Thymosin beta-4 is a low molecular weight, naturally occurring peptide that binds actin. It is released by platelets and macrophages at sites of injury, and in preclinical work it promotes cell migration, mobilizes and differentiates stem and progenitor cells, supports new blood vessel formation, and reduces myofibroblast number and scar formation (Goldstein 2012, PMID: 22074294; Kleinman 2016, PMID: 27450738). The 17-23 segment LKKTETQ is the actin-binding active site within the parent protein, and TB-500 supplies exactly that fragment with the N-terminus acetylated to slow degradation (Ho 2012, PMID: 23084823).
Two honest caveats about that mechanism story. First, a fragment is not the parent molecule. Full-length thymosin beta-4 has activities distributed across the whole 43-residue sequence, and no published human study has shown that Ac-LKKTETQ reproduces them at any dose. Second, mechanism has repeatedly failed to predict outcome here. In mice, thymosin beta-4 combined with prothymosin alpha supported cardiomyocyte proliferation after ischemic injury when the two genes were delivered into the myocardial wall as a gene therapy cocktail. That study delivered genes into heart tissue, it did not test a circulating peptide (Gladka 2023, PMID: 36125329). Compelling biology plus zero human efficacy trials is not evidence of benefit.
No human drug interaction study of TB-500 or of thymosin beta-4 has been published. Every entry below is mechanism-based and theoretical. Absence of documented interactions here reflects absence of research, not established safety.
Independently graded against 173,636 indexed supplements with 177 published clinical interactions, sourced from PubMed, FDA CAERS, openFDA, and NIH DSLD | Last updated:
Not medical advice. Based on published clinical research and systematic reviews.