P21
Research OnlyA hexapeptide (Ac-DGGLAG-NH2) derived from ciliary neurotrophic factor (CNTF) that is claimed to mimic BDNF effects and promote neurogenesis. Developed primarily at the New York State Institute for Basic Research. Limited to preclinical rodent studies with no human clinical trials. Sold as a research chemical with unknown safety profile.
Ac-DGGLAG-NH2 · P021 · CNTF-derived peptide
Preclinical evidence only
- Preclinical
- 100%
- Human research
- 0%
Based on 15 cited sources
Numeric assessment unreviewed
A historical numeric score is recorded but has not passed a current, compound-specific assessment review. No numeric score is displayed.
This is a limitation of the numeric assessment, not a measured absence of benefit. It does not re-review the separately recorded catalogue classification or establish efficacy or safety.
The proposed mechanisms of P21 are based entirely on animal and in vitro studies. No human mechanistic data exists.
How It Works (Simplified)
P21 is designed to bypass the blood-brain barrier and activate neurotrophic signaling:
Increases brain-derived neurotrophic factor expression by inhibiting leukemia inhibitory factor (LIF) signaling pathway.
Promotes formation of new neurons in dentate gyrus through enhanced proliferation and maturation of neural progenitor cells.
Via BDNF/TrkB/PI3K/Akt pathway, inhibits GSK-3beta activity - reducing abnormal tau hyperphosphorylation.
Restores synaptic proteins (PSD-95, synapsin-1) and glutamate receptors supporting plasticity and memory.
Key Research: Li B et al. (2010) demonstrated neurogenesis enhancement in normal mice. PMID:20600002
Important Limitations
- All studies from a single research group (Iqbal laboratory at IBR)
- No independent replication of key findings
- Translation to human physiology is completely unknown
- No human pharmacokinetics or safety data
- 15+ years of research with no clinical trial advancement
- “BDNF-mimetic” claim not fully validated at receptor level
Based on preclinical observations: Initial BDNF pathway activation may begin. Animal studies show early changes in CREB phosphorylation and neurotrophin signaling within days. No human timeline data available.
PMID:20600002Animal studies suggest neural progenitor proliferation increases. In mouse models, Ki-67+ cells (proliferating) and DCX+ cells (immature neurons) show measurable increases by 2-4 weeks of treatment.
PMID:25046994Preclinical models show continued neurogenesis and early synaptic protein restoration. Tau phosphorylation changes and GSK-3beta inhibition effects observed in AD mouse models within this timeframe.
PMID:27400746Long-term animal studies (3-12 months) suggest sustained cognitive improvements and ongoing neuroprotection. However, human pharmacokinetics, optimal dosing, and treatment duration are completely unknown.
PMID:28655344Research-based observations
This timeline reflects observations from published clinical and preclinical studies. Individual responses may vary significantly. This is not a guarantee of effects or a dosing schedule. Consult qualified healthcare providers for personalized guidance.
Dihexa
CompatibleBoth target cognitive enhancement through different mechanisms. P21 focuses on BDNF/neurogenesis while Dihexa acts on HGF/c-Met pathway. No interaction studies available; theoretical complementary nootropic effects.
Semax
CompatibleDifferent neurotrophic mechanisms. P21 is CNTF-derived targeting BDNF while Semax is ACTH-derived with broader neuroprotective effects. No known contraindications; both aim to support cognitive function.
Cerebrolysin
CompatibleCerebrolysin is a complex peptide mixture with neurotrophic properties. P21 has a more targeted mechanism via BDNF pathway. No interaction data available; both target neuroregeneration.
Selank
CompatibleNon-overlapping mechanisms. P21 targets neurogenesis while Selank modulates anxiety and immune function. Theoretical complementary cognitive benefits.
BPC-157
CautionBoth have neuroprotective claims but through different pathways. BPC-157 affects dopaminergic system while P21 targets BDNF/LIF signaling. Limited data on CNS interactions; exercise caution.
Research Note: Interaction data is based on published literature, mechanistic understanding, and theoretical considerations. Most peptide combinations lack direct clinical study. This information is for educational purposes only and does not constitute medical advice. Always consult qualified healthcare providers.
Key Studies Cited
Use the source links in the research discussion above to inspect the referenced records.
This dossier synthesizes available evidence from peer-reviewed literature, regulatory documents, and clinical trial registries. Evidence strength labels summarize the cited material for this entry and should be read alongside its population, model, and study limitations.
For complete methodology details, see our Methodology page.
Important Disclaimer
This dossier is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before making health decisions.
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Compared With
3 comparisonsConditions Studied
3 entries- P21 for Age-Related Cognitive Decline P21 has been studied for its potential effects on age-related cognitive impairment in preclinical models. Research from the Iqbal…
- P21 for Alzheimer's Disease Research Multiple preclinical studies have examined P21 in transgenic Alzheimer's mouse models (3xTg-AD). Research showed reduced tau hyper…
- P21 for Neurogenesis Enhancement P21 was specifically designed to promote adult hippocampal neurogenesis. Studies in normal mice showed increased proliferation and…