P021

P021 (CNTF-derived neurotrophic research peptide)

Evidence & Status

  • Preliminary / Experimental
  • Preliminary

At a Glance

A modified CNTF-derived pentapeptide studied only in verified animal models. It has no verified human interventional evidence, established human pharmacokinetics, or established human safety profile.

Plain English

Researchers study the exact modified P021 construct in animal models. These findings do not establish human neurogenesis, clinical benefit, pharmacokinetics, safety, or a treatment protocol.

Overview

P021 is a modified CNTF-derived pentapeptide, Ac-DGGL(A)G-NH2, in which the adamantyl group modifies the C-terminal glycine rather than adding a sixth amino-acid residue. The approved evidence concerns chronic oral treatment in mouse models; it does not establish human pharmacokinetics, clinical efficacy, or dosing.

Research Summary

Two approved publications report P021 in transgenic mouse models of Alzheimer's disease–related pathology. These are preclinical findings from a limited evidence base and must not be converted into claims of human neurogenesis, cognitive benefit, safety, or a treatment protocol.

Research Areas

  • Hippocampal neurogenesis
  • Cognitive aging
  • Alzheimer's disease
  • CNTF signaling pathway
  • Synaptic plasticity

Safety & Risks

Serious Risks

  • Complete absence of human safety data
  • Unknown CNS effects at non-physiological concentrations
  • Theoretical risk of aberrant neurogenesis or gliosis at supratherapeutic doses
  • Field of adult human hippocampal neurogenesis itself is scientifically contested

Reported Side Effects

  • Unknown in humans
United States
The cited evidence is preclinical and does not establish regulatory authorization or a human clinical indication.
United Kingdom
The cited evidence is preclinical and does not establish regulatory authorization or a human clinical indication.
Australia
The cited evidence is preclinical and does not establish regulatory authorization or a human clinical indication.
Canada
The cited evidence is preclinical and does not establish regulatory authorization or a human clinical indication.

Citations & Sources