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P021

Peptide 021, GLXC-21260

A tetrapeptide derived from CNTF, designed to promote neurogenesis, enhance cognition, and mitigate Alzheimer's pathologies by modulating neurotrophic signaling.

Molecular Profile
Formula C27H42N6O8
Mol. Weight 578.7 g/mol
Sequence Gly-Glu-Pro-Pro...
Route
Oral
60 nmol/g diet (in mice)
ORA
Subcutaneous (SC)
25 nM/day (in mice)
SUB

How It Works

How It Works: P021 is a modified tetrapeptide from CNTF that competitively inhibits LIF signaling and increases BDNF expression to promote neurogenesis and neuroprotection.

  • Competitively inhibits leukemia inhibitory factor (LIF) signaling, reducing neural progenitor cell inhibition
  • Increases BDNF expression, activating TrkB-PI3K-Akt pathway to inhibit GSK-3β and reduce tau phosphorylation
  • Enhances neurogenesis in hippocampal dentate gyrus (increases Ki-67+ and DCX+ cells)
  • Restores synaptic markers (e.g., synaptophysin, PSD-95, MAP2, glutamate receptors like GluN1, GluA1)
  • Reduces soluble Aβ40/Aβ42 and phosphorylated tau levels in Alzheimer's models
  • Prevents neurodegeneration and amyloid/tau pathologies in models of aging, Down syndrome, and macular degeneration.

Latest Clinical Trials

Completed PHASE2 NCT00537017

Follow Up Safety Study of SCH 420814 in Subjects With Parkinson's Disease (P05175)

Merck Sharp & Dohme LLC
INTERVENTIONAL
Updated Dec 15, 2025
Completed NA NCT03894709

A Care Model for Elderly Hip-fractured Persons With Cognitive Impairment and Their Family Caregivers

Chang Gung Memorial Hospital
INTERVENTIONAL
Updated Dec 15, 2025
View All Clinical Trials

Latest Studies

Utility 2
pubmed Nov 26, 2024

Effects of a ciliary neurotrophic factor (CNTF) small-molecule peptide mimetic in an in vitro and in vivo model of CDKL5 deficiency disorder.

Mottolese. Nicola N; Loi. Manuela M; Trazzi. Stefania S; Tassinari. Marianna M;...

The peptide P021 helped brain cells grow and survive in a dish made from CDKL5‑deficient cells, but when given to CDKL5‑deficient mice it did not raise BDNF levels, fix brain structure, or meaningfully improve behavior. More work is needed to see if starting treatment earlier or giving it longer could work.

pubmed Mar 13, 2024

Variants located in intron 6 of <i>SMN1</i> lead to misdiagnosis in genetic detection and screening for SMA.

Qu. Yujin Y; Bai. Jinli J; Jiao. Hui H; Qi. Hong H; Huang. Wenchen W; OuYang. Sh...

The study shows that certain DNA changes inside the SMN1 gene can trick standard genetic tests into wrongly saying a person has two missing copies of the gene, which could lead to a misdiagnosis of spinal muscular atrophy. Using a different test (MLPA‑P021) or sequencing avoids this error.

Browse All Studies