TB-500 (Thymosin β4)
An actin-sequestering protein that governs cell migration and wound healing.
Repair & recovery · 7 min read · updated 13 Aug 2026
Research use only. The ranges below are what published studies and community protocols report. They are reference material for laboratory research, not medical advice or a recommendation for human or veterinary use.
The compound
TB-500
View- Type
- Synthetic Peptide
- CAS
- 77591-33-4
- Formula
- C₂₁₂H₃₀₅₀N₆₆O₇₈S
- Mass
- ~4963 Da
At a glance
- Class
- Synthetic thymosin beta-4
- Length
- 43 amino acids
- Molecular weight
- ~4963 Da
- CAS
- 77591-33-4
- Key domain
- LKKTETQ — the actin-binding heptapeptide
- Vial size stocked
- 10 mg
Thymosin β4 is one of the most abundant proteins in mammalian cells and the body's principal G-actin sequestering agent. It binds monomeric actin and holds it in a pool available for rapid polymerisation. Because actin polymerisation is what drives a cell to extend a lamellipodium and move, Tβ4 sits at the mechanical heart of cell migration.
That single function explains the breadth of what has been studied. Wound closure requires keratinocytes to migrate. Angiogenesis requires endothelial cells to migrate. Cardiac repair after ischaemia involves epicardial progenitor migration. In each case Tβ4 is upstream of the movement rather than of the tissue-specific programme.
The naming is a persistent source of confusion. "TB-500" is a market term that sometimes refers to the full 43-residue protein and sometimes to the short LKKTETQ fragment. The material described here is the full-length protein — the molecular weight of ~4963 Da confirms it. The fragment has a molecular weight under 900 Da and different pharmacokinetics.
Mechanism in detail
- Actin sequestration: binds G-actin 1:1 through the LKKTETQ domain, maintaining the unpolymerised pool that cells draw on when they need to move quickly.
- Cell migration: the direct consequence — keratinocytes, endothelial cells, fibroblasts and stem/progenitor populations all migrate more readily.
- Angiogenesis: promotes endothelial tube formation and vessel sprouting, complementing rather than duplicating the VEGFR2-mediated route BPC-157 uses.
- Inflammation: downregulates pro-inflammatory cytokines and NF-κB signalling in several injury models, shifting the balance toward resolution.
- Extracellular matrix: influences laminin-5 and matrix metalloproteinase expression, which affects how repairing tissue is remodelled rather than just how fast it closes.
Why it pairs with BPC-157
The two compounds are almost always discussed together, and the pairing has a real mechanistic logic rather than being a marketing convention. BPC-157 acts predominantly on the vascular supply — angiogenesis, blood flow, the nitric oxide system. Tβ4 acts predominantly on cell motility and the migration of repair cells into the site. One improves the supply line; the other moves the workforce.
The GLOW and KLOW blends stocked here are built on exactly this pairing, with GHK-Cu added for the matrix-remodelling arm and, in KLOW, KPV for inflammation resolution.
Loading and maintenance
Reported TB-500 protocols almost universally use a two-phase structure: a loading phase of four to six weeks at a higher frequency, then a maintenance phase at the same dose but a much longer interval. The rationale offered is the long tissue residence time of the protein — it distributes widely and clears slowly compared to a short peptide, so once tissue levels are established they are maintained with infrequent dosing.
Storage
- Lyophilised: 2–8 °C, or −20 °C for extended storage, protected from light.
- Reconstituted: 2–8 °C, used within about 28 days. Never freeze.
- The infrequent maintenance dosing means a reconstituted vial can easily sit past its window. Date the label.
Cautions
- No controlled human trials for the repair indications. There have been human trials of Tβ4 in dry eye — including completed phase 3 topical eye-drop studies enrolling several hundred participants — and small phase 2 topical wound-care studies, but not at these doses or routes.
- Both the angiogenic and the migration-promoting mechanisms are non-selective. As with BPC-157, existing neoplastic processes are the principal concern.
- Tβ4 is on the WADA prohibited list. This is relevant to any research context involving competitive athletes.
- Reported effects are slow to appear — weeks, not days — which makes self-limiting the block duration important.
References & credit
- 1Goldstein AL, Hannappel E, Kleinman HK — Trends in Molecular Medicine 2005 — Thymosin β4 biology and its actin-sequestering function.
- 2Malinda KM et al., J Invest Dermatol 1999 — Thymosin β4 accelerates wound healing (J Invest Dermatol 1999;113:364–368).
- 3Bock-Marquette I et al., Nature 2004 — Thymosin β4 activates integrin-linked kinase and promotes cardiac cell migration and survival.
This article was written in-house. Where a dose range reflects community practice rather than a published trial, the community references we consulted are credited above and the article says which is which.