Marketed as a systemic tissue-repair peptide; commonly stacked with BPC-157 in community protocols for tendon, muscle, and ligament recovery.
TB-500 is a synthetic 7-amino-acid peptide (Ac-LKKTETQ) corresponding to residues 17–23 of full-length Thymosin Beta-4 (Tβ4), the 43-amino-acid actin-binding protein found in virtually every cell. Important nomenclature note: the “500” in TB-500 is just a product designator and the “17” you may have seen in marketing is a residue position number, not a length — TB-500 itself is 7 amino acids, not 17.
The actin-binding LKKTETQ motif is preserved in this fragment, but full Tβ4’s C-terminal AGES domain (cardiac repair) and N-terminal Ac-SDKP motif (anti-fibrotic, angiogenic) are not present in TB-500. This means clinical-trial data from full-length Tβ4 (RGN-259, RGN-352, RGN-137) does not transfer cleanly to TB-500 — the fragment lacks the domains those trials relied on.
While BPC-157 tends to work locally (near the injection site), TB-500 is often described in community literature as systemic. There are essentially no peer-reviewed human trials of the TB-500 7-aa fragment specifically; the systemic-distribution and longer-half-life claims trace back to full-Tβ4 work, not TB-500.
Not FDA approved. WADA prohibited under S2.3 (Growth Factors and Growth Factor Modulators). Procedurally removed from FDA 503A Category 2 on April 22, 2026 (nominators withdrew); PCAC reviews scheduled for July 23, 2026 — not currently legally compoundable. Available as a research chemical.
Binds and sequesters G-actin, regulating the actin cytoskeleton — the structural backbone that enables cells to change shape, migrate to injury sites, and rebuild tissue.
Promotes migration of stem cells, endothelial cells, and fibroblasts into damaged tissue. PMID 41490200 frames Tβ4 more broadly as driving angiogenesis, integrin-mediated extracellular matrix remodeling, and fibroblast activation — cell migration is one component of a larger repair program, not the single defining mechanism.
Stimulates new blood vessel formation in injured tissue (full-length Tβ4 in animal models; mechanism: VEGF upregulation and integrin-linked kinase activation per Bock-Marquette 2004 Nature, PMID 15565145). Whether the TB-500 heptapeptide reproduces this effect in vivo has not been established.
Full-length Tβ4 modulates inflammatory cytokines and reduces fibrosis; much of the anti-fibrotic activity is attributed to the N-terminal Ac-SDKP motif, which is not present in TB-500 (Goldstein 2012, PMID 22074294). The fragment may retain partial activity via actin-related effects but should not be assumed to reproduce full-Tβ4 anti-scar performance.
Most TB-500 research is preclinical (animal and in vitro). Human clinical data is limited, but the peptide’s parent molecule (Tβ4) has been studied in Phase 2 wound-healing trials.
| Benefit | Evidence |
|---|---|
| Soft tissue repair | Animal: skeletal-muscle regeneration in dystrophin-deficient mdx mice (full-length Tβ4, Spurney 2010 PLoS ONE, PMID 20126456). Tendon/ligament TB-500-specific evidence is largely extrapolated from full-Tβ4 wound-healing literature and veterinary use reports — peer-reviewed heptapeptide-specific data is sparse. |
| Wound healing | Tβ4 Phase 2 trials in chronic wounds: venous stasis ulcers (Guarnera 2007 Ann NYAS, PMID 17495250; 2010 PMID 20536470) and dermal review (Treadwell 2012 Ann NYAS, PMID 23050815) |
| Cardiac repair | Animal: cardiomyocyte survival and regeneration post-MI via integrin-linked kinase (Bock-Marquette 2004 Nature, PMID 15565145). Phase 2 cardiac efficacy has not been demonstrated in humans for either Tβ4 or TB-500. |
| Dry eye disease | Full-length Tβ4 (RGN-259) ophthalmic Phase 2 RCT, n=72 (Sosne 2015 Cornea, PMID 25826322): corneal staining and symptom improvement vs vehicle. Ophthalmic route only — not relevant to systemic SC TB-500. |
| Flexibility | Anecdotal user reports of improved joint mobility — no clinical trial evidence. (Anti-fibrotic activity in full-length Tβ4 is partly Ac-SDKP-mediated, and SDKP is absent from TB-500.) |
| Hair regrowth | Demonstrated for full-length Tβ4 in mouse skin (Philp 2004 Mech Ageing Dev, PMID 15037013); not independently validated for the TB-500 heptapeptide. |
| Neuroprotection | Animal: may support neurite outgrowth and recovery from traumatic brain injury in rodent models (full-length Tβ4) |
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Start Tracking FreeThese figures reflect community-practice and veterinary-extrapolated dosing conventions. There is no Phase 1 SC dose-finding study of the TB-500 heptapeptide in humans. No regulatory authority has approved TB-500 for any indication or any dose. The full-length Tβ4 Phase 1 (Ruff 2010, PMID 20536472) used IV doses 42–1260 mg — entirely different molecule, route, and PK.
