P21 10mg

The compound sold under the name P21 is P021 (CAS 1246751-68-7; PubChem CID 56599151; FDA substance registry UNII VV8CZC8PAS), a synthetic peptidomimetic with the molecular formula C27H42N6O8 and an average molecular weight of about 578.7 g/mol. Structurally it is an adamantylated tetrapeptide: the four-residue sequence Asp-Gly-Gly-Leu (DGGL), corresponding to residues 148-151 of human ciliary neurotrophic factor, carrying an N-terminal acetyl group and a C-terminal amide bond to 3-amino-adamantane-1-carboxamide. The literature usually writes this shorthand as Ac-DGGLAG-NH2, which is a common source of confusion — the trailing "AG" denotes the adamantane cap, not alanine and glycine, so the molecule is a tetrapeptide rather than the six-residue peptide the shorthand appears to describe.

A separate and more important naming distinction: P21 in this catalog is not p21^Cip1/Waf1, the endogenous human cyclin-dependent kinase inhibitor encoded by the CDKN1A gene, nor is it p21^ras, the 21 kDa Ras protein. Those are naturally occurring proteins associated with cell-cycle arrest and with Ras signaling respectively, and the large literature on them describes entirely different molecules. Material published about cell-cycle arrest, p53, or tumor suppression under the name "p21" does not refer to this compound.

P021 originates from the laboratory of Khalid Iqbal at the New York State Institute for Basic Research in Developmental Disabilities, which derived it by epitope-mapping an earlier eleven-residue CNTF fragment ("Peptide 6") down to its active core and then acetylating and adamantylating that core; the design intent described in the associated patents (for example US 8,796,214 and US 9,327,011) was greater lipophilicity and resistance to peptidase breakdown. The mechanism proposed by that group involves competitive inhibition of leukemia inhibitory factor signaling and increased BDNF expression. That mechanism is the originating laboratory’s model, supported by their in vitro data rather than independently established.

The published evidence is entirely preclinical. Studies in mice and rats have reported effects on behavioural measures, hippocampal neurogenesis markers, and tau phosphorylation in transgenic and aged-rodent laboratory models (Kazim et al., Neurobiology of Disease 2014, PMID 25046994; Bolognin et al., Alzheimer’s Research & Therapy 2017, PMID 28655344; Kazim et al., Scientific Reports 2017, PMID 28368015; Bolognin et al., Neurobiology of Aging 2014, PMID 24702821). Two honest caveats belong alongside those results. First, every primary experimental study of P021 in the indexed literature includes the originating investigator as an author, so there is no fully independent replication; the one study led primarily by an outside laboratory in a new rodent model (Journal of Neurodevelopmental Disorders 2024, PMID 39592934) was largely negative on its in vivo endpoints. Second, although the adamantane modification was intended to aid brain penetration, how much P021 reaches the brain has not been directly measured, and sources conflict on whether penetration is established. P021 is not an approved drug, and this product is supplied strictly for in vitro and laboratory research and is not for human or veterinary use.