TB-500

Thymosin Beta-4 Fragment | Regenerative System

Access to the catalog is structured — not open by default.

Technical card
  • System
    Regenerative System
  • Type
    Synthetic peptide — 7 amino acids (heptapeptide)
  • Gene (parent protein)
    TMSB4X (Thymosin Beta-4)
  • Sequence
    Ac-LKKTETQ (positions 17–23 of Thymosin Beta-4)
  • PubChem CID
    62707662
  • Formula
    C₃₈H₆₈N₁₀O₁₄
  • Mol. weight
    889.02 Da
  • Form
    Lyophilized vial
  • Purity
    >98% by HPLC
  • Status
    Active
View Research Library

TB-500 Overview

TB-500 is a synthetic heptapeptide corresponding to positions 17–23 of Thymosin Beta-4 — a naturally occurring protein encoded by the TMSB4X gene and found in virtually all nucleated mammalian cells. As a fragment, TB-500 isolates the actin-binding domain (Ac-LKKTETQ) identified as the primary effector region of the parent molecule. It belongs to AXION’s Regenerative System, a research compound cluster organized around signaling pathways associated with tissue integrity, cellular repair, and structural biology.

The parent protein, Thymosin Beta-4, is one of the most extensively studied endogenous peptides in repair biology. Published literature includes landmark studies in Nature (2004 and 2007) documenting cardioprotective and progenitor-mobilizing effects in murine models, as well as Phase II and Phase III clinical programs conducted by RegeneRx Biopharmaceuticals using the full-length recombinant protein. TB-500, as the synthetic fragment, is investigated as a research tool for studying the actin-sequestering mechanisms that underlie cell migration, angiogenesis, and inflammatory modulation in injury contexts.

A critical distinction governs the use of this compound in research: no published clinical trial has been conducted specifically with the TB-500 fragment (Ac-LKKTETQ) in humans. The available clinical evidence — Phases I, II, and III — derives from full-length Thymosin Beta-4. While pharmacological equivalence is mechanistically plausible, it has not been clinically validated. This distinction is documented and must be preserved in all research communications.

TB-500 Research Directions

The published literature on Thymosin Beta-4 and its synthetic fragment TB-500 spans multiple decades and biological contexts. Below is an overview of the principal research areas documented in preclinical studies and — where applicable — in clinical programs using the full-length parent protein.

  • Actin dynamics and cytoskeletal remodeling — G-actin sequestration (1:1 binding to monomeric actin), regulation of G/F-actin equilibrium, and downstream effects on cell morphology and motility in injury models
  • Cell migration in tissue repair contexts — keratinocyte and endothelial cell migration models; lamellipodia formation; extracellular matrix remodeling at wound sites
  • Cardioprotection and progenitor mobilization — ILK-Akt pathway activation in murine infarction models; epicardial progenitor activation and neovascularization (landmark Nature publications, 2004 and 2007) — data from full-length Thymosin Beta-4
  • Corneal healing — murine alkali-injury models demonstrating accelerated re-epithelialization and reduced PMN infiltration; Phase III clinical data for RGN-259 (full-length Thymosin Beta-4) in neurotrophic keratopathy
  • Anti-inflammatory signaling — NF-κB pathway modulation in corneal epithelial cells; reduction of pro-inflammatory cytokine expression (IL-8) in in vitro models
  • Dermal wound closure — multiple rodent models; collagen deposition, organized architecture, and reduced scar formation relative to controls
  • Angiogenesis — endothelial cell migration assays; new vessel formation in ischemic tissue models; interaction with VEGF-related pathways
  • Chronic wound research — Phase II data from RegeneRx for venous and pressure ulcers using topical RGN-137 formulation (full-length Tβ4)
G-actin sequestration

TB-500 binds monomeric G-actin in a 1:1 complex via its Ac-LKKTETQ domain, regulating the dynamic equilibrium between G-actin (globular) and F-actin (filamentous). This modulation directly controls cytoskeletal reorganization, cell morphology, and directed cell migration in injury contexts.

