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Thymosin β4 fragment · 43 residues · actin-binding
Thymosin Beta-4 fragment. A 43-amino acid synthetic peptide. Supplied as a lyophilized powder for research purposes only.
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Assayed by Janoshik to ≥99% purity — the certificate is included with every order.
Valtrax Research supplies materials strictly for in-vitro laboratory research. They are not drugs, supplements, cosmetics, or medical devices, and are not intended for human or animal use, ingestion, or administration. By ordering, you confirm you are a qualified researcher purchasing for lawful research use, in accordance with all applicable Canadian laws and regulations.
TB-500 is the synthetic version of a 43-residue stretch of thymosin β4 — the parent protein is one of the most abundant peptides inside motile cells, and its job is to hold a reserve pool of G-actin monomers. The fragment keeps the part that does the binding, including the central actin-contact motif most of the activity is pinned to.
That actin handle is the whole reason it stays on the bench. Sequester or release monomeric actin and you change how a cell builds and tears down its cytoskeleton — which is the lever behind the migration and wound-closure models that keep returning to this peptide.
Everything routes back to actin. The literature on thymosin β4 / TB-500 measures cell migration, wound closure, and tissue remodeling, then ties those outputs to the peptide’s grip on monomeric actin. Cardiac and dermal preparations recur because both depend on cells moving into a damaged field.
Strip TB-500 down and the mechanism is actin handling. The peptide carries thymosin β4’s actin-sequestering motif, so studies read it through the cytoskeleton: how monomer availability shifts, how cells polarize, and how that translates into directed migration across a wound bed.
The foundational papers are about the parent protein — Malinda on wound closure, Bock-Marquette on cardiac cell migration and survival, Smart on epicardial progenitor mobilization. TB-500 inherits that record as the synthetic, defined-sequence stand-in used to probe the same actin-driven behaviors.
Thymosin β4 first surfaced in thymic-extract work, catalogued among the thymosins before its real function — binding and buffering G-actin — was understood. Once the actin role was clear, attention shifted from immunology to cytoskeletal dynamics and tissue repair.
TB-500 is the practical offshoot: a synthesized fragment that keeps the active region, giving labs a defined sequence to study where the full protein would be cumbersome to work with.
Malinda, K.M. et al. (1999). Thymosin beta4 accelerates wound healing. J Invest Dermatol 113(3):364–368.
PubMedBock-Marquette, I. et al. (2004). Thymosin beta4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair. Nature 432(7016):466–472.
PubMedSmart, N. et al. (2007). Thymosin beta 4 induces adult epicardial progenitor mobilization and neovascularization.
PubMedThird-party tested for purity, identity, quantity.
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