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For in vitro laboratory research use only. Not for human consumption, diagnostic, or therapeutic use.
Research Data
Mechanisms of Action
Data presented from peer-reviewed in vitro studies. All findings are laboratory observations only.
TB-500's primary mechanism is sequestration of G-actin monomers, preventing their polymerisation into F-actin filaments. This frees the cellular cytoskeleton to assume the morphology required for rapid directional migration toward injury sites.
TB-500 promotes survival and migration of cardiac progenitor cells in in vitro models of ischaemia, with published data showing significant reduction in apoptosis markers and improved cardiomyocyte viability.
TB-500 upregulates SDF-1/CXCR4 signalling to recruit circulating stem cells to injury sites, while simultaneously promoting new vessel formation via eNOS and VEGF pathways — supporting systemic rather than localised repair.
In vitro scratch assay data showed TB-500-treated myoblast cultures closed the wound gap at 2.8× the rate of untreated controls, with actin sequestration confirmed as the primary mechanism.
Analytical Data
| Specification | Value |
|---|---|
| CAS Number | 77591-33-4 |
| Molecular Formula | C₂₁₂H₃₅₀N₅₆O₇₈S |
| Molecular Weight | 4963.44 g/mol |
| Purity (HPLC) | 99.0% |
| Appearance | White lyophilised powder |
| Solubility | Soluble in water (0.5 mg/mL) |
| Storage | −20°C long-term / 2–8°C short-term |
| Shelf Life | 24 months from production date |
| Research Grade | Yes — For In Vitro Use Only |
What Research Has Shown
In Vitro Scratch Assay & Cardiac Cell Study — Accredited Laboratory
Cell Migration Rate vs. Untreated Control
Comparative Activity Profile
In Vitro Safety Data
TB-500 demonstrates a clean preclinical safety profile across in vitro and rodent models. No significant adverse effects reported at standard research concentrations.
Observed Adverse Indicators
Cytotoxicity at 1 µM
NoneGenotoxic effects
NoneAngiogenic promotion
MinimalInflammatory modulation
None⚠️ Theoretical Concern
TB-500 promotes angiogenesis via actin modulation. Researchers working with angiogenesis-sensitive models should account for this systemic activity.
Researcher Reference
TB-500 is the synthetic form of the 43-amino-acid fragment corresponding to the actin-binding domain of Thymosin Beta-4 (TB4), a naturally occurring protein found in virtually all nucleated human cells. TB-500 isolates the bioactive region responsible for actin sequestration and cell migration activity.
Published in vitro and animal studies document: G-actin sequestration promoting cell motility, upregulation of matrix metalloproteinases (MMPs) supporting ECM remodelling, promotion of angiogenesis via VEGF and eNOS pathways, and stem cell recruitment to injury sites via SDF-1/CXCR4 signalling.
BPC-157 acts primarily via FAK-paxillin pathway activation with site-specific localised repair activity. TB-500 works systemically via actin sequestration and stem cell mobilisation. They are frequently combined in research as complementary mechanisms — BPC-157 for local repair initiation, TB-500 for systemic healing support.
TB-500 shows no cytotoxicity at research concentrations up to 10 µM. No genotoxic or mutagenic effects in published models. The main research consideration is its angiogenic activity, which should be accounted for in angiogenesis-focused experimental designs.
Peer-Reviewed Literature
All citations refer to published peer-reviewed in vitro research. Data presented for scientific reference only. No claims made regarding human therapeutic use.
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