Synthetic Thymosin β4 fragment — Studied for actin sequestration, VEGF-mediated angiogenesis, stem-cell mobilization, and accelerated wound healing in musculoskeletal and dermal tissue research models.
TB-500 is the synthetic version of the 43-amino-acid Thymosin β4 (Tβ4) peptide, naturally produced in the thymus and many other cell types. It functions through three principal pathways: cytoskeletal regulation via G-actin sequestration, vascular remodelling through VEGF upregulation, and pluripotent cell mobilization to sites of injury.
The conserved central region (17-LKKTETQ-23) binds G-actin with high affinity (Kd ≈ 0.5 µM), sequestering monomers from the polymerising F-actin pool and remodelling cytoskeletal architecture in motile cells.
Tβ4 induces VEGF-A and VEGF-C transcription via HIF-1α stabilisation under hypoxic injury conditions. Downstream endothelial proliferation and tube formation are measurable in Matrigel angiogenesis assays within 48–72h.
Tβ4 inhibits NF-κB pro-inflammatory signalling and upregulates anti-apoptotic Bcl-2 expression. Cardiac ischaemia-reperfusion models show ~40% infarct-size reduction with sustained dosing in murine studies.
Rodent models of Achilles tendon laceration and skeletal muscle injury show that systemic Tβ4 administration accelerates fibre regeneration, increases tensile strength of healing tendons, and reduces collagen-III to collagen-I ratios — a profile associated with functional rather than scar repair. Effects are dose-dependent over 2–8 mg/kg ranges in mice.
Refs: Philp D et al., Mech Ageing Dev (2007); Goldstein AL et al., FASEB J (2012)
In mouse and porcine cardiac infarct models, Tβ4 administration within 24h of ischaemia reduces infarct volume by 25–45% and improves left ventricular ejection fraction. Mechanistically, this involves epicardial progenitor cell mobilization and angiogenic remodelling of the peri-infarct border zone.
Refs: Bock-Marquette I et al., Nature (2004); Smart N et al., Nature (2011)
Each batch is independently tested by a third-party ISO-accredited laboratory prior to release. The analysis below reflects Batch AV-2025-TB4-041, tested 25 February 2025.
| Test Parameter | Method | Specification | Result | Status |
|---|---|---|---|---|
| Identity (sequence) | ESI-MS / MS-MS | Matches theoretical m/z | Confirmed (4963.5 Da) | PASS |
| Purity (HPLC) | RP-HPLC C18, 210nm | ≥98.0% | 99.2% | PASS |
| Water content | Karl Fischer | ≤8.0% | 6.1% | PASS |
| Heavy metals | ICP-MS (EPA 200.8) | ≤10 ppm | <2 ppm | PASS |
| Bacterial endotoxins | LAL chromogenic | ≤10 EU/mg | <1 EU/mg | PASS |
| Form | Temperature | Duration |
|---|---|---|
| Lyophilised powder | −20°C (preferred) or 2–8°C | 24 months / 12 months |
| Reconstituted (BAC water) | 2–8°C | ≤28 days |
| Reconstituted (saline) | 2–8°C | ≤7 days |
Work under laminar flow. Wipe vial septa with 70% IPA and allow to dry before penetration.
For a 5 mg vial, add 2.5 mL bacteriostatic water → 2 mg/mL stock. Inject slowly along the inner vial wall, never directly onto the lyophilised cake.
Gently swirl until clear — do not vortex or shake (mechanical agitation may damage tertiary structure of the 43-AA chain).
Refrigerate at 2–8°C. Avoid freeze-thaw cycles. Aliquot for repeated use if necessary.
TB-500 is the synthetic version corresponding to the 43-amino-acid fragment (or sometimes the full 43-AA Tβ4 itself, depending on supplier definition). Endogenous Thymosin β4 is naturally produced by the thymus and most cell types. The synthetic TB-500 retains the central LKKTETQ actin-binding domain and exhibits comparable biological activity in preclinical models.
Both are studied for tissue repair but operate through distinct mechanisms. BPC-157 (15 AA) acts primarily on the VEGFR2/NO pathway and is associated with rapid local healing of tendons, ligaments, and GI mucosa. TB-500 (43 AA) acts via systemic G-actin sequestration and stem-cell mobilization, with slower onset but broader distribution including cardiac and dermal beds. Some research protocols combine the two for synergistic effects.
TB-500 is classified under WADA Prohibited List class S2 (Peptide Hormones, Growth Factors, Related Substances) because of its potential to accelerate musculoskeletal recovery and enhance athletic performance through angiogenic and tissue-repair mechanisms. It is banned in human sport at all times (in and out of competition) and also in equine sport.
Published preclinical studies typically employ a loading phase of 4–8 mg weekly (split doses) for 4–6 weeks, followed by a maintenance dose of 2 mg every 1–2 weeks. The long extravascular half-life (~24h) and slow tissue redistribution permit infrequent administration. Dosing should always be specified by the relevant research protocol and IACUC approval.
Independently verified by third-party ISO-accredited laboratory. COA available on request.
View TB-500 in Store → Reconstitution Protocol Guide