Cartalax

peptide · musculoskeletal · Oral · Subcutaneous

Cartalax, a peptide. Synthetic tripeptide Ala-Glu-Asp from the Khavinson short-peptide programme, assigned to cartilage and studied against the ageing-associated…

Synthetic tripeptide Ala-Glu-Asp from the Khavinson short-peptide programme, assigned to cartilage and studied against the ageing-associated secretory phenotype of chondrocytes. In that phenotype the cells raise synthesis of p16, p21, p53, TNF-alpha and IL-1-alpha and lower sirtuin-1; the peptide is reported to normalise those molecules, which is the proposed basis for peptide chondroprotection in osteoarthritis. Unlike the other entries in this family the tissue attribution is corroborated, by both the cartilage cell work and the review that names the brand beside the sequence.

PubChem CID 87815447 (C12H19N3O8), CAS 85806-95-7. THE IDENTITY VERIFIES TWICE, INDEPENDENTLY, which makes this the strongest of the four grey-market peptides in this batch: PubChem lists both Cartalax and T-31 peptide as synonyms of Ala-Glu-Asp (those are PubChem synonyms, not sentences from any abstract), and PMID:37782637 carries brand, sequence, tissue and route in one sentence — "Sigumir, a polypeptide complex of cartilage and bone tissues of young animals, and the AED tripeptide (Kartalax) have shown high efficacy in animal models of OA and oral administration in patients with OA of older age groups." NOTE THE INDEXED SPELLING IS KARTALAX; `Cartalax` returns 6 hits and `Kartalax` 1, so both belong in aliases[]. The internal code is confirmed by PMID:26033601 ("Short peptides T-31 (AED) and T-35 (EDL)") and PMID:18306703 studies "T-31 substance" in an ovariectomy osteoporosis model in rats. PUBCHEM DATA-QUALITY CAVEAT: that CID's synonym list contains two entries wrong for the structure, "H-Asp-Glu-Asp-OH" and "alanyl-glutamyl-aspartic acid". Trust the formula and SMILES over them — Ala + Glu + Asp less two waters is C12H19N3O8 at 333.29, which is what is stored. MECHANISM verbatim from PMID:37356100: chondrocyte SASP "is characterized by an increase of the synthesis of p16, p21, p53 pro-apoptotic proteins, TNF-alpha, IL-1alpha pro-inflammatory cytokines and a decrease of Sirt1 synthesis. Peptides AED and CPC normalize the synthesis of molecules that form SASP of chondrocytes." Human-cell gene data in PMID:32399807 ("IGF1 gene expression levels ... being enhanced by 3.5-5.6 fold upon the addition of the peptides", at nanomolar concentrations). A NEGATIVE RESULT WORTH RECORDING: PMID:22238759 tested T-31 on aged thymocytes and found "Only AB-9 peptide exhibited a complex geroprotective effect" — i.e. negative for AED, so that paper is not supporting evidence. SEARCH TRAP: "AED" alone collides with antiepileptic drug. The DNA-binding class claim shares Ovagen's limitation: the peptides imaged entering nuclei in PMID:22117547 were epithalon, pinealon, testagen and bronchogen, not AED, so the mechanism reaches this sequence by extrapolation.

Sources: PMID:37782637, PMID:37356100, PMID:25946838, PMID:26033601, PMID:32399807, PMID:37782646