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TB-500, Actin binding fragment
The synthetic actin binding fragment (LKKTETQ) of thymosin beta-4, studied for cell migration, angiogenesis, and systemic tissue repair in animal models.

In animal studies, the actin binding fragment of thymosin β4 is thought to drive cell migration and new blood vessel growth, the basis for its tissue repair reputation.
Tendon, ligament & muscle
Infarct size & function
Dermal & corneal
Endothelial migration
Bars indicate how far the evidence has progressed (in vitro to animal to human), not the size of any effect.
Crockford D, Turjman N, Allan C, Angel J
Reviews Tβ4 as the major G-actin sequestering molecule, promoting cell migration, angiogenesis, and survival, the rationale for dermal, corneal, and cardiac trials.
Marketed for tendon/joint/muscle healing and cardiac repair. The full Tβ4 molecule (as RGN-137) reached human trials for chronic skin wounds and cardiac repair with mixed results; Phase 2 data in hundreds of patients showed a favorable safety profile. There are no large randomized human trials of TB-500 itself for the musculoskeletal/athletic uses it is sold for.
The dominant concern is angiogenesis driven tumor support: Tβ4 is overexpressed in numerous cancers and correlates with metastatic potential in melanoma models (correlative, not proof exogenous dosing causes cancer). Pro angiogenic effects also raise concern in proliferative retinopathy.
Active/untreated cancer; proliferative retinopathy; pregnancy.
Not FDA approved; Category 2 (2023) then removed April 2026 (grey zone); PCAC review July 23, 2026 (wound healing). WADA prohibited (S2, Tβ4 and derivatives explicitly named).
Subcutaneous/IM. Long tissue residence; systemic distribution.
Source: Fnx Performance Peptide Research Database, a synthesis of the scientific and regulatory literature, not medical advice. For medical questions, consult a qualified physician.