Neuro & cognitive

P21 (P021)

Also called P021, Peptide 021, Ac-DGGLAG-NH2, CNTF peptide mimetic, GLXC-21260

P21, also written P021, is a small lab-made peptide based on a short piece of ciliary neurotrophic factor (CNTF), a natural protein that supports nerve cells. In mice and rats it increased the birth of new brain cells and improved memory, including in animals bred to develop Alzheimer's-like changes. It has never been tested in people, and almost all of the research comes from one New York lab whose lead scientist co-founded a company developing it.

Preclinical onlyStudied in cells or animals only. Effects in people are unknown.

New · under editorial review. Added October 30, 2026 by our automated research, with every claim sourced. A person has not checked this page yet; treat it with extra care. How we research

All printable flashcards

Illustrative chain. The exact sequence has not been published in a source we could verify.

At a glance

Type: Peptide
Size: 4 amino acids (Asp-Gly-Gly-Leu) plus an adamantane-based glycine-like unit at the C-terminal end; N-terminal acetyl cap and C-terminal amide
Formula: C27H42N6O8
Molecular weight: 578.7 g/mol (PubChem)
Origin: Designed by the Iqbal laboratory from an active region of human CNTF found by epitope mapping. Its parent is Peptide 6, an 11-amino-acid CNTF fragment (residues 146-156) [3]; P021 keeps a four-residue core (Asp-Gly-Gly-Leu, with an acetyl cap at the start) and adds an adamantane group at the C-terminal end to slow breakdown and help it reach the brain [8][12]. How to write that end unit is not settled: the papers write the compound as Ac-DGGLAG-NH2 or Ac-DGGL(A)G-NH2 and call the last unit an 'adamantylated glycine' [1][4][8], while PubChem's structure shows it as an amino-adamantane carboxamide joined to leucine [15]. Because of this, we do not give a one-letter sequence. The formula and weight above are PubChem's; the developers give a molecular weight of 578.3 Da, which matches the exact mass of that formula [14][15].
Evidence: Preclinical only
US FDA status: Not FDA-approved and no registered human trials were found on ClinicalTrials.gov ²⁰. A 2025 independent review described it as in early development by Phanes Biotech, with no clinical trials ¹⁶.

Overview

How it works

Proposed, from animal and cell studies only: P021 is reported to block signaling by leukemia inhibitory factor (LIF), which normally holds back the making of new neurons, and to raise levels of brain-derived neurotrophic factor (BDNF) ²¹²¹³. BDNF in turn is thought to switch off the enzyme GSK-3β, a major driver of tau phosphorylation, which the developers suggest explains the lower tau changes seen in treated mice ⁴¹²¹³. Unlike the full CNTF protein, it is described as small enough to cross the blood-brain barrier and to work when given by mouth in food ⁶¹³; the developers report it crosses into the brain in rats ⁶, but a 2025 nonprofit review listed its blood-brain barrier penetration as 'not documented' ¹⁶. None of this has been confirmed in humans.

What research shows

Normal adult mice (2010): P21 given outside the brain improved learning and short-term and spatial memory and increased new neuron birth and maturation in the hippocampus ¹.
3xTg-AD Alzheimer's model mice, treatment from 9-10 months for 12 months in food: lower abnormal tau, lower soluble amyloid-beta, a trend to fewer plaques, and better memory, neurogenesis and synaptic markers ⁴.
3xTg-AD mice treated from 3 months of age (prevention design): reduced nerve-cell loss, amyloid and tau changes, rescued object-recognition memory and lower death rate; separate report of preserved dendrites and synapses ⁸⁹.
Aged rats (22-24 months): reduced age-related learning and memory decline, more new neurons and higher BDNF ⁵; lower total tau in brain and spinal fluid, with no detectable immune reaction ⁶.
Down syndrome model mice (Ts65Dn), treatment before and shortly after birth via the mother: less developmental delay and better adult memory ⁷. Similar early-life treatment in 3xTg-AD mice prevented later memory loss and reduced tau and plaques at 22 months ¹⁰.
CDKL5 deficiency model (2024): P021 fixed growth and survival defects in human-derived nerve cells in a dish, but long-term treatment in knockout mice did not raise BDNF or fix brain structure and gave only limited behavior benefit ¹¹.
Diffusion MRI study in 3xTg-AD mice (2026, n=78): early treatment moved white-matter measures partly back toward normal; the authors say this suggests myelin effects but did not confirm it with tissue studies ¹⁴.
Most P021 studies come from one lab whose senior author holds patents and co-founded the developing company ¹¹¹⁴; a 2025 review by the Alzheimer's Drug Discovery Foundation found no human studies of any kind ¹⁶.

Doses studied in people

No human studies exist, so there is no human dose. Animal studies mostly mixed it into food (60 nmol per gram of feed in mice) ¹²¹⁶; these figures do not translate to people.

Read this first: these are the amounts given to participants in published studies or written on official prescribing labels, reported for reference. They are not recommendations. Trial doses were chosen for specific patients under medical supervision, and a dose that is safe in one person can be harmful in another.

