TB-500 is a seven-residue fragment of a forty-three-residue protein — and that gap is the whole story.

What TB-500 actually is

TB-500 is the synthetic, N-acetylated heptapeptide Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln — seven residues, molecular weight approximately 889 Da. It corresponds to residues 17 through 23 of thymosin beta-4 (Tβ4), the body's principal actin-sequestering protein, and it carries that protein's actin-binding motif. That is the entire molecule. It is not a blend, not a stack, and not the full protein.

Here is the part most pages skip. The overwhelming majority of the efficacy research attached to the name TB-500 was not run on the 889 Da fragment. It was run on full-length thymosin beta-4 — a 43-residue protein of about 4,963 Da, roughly five and a half times the mass ^[5]. A seven-residue piece is being asked to stand in for the whole protein it came from. Whether the fragment reproduces the protein's effects at the doses used in peptide research has not been established in controlled human trials ^[11].

This site treats that distinction as load-bearing, not as a footnote. Every finding below is labeled by what was actually administered: the 7-mer fragment, or the full-length protein. Where the data is on the protein, we say so.

TB-500 Peptide: The Ac-LKKTETQ Fragment of Thymosin Beta-4

As a research peptide, the TB-500 peptide is supplied as a lyophilized (freeze-dried) powder and reconstituted in sterile or bacteriostatic water for laboratory use. It is a short acetylated peptide, chemically more robust than the long parent protein but still subject to proteolysis and freeze-thaw degradation ^[5].

The sequence matters because LKKTETQ is the WH2-type actin-interacting region of the beta-thymosins — the segment through which thymosin beta-4 grips monomeric actin. X-ray crystallography of a gelsolin-domain-1–Tβ4 hybrid bound to actin, solved to 2 Å, showed the parent protein forms a 1:1 complex with G-actin and sequesters the monomer by capping both ends, preventing it from polymerizing ^[1].

One caution the literature insists on: Ac-SDKP, an N-terminal cleavage product of thymosin beta-4 with its own anti-fibrotic and angiogenic activity, comes from the opposite end of the protein and is not produced by the C-terminal-region TB-500 fragment ^[5]. Effects attributed to Ac-SDKP do not transfer to the 7-mer.

What the research record shows

The strongest results are reproducible and quantitative — and almost all of them are on the full-length protein. In a rat full-thickness wound model, topical or intraperitoneal thymosin beta-4 raised re-epithelialization by 42% at four days and up to 61% at seven days versus saline, with as little as 10 pg stimulating keratinocyte migration two- to three-fold ^[3]. In mice, thymosin beta-4 activated the PINCH–ILK–Akt survival pathway and, after coronary artery ligation, improved cardiac function ^[2].

The honest gaps are just as concrete. There are zero completed controlled clinical trials of the TB-500 heptapeptide for any indication ^[11]. The only human data is on full-length Tβ4: a randomized Phase 1 intravenous safety study, well tolerated to 1,260 mg ^[6]. And a recognized safety signal sits over the whole class — thymosin beta-4 is overexpressed in several cancers and implicated in tumor angiogenesis ^[5].

For the regulatory picture — FDA 503A status, the September 2023 Category 2 placement, and where compounded access stands — see the dedicated TB-500 legal status page.

Why the scale gap matters, in plain numbers

Two numbers carry this whole site: 7 and 43. TB-500 is 7 residues, about 889 Da, with the molecular formula C38H68N10O14. Thymosin beta-4 is 43 residues, about 4,963 Da. The fragment is a single segment — residues 17 to 23 — clipped out of a protein roughly five and a half times its mass ^[5].

That is not a pedantic distinction. A protein's behavior depends on its whole structure, and a short motif lifted out of context does not automatically inherit the parent's full activity. The literature is explicit that it is not established whether the isolated 7-mer reproduces thymosin beta-4's effects at the doses used in peptide research ^[5]. Marketing that quotes the protein's animal results under the fragment's name is borrowing evidence the fragment has not earned.

There is also a concrete mechanistic example of where the two diverge. Full-length thymosin beta-4 can be cleaved at its N-terminus to release Ac-SDKP, a small peptide with its own anti-fibrotic and angiogenic activity. TB-500 comes from the protein's C-terminal region and does not produce Ac-SDKP ^[5]. So any benefit attributed to that cleavage product belongs to the protein, not to the fragment — a clean illustration of why "part for whole" fails here.

How to read this digest

Every page here follows three habits. First, the headline finding comes first and the attribution follows — a study is named after the number it produced, not before. Second, each finding is tagged by what was actually administered: the 889 Da fragment, or the 4,963 Da full-length protein. Third, the misses are surfaced as plainly as the hits, because a record that only reports successes is not a record.

The pages split by intent. The research page covers mechanism, the wound and stroke and muscle data, and the human-trial situation. The TB-500 cardiac research page handles the cardiac and angiogenesis literature — the part of the story where thymosin beta-4 reportedly reawakens an embryonic program in the adult heart. The dosage page reads what investigators administered, and states plainly that no validated human half-life exists for the fragment. The TB-500 legal status page reads the FDA 503A record and the WADA standing.

What this site is not: a clinic, a vendor, or a prescription. Nothing here is dosing advice, medical advice, or legal advice, and nothing is for sale. It is an editorial digest of published research and the public regulatory record, with every quantitative claim tied to a numbered source on the references page.

Frequently asked, answered up front

What is TB-500?

TB-500 is the synthetic, N-acetylated heptapeptide Ac-LKKTETQ — residues 17 to 23 of thymosin beta-4 and its actin-binding motif. It is sold for research and veterinary use. Most published efficacy data are on the full-length thymosin beta-4 protein, not the 7-mer fragment, so claims for the fragment in humans are not established ^[5][11].

What does TB-500 stand for?

TB refers to thymosin beta (β). TB-500 is a research and veterinary designation for the synthetic Ac-LKKTETQ fragment of thymosin beta-4; it is not an abbreviation with an official chemical expansion beyond that thymosin-beta-4 origin ^[5]. The veterinary literature also uses the related designation TB1000.

What is TB-500 used for in research?

Research interest centers on tissue repair, wound healing, cardiac and neurological recovery, angiogenesis, and anti-fibrotic effects — largely from full-length thymosin beta-4 animal models ^[5]. A rat wound study reported up to 61% greater re-epithelialization at seven days ^[3]. The fragment's human efficacy is not established ^[11].