The Compound Report is an educational resource. Nothing on this site constitutes medical advice or encourages personal use of any compound. Always consult a qualified healthcare provider.
Educational reference only. Nothing on this page constitutes medical advice or encourages personal use of this compound. Always consult a qualified healthcare provider before any decision involving your health.
TB-500 · Thymosin Beta-4 Fragment · Ac-LKKTETQ
Effect demonstrated in multiple animal studies; human data sparse or extrapolated. Grades summarize evidence quality, not whether a compound is appropriate, legal, or risk-free.
Same compound, route-specific context. Switch forms instead of opening separate pages.
The default community route. Distributes systemically — unlike BPC-157, there is no localized perilesional injection advantage documented for TB-500, and no evidence tha…
No route-matched protocol rows were parsed for this form; use the route notes and full dosing chapter before comparing options.
Open the full report at the dosing chapter for protocol rows, cycle context, and administration notes.
43 amino acids, ~4,963 Da. This is what was used in Phase 1 human safety trials, Phase 2 wound healing trials (pressure ulcers, stasis ulcers), Phase 2 cardiac trials, and Phase 3 dry eye trials. When research says 'Thymosin Beta-4 showed X in humans,' they mean this compound. It is more expensive to synthesize and less stable than TB-500, but it contains all functional domains.
The default community route. Distributes systemically — unlike BPC-157, there is no localized perilesional injection advantage documented for TB-500, and no evidence that injection near the injury produces superior outcomes versus abdominal SubQ. Inject anywhere; the peptide distributes systemically and is drawn to areas of active inflammation and injury. The loading/maintenance structure has no published pharmacokinetic basis — it is community-derived, adapted from general principles of peptide saturation protocols.
The route with the most human evidence. Not an established route for injectable TB-500. Full TB4 topical gels were used in RegeneRx wound trials.
TB-500 is a compound in a genuinely unusual position: the animal model evidence is consistent and replicated, the full-protein human data is more advanced than almost any other peptide in this reference, and the community has years of practical experience with it — yet the compound the community injects may not directly produce the effects attributed to it, and the human data was generated with a structurally different molecule.
The central tension resolved: TB-500 was synthesized to mimic the actin-binding function of full Thymosin Beta-4. What it cannot mimic are the other functional domains of the full protein — the ILK activation, the Ac-SDKP generation, the broader structural interactions. And now a 2024 study suggests TB-500 itself may not be the active form at all: its metabolite Ac-LKKTE shows the wound-healing activity that TB-500 did not demonstrate in vitro. The community injects TB-500; the body may convert it to Ac-LKKTE; the clinical data was generated with a 43-amino acid protein none of these things are. This is not a reason to dismiss TB-500 — it is a reason to understand it accurately.
The strongest argument for TB-500: the mechanistic foundation is real (actin sequestration, VEGF angiogenesis), the full-protein human safety data is favorable (84 healthy volunteers, IV administration, no serious adverse events), the animal model evidence for musculoskeletal healing is replicated across multiple independent groups, and years of community use have not produced a serious adverse event signal. If TB-500 works as a prodrug — converting to an active metabolite that performs the same functions — the practical outcome may be similar to what the community expects, even if the mechanism is more indirect than assumed.
The strongest argument for caution: the community injects a compound that has never been tested in a controlled human trial for the application they use it for (musculoskeletal repair). The most mechanistically significant finding (cardiac progenitor activation) may not apply to the fragment. The loading/maintenance protocols are empirical, not PK-validated. And the 2024 metabolite finding introduces genuine uncertainty about dose-response and inter-individual variability. This is not a compound that has been clinically validated in the way its community use implies.
The default page keeps the decision layer visible first: summary, routes, evidence, and risks. Open the full report for mechanisms, chapter sections, citations, updates, and print/share controls.
The Fragment Every Community Vendor Sells as ‘TB-500.’ The Actin-Sequestering Domain of Thymosin Beta-4. Why the Full 43-AA Protein Is Used in Clinical Trials While the Community Uses a 7-AA Fragment. The Phase 2b Cardiac Trial That Used Full Tβ4. Whether the Fragment Recapitulates the Parent Protein’s Pharmacology. What Actin Sequestration Actually Does in Tissue Repair. Polaris and Limitless Community Formats.
NOTE: This chapter covers GHK as a free tripeptide — its endogenous biology, copper-carrier function, and primary topical cosmetic applications. The systemic, injectable, and regenerative applications of the copper-chelated complex are covered in the GHK-Cu chapter, which should be read alongside or before this chapter. Plasma Levels: 200 ng/mL at Age 20, Declining to 80 ng/mL by Age 60. The Connectivity Map and 4,000 Genes. Loren Pickart (1938–2023). The Copper Switch.
The Body's Own Repair Signal — And the Evidence Gap Between What It Does and How People Use It