P21 Peptide
A fragment derived from CNTF wearing an adamantane cage so it can cross into the brain. Orally active in mice, studied in dementia models, and no human has ever taken it in a trial.
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For research use only. Not for human or veterinary use.
What P21 Peptide is
The plain-language version, first.
A neurotrophin fragment wearing a chemical crash helmet.
P21 peptide (also written P021, Ac-DGGL(A)G-NH2, acetyl-Asp-Gly-Gly-Leu-(adamantyl)Gly-amide, C27H42N6O8, molecular weight 578.7, PubChem CID 56589645) is a synthetic non-natural peptide derived from a short region of ciliary neurotrophic factor, carrying an adamantane substitution on its C-terminal glycine to permit blood brain barrier penetration. It has been studied as an orally active compound in 3xTg-AD mice, with no human studies published to date.
The parent story matters here, because P21 exists to fix the parent's specific failure.
CNTF is a growth factor your nervous system uses. It went into development decades ago, and it ran into problems including immune reactions and a molecule too large and fragile to deliver well.
P21 is a small fragment derived from it, wearing an adamantane group, which is a rigid carbon cage bolted on so the fragment can cross the blood-brain barrier.
Adamantane is a real trick with real precedent. Several approved drugs use that cage for exactly this purpose.
So the design reads sensibly: keep a working piece, armour it, get it into the brain by mouth.
A rational repair job on a failed molecule. The design is the strong part of this file.
What is P21 peptide?
Mechanism studied, not outcome promised.
Leukaemia inhibitory factor signalling prevents neural progenitor cells from forming neurons. P021 competitively inhibits that signalling, which is why an inhibitor ends up on the pro-neurogenesis side of the ledger.
A rigid, fat-loving hydrocarbon cage is attached to the C-terminal glycine. That single modification is what gets a small water-loving peptide across the blood brain barrier well enough to work when eaten.
Chronic P021 increased brain-derived neurotrophic factor in 3xTg-AD mice alongside the reported cognitive and synaptic findings (Kazim, 2014, PMID 25046994).
The parent molecule failed for a fixable reason, and this is the attempted fix.
The proposed mechanism sits in an interesting corner of brain biology: the birth of new neurons.
The mouse work points at P21 nudging neural progenitor cells toward becoming neurons, partly by interfering with a signal called LIF that normally holds them back.
Releasing a handbrake rather than pressing an accelerator. As mechanisms go it is a genuinely elegant one.
It is also, so far, a mouse mechanism. The models used are dementia models, the durations run long for rodent work, and the oral activity claim has held up in that setting.
Here's the honest part, in the plainest terms available.
No human has taken this compound in any registered trial. The entire file lives in animals, and elegance in a mouse is still a mouse.
The research so far for P21 Peptide
Where the evidence is thin, we say so.
Chronic oral P021 in 3xTg-AD mice reduced tau hyperphosphorylation and soluble amyloid beta, increased BDNF, and was reported to rescue deficits in cognition, neurogenesis and synaptic plasticity (Kazim, 2014, Neurobiology of Disease, PMID 25046994). Rodent tolerability out to eighteen months with no weight loss or pain behaviour, which is the specific failure mode of the parent protein.
Any human study. There are no registered or published trials of P021 in people, which is notable for a molecule explicitly designed to solve a human trial failure. There is also no CAS number in any primary source we could find, and independent replication outside the originating lab is thin.
Most neurotrophic fragments are derived because the parent protein is too large or too short-lived to administer. P021 is unusual in that its design constraint was a documented adverse event profile, since full-length ciliary neurotrophic factor produced anorexia, myalgia and cramping in ALS trials, and the fragment was selected to retain receptor-level activity while shedding whatever produced those effects. The rodent tolerability data, spanning administration periods up to eighteen months without weight loss or pain behaviour, is therefore not a routine safety appendix but a direct test of the design hypothesis. What remains untested is whether that separation holds in the species where the original problem was observed, because P021 has never been administered to a human being.
Mouse work with an interesting shape, and a human column that is empty.
The animal file has a specific strength worth naming: duration.
Rodent studies have run up to eighteen months, which is long for this kind of work, without the toxicity pattern that helped sink the parent molecule.
Long, clean animal runs are genuinely encouraging. They are also exactly where every failed neurology drug looked good, because the brain is where animal models betray you most.
Neurology has the worst translation rate in all of drug development. Compounds that cure mouse dementia are a crowded graveyard.
No human trials. Nothing approved. No safety data in people at all.
A well-designed molecule with promising mouse work, standing at the exact spot where hundreds of promising molecules have previously fallen over. Respect the design. Price in the graveyard.
P21 peptide, research grade, sold for laboratory use only.
P21 Peptide specs
The chemistry, exactly as released.
Who studies P21 Peptide
Who tends to order this one, and why.
A research compound does not have one audience. It has a handful of rooms where the same question keeps coming up, and the question is a different question in each of them.
Groups working on oral peptide delivery
The adamantane cage is a concrete, reproducible answer to the blood brain barrier problem, and the feed-dosed study is the proof point.
Tau and amyloid model labs
The 3xTg-AD readouts in the Kazim work cover tau phosphorylation and soluble amyloid beta in the same animals, which is a convenient combined endpoint set.
Neurogenesis researchers
The LIF inhibition mechanism is an unusual route to progenitor differentiation and is not widely used as a tool approach.
Anyone confusing this with p21 the protein
P021 the peptide and p21 the cyclin-dependent kinase inhibitor share nothing but a label. Literature searches on the bare term return mostly the protein.
Sold for laboratory research only. This is not guidance for personal use, and nothing here is a recommendation.