ILK → Akt (PKB)

Thymosin Beta-4 (full-length) activates Integrin-Linked Kinase (ILK), resulting in Akt phosphorylation, promoting cell survival and inhibiting apoptosis — documented in murine cardiac injury models (Bock-Marquette et al., Nature 2004). Specific replication by the TB-500 fragment has not been separately validated.

NF-κB modulation

In corneal epithelial cell models, Thymosin Beta-4 inhibits TNF-α-stimulated NF-κB (p65) nuclear translocation, reducing pro-inflammatory cytokine expression (IL-8) and PMN infiltration. Data from full-length protein; fragment-specific data limited.

Angiogenesis / VEGF axis

Thymosin Beta-4 promotes endothelial cell migration and new vessel formation in vitro and in vivo. VEGF-related pathway interaction proposed but not fully characterized for the TB-500 fragment specifically.

Epicardial progenitor activation

Thymosin Beta-4 (full-length) demonstrated capacity to activate epicardial progenitor cells in adult mice and promote simultaneous myocardial regeneration and neovascularization (Smart et al., Nature 2007). Specific activity of the TB-500 fragment in this context has not been separately validated.

The compound offered by AXION is a research-grade (RUO) synthetic fragment of Thymosin Beta-4. It is not related to, nor a substitute for, any clinical program or approved pharmaceutical product involving the full-length Thymosin Beta-4 protein. No therapeutic claim is made or implied.

TB-500 Quality & Traceability

Every AXION compound is subject to analytical verification before release. Purity and traceability are not marketing attributes — they are part of the integrity of the research itself.

  • Certificate of Analysis

    Available per lot on request.

  • Lot Traceability

    Each vial carries a unique lot number linked to its full analytical record.

  • QR Verification

    QR code on packaging links directly to the COA for that specific lot.

  • HPLC Verified

    >98% purity per lot. Verified by HPLC + Mass Spectrometry.

Learn more about our verification process: Quality & Testing

Related Compounds Compounds in the Regenerative System

All compounds below belong to the same biological system as TB-500. Each is supplied as an RUO research compound.

KLOW Blend

Regenerative System

TB-500 is a synthetic heptapeptide corresponding to positions 17–23 of Thymosin Beta-4 — a naturally occurring protein encoded by the TMSB4X gene and found in virtually all nucleated mammalian cells.…

View molecule

GHK-Cu

Regenerative System

TB-500 is a synthetic heptapeptide corresponding to positions 17–23 of Thymosin Beta-4 — a naturally occurring protein encoded by the TMSB4X gene and found in virtually all nucleated mammalian cells.…

View molecule

BPC + TB Blend

Regenerative System

TB-500 is a synthetic heptapeptide corresponding to positions 17–23 of Thymosin Beta-4 — a naturally occurring protein encoded by the TMSB4X gene and found in virtually all nucleated mammalian cells.…

View molecule

BPC-157

Regenerative System

TB-500 is a synthetic heptapeptide corresponding to positions 17–23 of Thymosin Beta-4 — a naturally occurring protein encoded by the TMSB4X gene and found in virtually all nucleated mammalian cells.…

View molecule

Related Articles - Research Library Explore the Science Behind This System

The Research Library provides in-depth editorial coverage of the mechanisms, evidence, and investigative directions relevant to this system. Each article connects to one or more related compounds in the AXION catalog.

Part of the Regenerative System
Explore the full system — its biological role, signaling pathways, and all related research compounds.
RUO — Research Use Only | Not for Human or Veterinary Use

GHK-Cu (Copper Tripeptide-1) is supplied by AXION Biotech exclusively for research purposes. This compound is not approved by the FDA, ANVISA, or any regulatory agency for human or veterinary use. No therapeutic claims are made or implied. All scientific data referenced on this page derives from preclinical (animal / in vitro) models or limited pilot studies unless explicitly stated otherwise.