Vial math

Many research vials hold 5 or 10 mg of powder. This table shows how much ends up in each mark on a U-100 insulin syringe for common amounts of added liquid. It is arithmetic only, not a dose.

Vial	Liquid added	Concentration	Per unit (0.01 mL)
5 mg	1 mL	5 mg/mL	50 mcg	Open in calculator
5 mg	2 mL	2.5 mg/mL	25 mcg	Open in calculator
5 mg	3 mL	1.67 mg/mL	16.7 mcg	Open in calculator
10 mg	1 mL	10 mg/mL	100 mcg	Open in calculator
10 mg	2 mL	5 mg/mL	50 mcg	Open in calculator
10 mg	3 mL	3.33 mg/mL	33.3 mcg	Open in calculator

More sizes: all vial sizes · How this works: Syringes and units · Reconstitution guide.

Safety

Unknown in humans: no human safety, pharmacokinetic or toxicology data have been published ¹⁶.
In mice, up to 18 months of oral dosing was reported by the developers to cause no adverse effects ¹²; a 2025 review noted no weight loss, tumors or pain signs in rodents ¹⁶, and the developers found no detectable immune reaction in rats ⁶. The same review notes that antibody formation against P021 has been raised as a possible risk, though none had been found ¹⁶.
The parent protein CNTF, given to people with ALS in a 1990s trial, caused loss of appetite, muscle loss, cramps and pain; P021 is claimed to avoid these, but this is shown only in animals ¹⁶.
Products sold online as 'P21' are not regulated drugs, so their identity and purity are not verified by any regulator. P021 is not named on FDA's compounding safety-risk list ²².

Report side effects of any drug or product to the FDA through MedWatch. For a possible poisoning in the US, call Poison Control at 1-800-222-1222.

Legal status

FDA: Not FDA-approved and no registered human trials were found on ClinicalTrials.gov ²⁰. A 2025 independent review described it as in early development by Phanes Biotech, with no clinical trials ¹⁶.
Compounding: Not named on FDA's 503A/503B bulk-substance safety-risk (Category 2) page or its withdrawn-nominations list as of April 2026 ²².
Sports (WADA): Not named on the WADA 2026 Prohibited List. Because it has no approval from any health authority, it appears to fall under S0 (non-approved substances), which is banned at all times ²¹. This is our reading; check with your anti-doping body.
Other: Not approved in any country that we found. The peer-reviewed papers describe it as a CNTF-derived peptide, not as a component of Cerebrolysin ¹¹².

Rules change often. See Legal status of peptides for how these categories work.

History

The Iqbal and Grundke-Iqbal lab at the New York State Institute for Basic Research reported Peptide 6, an 11-mer from CNTF, around 2009-2010 ²³. In 2010 the same group described the shorter adamantane-modified version, called P21, which boosted new neuron formation and memory in normal mice ¹. Studies through 2026 tested it in Alzheimer's model mice, aged rats, and Down syndrome and other mouse models ⁴⁵⁷¹⁰¹⁴. Khalid Iqbal holds patents on P021 and co-founded Phanes Biotech, which holds a worldwide license to develop it as a drug ¹⁴. In the papers we reviewed, the links to Cerebrolysin are indirect: Cerebrolysin's maker, EVER NeuroPharma, partly funded a 2015 rat study of the parent Peptide 6 ¹⁹, and a 2011 mouse paper comparing CNTF peptides with Cerebrolysin was retracted by the journal in April 2026; the PubMed record does not give a reason ¹⁷¹⁸.

Common questions

Has P21 (P021) been tested in humans?

No. No human studies or registered clinical trials have been published; all results come from mice, rats and cells ¹⁶²⁰.

Is P21 made from Cerebrolysin?

No. The published papers describe it as a designed peptide based on a short active region of the protein CNTF, with an adamantane group added ¹¹². A 2011 mouse study comparing CNTF peptides with Cerebrolysin was retracted in 2026 ¹⁷¹⁸.

What did the animal studies show?

In normal mice, aged rats and Alzheimer's model mice, P021 increased new neuron formation, raised BDNF and improved memory tests, and in model mice it lowered tau changes ¹⁴⁵. One 2024 study in a different disease model found only limited benefit in living mice ¹¹.

Is the research independent?

Mostly not. Nearly all studies come from the lab of Khalid Iqbal, who holds patents on P021 and co-founded Phanes Biotech, which holds a worldwide license to develop it ¹⁴¹¹. Independent replication is limited.

Is P21 safe?

Its safety in people is unknown because it has never been tested in humans ¹⁶. Rodent studies of up to 18 months, run by the developers, reported no obvious side effects ¹².

Is P21 banned in sport?

It is not named on WADA's 2026 list, but as an unapproved drug it appears to fall under the S0 class, which is banned at all times ²¹.

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Sources

Wondering how to judge the claims made about compounds like this one? The Academy track Thinking clearly about peptide claims walks through it. You can try the Academy free first.

Last reviewed 2026-10-30 · How we research · Found an error? See our corrections policy.