P21 Peptide backstory
How it got here.
The New York State Institute for Basic Research sits on Staten Island, which is not where anybody expects Alzheimer's chemistry to come from. Khalid Iqbal's group there has been working on tau for a very long time.
The idea behind P021 is almost stubborn. CNTF failed in humans for reasons that had nothing to do with whether it helped neurons.
It failed because the whole protein did too many things at once and some of them were awful. So rather than declare the target dead, they asked which small piece carried the useful signal.
Then they solved the delivery problem with an adamantane cage, which is a genuinely elegant piece of medicinal chemistry dressed up as brute force. And then they proved the point in the least glamorous way available.
They put it in mouse chow and left it there for a year.
- 1
CNTF's bad trial
Ciliary neurotrophic factor went into ALS trials and produced anorexia, muscle pain and cramps. The protein was effectively shelved as a systemic therapeutic.
- 2
Staten Island, not Cambridge
Khalid Iqbal's lab at the New York State Institute for Basic Research took a short region of CNTF and built a peptide around it rather than abandoning the target.
- 3
Dosed in the chow
The pivotal twelve month 3xTg-AD study administered P021 in the feed. An orally active neuroactive peptide is rare enough that this is the headline detail.
Buying P21 Peptide in Canada
What ships, how fast, and the paperwork.
The hard part of buying research material is almost never the compound. It is the logistics. What leaves the building, how fast it moves, and what is in the box beside the vial. Here is ours, plainly.
Research use only
Sold for laboratory research use only, not for human or veterinary consumption. Health Canada's advisory of 9 April 2026 states that peptides are generally regulated as prescription drugs in Canada, and that "For Research Use Only" labelling does not make these products legal. P21 is not named in that advisory, which is not the same as being cleared.
No CAS number, on purpose
We could not locate a CAS registry number for P021 in any primary source. Some listings print one anyway. A blank you can trust beats a number you can't.
Two molecular weights in circulation
PubChem CID 56589645 gives 578.7. A second source gives 578.3. They agree to within 0.4 daltons and both describe the same compound, C27H42N6O8.
P21 Peptide vs Dihexa
Stacked together constantly, compared almost never.
The two brain-penetrant hopefuls of this catalogue, and the difference between their files is a lesson in how evidence ages.
P21 is a rationally designed CNTF fragment in an adamantane cage, with long-duration mouse work and zero human subjects ever. Its file is thin but intact.
Dihexa had a bigger reputation and then three of its foundational papers were retracted in 2025, leaving one independent rodent study upright.
A small file that holds beats a large one that had to be taken back. Neither has touched a human, and the mouse-to-human gap in neurology is the widest in all of drug development. Dihexa has its own page here
Stuff people ask about P21 Peptide
If your question is not here, email us. Real human answers.
No, and the name collision causes real confusion. p21, also called Cip1 or Waf1, is a cyclin-dependent kinase inhibitor involved in the cell cycle. P021 is a small synthetic peptide derived from ciliary neurotrophic factor, written Ac-DGGL(A)G-NH2. They're unrelated. If you search the bare term in a literature database, most of what comes back is the protein rather than the peptide.
Brain access. P021 is a small water-loving peptide, and the blood brain barrier is built to keep those out. Attaching a rigid adamantane cage to the C-terminal glycine makes the molecule fat-soluble enough to cross. It's the modification that turns an otherwise ordinary CNTF fragment into something that works when a mouse eats it rather than only when it's injected.
In rodents, yes, and that's the most distinctive thing about it. The pivotal twelve month study in 3xTg-AD mice dosed P021 in the feed rather than by injection (Kazim, 2014, PMID 25046994). Oral activity is uncommon for neuroactive peptides. Whether it carries into any other species is unknown, because no other species has been tested.
Because CNTF failed people. In ALS trials the full-length protein caused anorexia, muscle pain and cramps, which made it unusable systemically no matter what it did for neurons. Khalid Iqbal's lab kept the short region that carried the useful signal and dropped the rest. In rodents dosed up to eighteen months, P021 didn't produce weight loss or signs of pain.
Chronic oral P021 in 3xTg-AD mice reduced tau hyperphosphorylation and soluble amyloid beta, increased BDNF, and in the authors' words rescued deficits in cognition, neurogenesis and synaptic plasticity (Kazim, 2014, Neurobiology of Disease). Those are model-system endpoints in a genetically engineered mouse, which is a long way from a clinical outcome in a person.
None. Nothing registered, nothing published. A decade after the pivotal rodent paper, P021 has never been given to a human being. That's worth sitting with, because the molecule was specifically engineered around a problem that only showed up in humans, and the fix has never been checked in the species that had the problem.
Good pairing options with P21 Peptide
What researchers stack alongside it.
Pairing is where research gets ahead of itself. These are the compounds researchers put in the same order as P21 Peptide, which is a statement about ordering habits, not about evidence. Two things in one cart have not been studied together unless somebody studied them together.
Seven residues that shut a potassium channel called TREK-1. One laboratory, one paper, and a number so striking that the right response is to wait for somebody else to see it too.
A peptide preparation made from pig brain, used in clinics across half the world. A 2023 Cochrane review found no mortality benefit and a 2.39 relative risk of serious adverse events. We are leading with that on purpose.
Order P21 Peptide right now
One last look before you decide.
Freeze-dried, COA on the page, ships cold
If you are researching P21 Peptide and you want a source you do not have to second-guess, start with the paperwork on this page. For research use only.
Not for human consumption. Not approved by Health Canada or any other regulatory body.
Page last updated August 19, 2026
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