Peptide Schedule
P21Small moleculeNo amino acid sequence. Icon reflects category theme only.

P21 Dosage Calculator

CognitiveInjection/NasalResearch~3+ hours half-life

P21 (also designated P021) is a synthetic tetrapeptide derived from the biologically active region of human ciliary neurotrophic factor (CNTF), specifically amino acid residues 148-151.

Promoted hippocampal neurogenesis and dendritic maturation in multiple mouse modelsReduced tau hyperphosphorylation by 50-60% in triple transgenic Alzheimer's miceCrosses the blood-brain barrier after peripheral administrationEnhanced spatial learning and reference memory in normal adult mice4 weeks on / 4 weeks off

100mcg · Daily

100500
4.0 units
100 units (1mL)
Concentration
2,500
mcg/mL
Draw Volume
0.040
mL
Syringe Units
4.0
units
Doses / Vial
50
doses

Summary: Add 2mL BAC water to your 5mg vial. Draw to 4.0 units on a U-100 syringe for a 100mcg dose. This vial will last 50 doses.

Cycle Planner

Intranasal or Subcutaneous. Typical beginner frequency: daily.

P21 Pharmacokinetics

P21 Dosing Protocol

LevelDose / InjectionFrequency
Beginner100mcgDaily
Moderate300mcgDaily
Aggressive500mcgDaily

Note: CNTF-derived tetrapeptide (residues 148-151) with adamantylated glycine C-terminal cap. Crosses the blood-brain barrier. Intranasal or subcutaneous. Preclinical only — no human trials. Cycle 4 weeks on, 2-4 weeks off.

About P21

P21 (also designated P021) is a synthetic tetrapeptide derived from the biologically active region of human ciliary neurotrophic factor (CNTF), specifically amino acid residues 148-151. An adamantylated glycine group was added to the C-terminal to improve blood-brain barrier permeability and protect against enzymatic degradation by exopeptidases. Unlike full-length CNTF, which is too large to cross the blood-brain barrier and carries systemic side effects including weight loss and antibody formation, P21 was engineered to retain the neurotrophic benefits while eliminating these drawbacks. Its primary mechanism involves competitive inhibition of leukemia inhibitory factor (LIF) signaling, which normally acts as a brake on hippocampal neurogenesis. By suppressing LIF, P21 allows endogenous neurogenic processes to proceed more effectively, leading to increased BDNF expression, TrkB receptor activation, and downstream CREB phosphorylation. Preclinical evidence comes primarily from the laboratory of Dr. Khalid Iqbal at the New York State Institute for Basic Research in Developmental Disabilities. In 3xTg-AD mice (a triple transgenic Alzheimer's model), P21 reduced tau hyperphosphorylation by 50-60%, increased hippocampal neurogenesis approximately threefold, and prevented synaptic loss. In normal adult C57BL/6 mice, it enhanced spatial reference memory and promoted maturation of newly born neurons in the dentate gyrus. All existing data comes from animal studies. No Phase I, II, or III human clinical trials have been conducted, and the long-term safety profile in humans remains entirely unknown. This compound should be considered strictly experimental.

Frequently Asked Questions