Most users stack TB-500 with BPC-157 for complementary healing: BPC-157 works locally via angiogenesis and FAK-paxillin activation, while TB-500 is conventionally treated as a systemic agent in community use (no human PK confirmation). Typical stack: BPC-157 250–500 mcg daily + TB-500 2–5 mg twice weekly. This combination has no published human clinical trial evidence; both peptides individually lack peer-reviewed Phase 2/3 efficacy data in humans, and the combination has zero published human studies.
TB-500 comes as a lyophilized powder. Standard reconstitution with bacteriostatic water.
5 mg vial + 2 mL BAC water = 2.5 mg/mL
| Dose | Volume | Syringe Units |
|---|---|---|
| 2 mg | 0.80 mL | 80 units |
| 2.5 mg | 1.00 mL | 100 units |
| 5 mg (full vial) | 2.00 mL | 200 units (split between 2 syringes) |
5 mg vial at 2 mg 2×/week lasts ~9 days (1.25 weeks); at 5 mg 2×/week lasts ~3 days
Pre-filled with a typical TB-500 setup. Edit any field — the draw updates live.
Insulin syringe — 100 units = 1 mL
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Beyond the general angiogenesis concern: full-length Tβ4 is overexpressed in colorectal carcinoma, melanoma, pancreatic, hepatocellular, and other malignancies, and overexpression correlates with epithelial-mesenchymal transition (EMT) and metastatic progression in published tumor-biology literature (Tang 2011 Cancer Lett, PMID 21621326; Nemolato 2012 Cancer Biol Ther, PMID 22233609; Cha 2003 J Natl Cancer Inst, PMID 14625258). The mechanism (ILK activation → E-cadherin suppression → EMT) is partly conferred by the actin-binding region preserved in TB-500. Whether the heptapeptide reproduces this risk in vivo is unknown; the preclinical signal is mechanistically direct enough that active or prior malignancy is a strong contraindication, not merely theoretical.
How fast does it work?
Most users notice initial effects (reduced pain, improved mobility) within 1–3 weeks. Full tissue remodeling takes 4–8 weeks.
TB-500 vs. BPC-157?
BPC-157 works locally — best for gut issues and near-site injuries. TB-500 is conventionally treated as a systemic agent in community use (no human PK confirmation). Most users run both together.
Why twice weekly instead of daily?
Community protocols settled on twice-weekly based on empirical results. The commonly cited “30–60 hour half-life” figure is not actually supported by the published metabolism literature — PMIDs 25469748 and 27569051 describe Tβ4 peptides as undergoing rapid proteolytic degradation in liver/kidney microsomes (“short half-life in plasma and rapid elimination”). Human PK for injectable TB-500 has not been well established; twice-weekly dosing likely works because of sustained downstream tissue effects, not a long plasma half-life.
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Start Tracking FreeNo. TB-500 (the synthetic Ac-LKKTETQ heptapeptide, not full-length thymosin beta-4) has never been approved as a drug. It was removed from the FDA Category 2 bulk drug substances list on April 22, 2026 as a procedural matter (nominators withdrew); the FDA Pharmacy Compounding Advisory Committee is scheduled to review it July 23–24, 2026. It is not legally compoundable in the US pending that review and is sold only as a research chemical.
Community-practice loading is approximately 2–2.5 mg twice weekly for 4–6 weeks, followed by 2 mg weekly for maintenance. These figures come from veterinary-extrapolated and community-empirical conventions — there is no Phase 1 subcutaneous dose-finding study of the TB-500 heptapeptide in humans and no regulatory authority has approved any dose for any indication.
The commonly cited "30–60 hour" half-life is NOT supported by published metabolism data. Available in vitro work (Thomas 2016, PMID 27569051; Liang 2024) describes rapid proteolytic cleavage in liver and kidney microsomes — plasma half-life is short. Twice-weekly community dosing likely works (if it works) because of sustained downstream tissue effects of metabolites like Ac-LKKTE, not a long plasma half-life.
A typical reconstitution is 5 mg of TB-500 + 2 mL of bacteriostatic water, yielding a concentration of 2.5 mg/mL. A 2 mg dose draws to 0.80 mL (80 units on a 100-unit insulin syringe). Always swirl gently — do not shake — to avoid denaturing the peptide.
No, and this distinction matters. TB-500 is a synthetic acetylated 7-amino-acid fragment (Ac-LKKTETQ) of the actin-binding region of thymosin beta-4 (Tβ4), a 43-amino-acid naturally occurring peptide. The bulk of published research on healing effects uses full-length Tβ4 (RegeneRx’s RGN-259/352/137 programs), not the TB-500 heptapeptide. Inferences from Tβ4 trials to TB-500 are extrapolation, not direct evidence.
Yes. TB-500 is prohibited at all times under WADA S2.3 (Growth Factors and Growth Factor Modulators). No therapeutic-use exemption is available for athletes in competition or out of competition.
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