, safety, or a recommendation.

02

At a glance

Residues
18 amino acids, N→C
Molecular weight
2,012.3 Da
Formula
C96H142N26O22
Discovered
2010 Described as a sortilin-derived TREK-1 blocker (Mazella et al., PLoS Biol 2010).
Routes studied
Subcutaneous Routes used in published research
FDA
Not approved
WADA
Prohibited · S0 Non-approved substances
03

Sequence

N → C · 18 residues · hover, tap, or use arrow keys to inspect

Note Sortilin propeptide residues 12–28 with an added N-terminal Tyr, as synthesized in the discovery paper.

04

Overview

A peptide derived from the sortilin propeptide that blocks TREK-1 potassium channels. It produced rapid antidepressant-like effects in mouse studies.

Research status Preclinical stage; in mice, a 4-day treatment produced antidepressant-like effects and markers usually seen only after weeks of SSRI treatment

05

Mechanism

Spadin corresponds to residues 12-28 of the sortilin propeptide (17 amino acids), synthesized with an added N-terminal tyrosine (18 residues: YAPLPRWSGPIGVSWGLR). It binds and blocks TREK-1 two-pore-domain potassium channels; in mice this increased dorsal raphe serotonin neuron firing, hippocampal CREB phosphorylation, and neurogenesis after 4 days of treatment.

06

Effects reported in research

Reported outcomes, not promises. These come mostly from preclinical (cell or animal) research and have not been confirmed in human trials.

  • Rapid antidepressant-like effects
  • Enhanced hippocampal neurogenesis
  • Improved stress resilience
  • Modulated TREK-1 potassium channel activity
07

Safety & unknowns

No human safety data. Only preclinical rodent studies published. Novel mechanism targeting potassium channels carries unknown risks. Not FDA-approved. Very early research stage.

Unknowns. No randomized controlled trials in humans have been published, so human safety has not been established in controlled studies.

Informational only — not medical advice. peptidemeta publishes no dosing, protocols, or sourcing. Talk to a qualified clinician about any treatment decision.

08

Studies [1]

  1. Preclinical 2010

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

    Mazella J, Pétrault O, Lucas G, et al. PLoS Biology

    Discovery paper showing spadin binds and blocks TREK-1 channels, increases serotonin neuron firing, and after 4 days of intravenous treatment produced antidepressant-like behavior, CREB phosphorylation, and neurogenesis in mice.

    [pubmed] [doi]

10

Status sources

Sources behind the tier, regulatory status, sequence and dates on this page.

11

Cite this entry

$ cite --format=apa

peptidemeta. (2026). Spadin. In peptidemeta: The peptide library, ranked by evidence. Retrieved November 8, 2026, from https://peptidemeta.com/p/spadin/

$ cite --format=bibtex 
@misc{peptidemeta-spadin,
  title = {Spadin},
  author = {{peptidemeta}},
  year = {2026},
  howpublished = {\url{https://peptidemeta.com/p/spadin/}},
  note = {Accessed 2026-11-08}
}

Accessed date reflects when you opened this page. Cite primary studies for scientific claims.

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