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No. 031 · Mind · Nootropic Peptide

P21

P021Peptide 021Ac-DGGLAG-NH2

C Tier C · Animal data how tiers work →
  • Not FDA approved
  • WADA ✗ S0
Compare Cite
Fingerprint 5 residues
P21 sequence fingerprint
  • Nonpolar 3
  • Negative charge 1
  • Modified / non-standard 1

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 mouse and rat studies from the developing laboratory (e.g. Li et al., FEBS Lett 2010); no published human studies.

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

02

At a glance

Residues
5 amino acids, N→C
Molecular weight
578.7 Da
Formula
C27H42N6O8
Discovered
2010 Designed from a CNTF-derived peptide at the NYS Institute for Basic Research (Li et al., FEBS Lett 2010).
Routes studied
Intranasal, Subcutaneous Routes used in published research
FDA
Not approved
WADA
Prohibited · S0 Non-approved substances
03

Sequence

N → C · 5 residues · hover, tap, or use arrow keys to inspect

Note Reported as Ac-DGGLAG-NH2, where the C-terminal residue is an adamantane-containing glycine surrogate (PubChem depicts 3-amino-adamantane-1-carboxamide).

04

Overview

A synthetic peptide derived from an active region of ciliary neurotrophic factor (CNTF), with an adamantane-modified C-terminus (Ac-DGGL-[adamantylglycine]-NH2, also called P021). Explored in mouse and rat models for neurogenesis and Alzheimer-related decline.

Research status Preclinical research only; mouse and rat studies, mostly from the developing laboratory, report neurogenic and cognitive effects

05

Mechanism

P21 (P021) is a CNTF-derived peptidergic compound. In mouse studies it increased brain-derived neurotrophic factor (BDNF) expression and decreased glycogen synthase kinase-3 beta (GSK-3β) activity, which was associated with reduced tau hyperphosphorylation and increased hippocampal neurogenesis and synaptic plasticity.

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.

  • Promoted hippocampal neurogenesis
  • Improved spatial learning and memory
  • Reduced tau hyperphosphorylation
  • Enhanced dendritic complexity
07

Safety & unknowns

No human safety data. Only preclinical animal studies available. Mechanism of promoting neurogenesis carries unknown long-term risks. Not FDA-approved. Data limited to rodent studies.

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 2014

    Disease modifying effect of chronic oral treatment with a neurotrophic peptidergic compound in a triple transgenic mouse model of Alzheimer's disease

    Kazim SF, Blanchard J, Dai CL, et al. Neurobiology of Disease

    Twelve months of oral P021 in 3xTg-AD mice reduced tau hyperphosphorylation and soluble Aβ, increased BDNF and decreased GSK-3β activity, and rescued deficits in cognition, neurogenesis, and synaptic plasticity.

    [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). P21. In peptidemeta: The peptide library, ranked by evidence. Retrieved November 8, 2026, from https://peptidemeta.com/p/p21/

$ cite --format=bibtex 
@misc{peptidemeta-p21,
  title = {P21},
  author = {{peptidemeta}},
  year = {2026},
  howpublished = {\url{https://peptidemeta.com/p/p21/}},
  note = {Accessed 2026-11-08}
}

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

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