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TB-500 / TB4 — Peptide Protocol Wiki reference

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TB-500 (Thymosin Beta-4): Tissue Repair Guide | Peptide Protocol Wiki Skip to main content 🧬 Peptide Protocol Wiki Peptides Side Effects New Learn Directory Tools Blog News About ⌘K ⌘K 🌱 New to Peptides? Start the 7-step beginner guide Peptides Side Effects New Directory Learn Tools Blog News About TB500 📋 Overview 🧬 Molecule 🔄 Similar ⚠️ Side Effects 💉 Dosing 🔬 Research 🚨 Risks 👥 Community 📊 Community Data Home Peptides TB500 Healing & Tissue Repair Immune Support phase2 TB500 Also known as: Thymosin Beta-4, TB-500, Timbetasin, Thymosin Beta 4, Tβ4 Compare with 3 peptide s Research compiled by Peptide Protocol Wiki 📅 Updated February 8, 2026 Citations Verified TL;DR TB500 is a synthetic version of Thymosin Beta-4 (Tβ4), a naturally occurring 43-amino acid peptide present in virtually all human and animal cells. It functions primarily through G-actin sequestration, promoting cell migration, angiogenesis, and tissue repair.

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evidence_reference, safety_reference, dosing_reference, mechanism, contraindication_reference

Findings (69) · awaiting review (32)
safety · pending
TB-500 (Thymosin Beta-4): Tissue Repair Guide | Peptide Protocol Wiki Skip to main content 🧬 Peptide Protocol Wiki Peptides Side Effects New Learn Directory Tools Blog News About ⌘K ⌘K 🌱 New to Peptides?
dosing · pending
Start the 7-step beginner guide Peptides Side Effects New Directory Learn Tools Blog News About TB500 📋 Overview 🧬 Molecule 🔄 Similar ⚠️ Side Effects 💉 Dosing 🔬 Research 🚨 Risks 👥 Community 📊 Community Data Home Peptides TB500 Healing & Tissue Repair Immune Support phase2 TB500 Also known as: Thymosin Beta-4, TB-500, Timbetasin, Thymosin Beta 4, Tβ4 Compare with 3 peptide s Research compiled by Peptide Protocol Wiki 📅 Updated February 8, 2026 Citations Verified TL;DR TB500 is a synthetic version of Thymosin Beta-4 (Tβ4), a naturally occurring 43-amino acid peptide present in virtually all human and animal cells.
mechanism · pending
It functions primarily through G-actin sequestration, promoting cell migration, angiogenesis, and tissue repair.
mechanism · pending
Browse all healing peptides → Table of Contents 📌 TL;DR • Promotes cell migration and tissue repair by sequestering G-actin and modulating cytoskeletal dynamics • Investigated in phase II clinical trials for dermal wound healing and corneal injuries • Demonstrated cardioprotective effects after myocardial infarction in p
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tion # Actin Sequestration and Cytoskeletal Regulation # The most well-characterized function of Thymosin Beta-4 is its role as the principal actin-sequestering protein in eukaryotic cells.
safety · pending
reclinical models • Modulates inflammatory responses by inhibiting NF-kB signaling and reducing pro-inflammatory cytokines • Reduces fibrosis and scar formation through decreased myofibroblast activity Community-Reported Side Effects Anecdotal ?
dosing · pending
📋 Protocol Quick-Reference Tissue repair, wound healing, and injury recovery 💉 Dosing Amount 2-2.5 mg per injection (loading); 750 mcg-2 mg (maintenance) Frequency 2-3 times per week (loading phase); 1-2 times per week (maintenance) Duration Loading: 4-6 weeks; Maintenance: 4-8 weeks; total 8-12 weeks Step-wise Titration (12 weeks) 💊 Administration Route SC Schedule 2-3 times per week (loading phase); 1-2 times per week (maintenance) Timing No specific time of day required; consistency preferred ✓ Rotate injection sites 📅 Cycle Duration Loading: 4-6 weeks; Maintenance: 4-8 weeks; total 8-12 weeks Repeatable Yes Loading phase followed by maintenance Preparation & Storage Diluent: Bacteriostatic water Storage: Store lyophilized (unreconstituted) vials at -20C for long-term storage or 2-8C (refrigerator) for short-term.
contraindication · pending
fects blood cell migration CMP with liver enzymes When: Baseline Why: Liver and kidney function baseline CRP or ESR When: Baseline Why: Baseline inflammation markers to track healing response Ferritin When: Baseline Why: Iron status if recovering from surgery or injury CBC When: 4 weeks Why: Monitor blood cell parameters CRP When: 4 weeks Why: Track inflammatory marker improvement with tissue healing 💡 Key Considerations → Contraindication: Avoid with active cancer or recent cancer history (promotes angiogenesis and cell migration); not for use in pregnancy Subscribe to unlock this content Get weekly peptide research summaries, new study alerts, and protocol updates — free.
outcome · pending
Restore access No thanks, continue reading Related Reading Peptide BPC-157 body protection compound peptide Peptide GHK-Cu copper peptide for tissue repair Article The Complete Guide to Peptide Stacks: Popular Combinations Explained How TB500 works at the cellular level Overview of TB500 benefits and applications Scientific Details Molecular Formula C212H350N56O78S Molecular Weight 4963.44 Da CAS Number 77591-33-4 Sequence Ac-SDKPDMAEIEKFDKSKLKKTETQEKNPLPSKETIEQEKQAGES What is TB500?
mechanism · pending
The peptide is encoded by the TMSB4X gene in humans and is expressed in virtually every cell type, with particularly high concentrations found in platelets, macrophages, and polymorphonuclear leukocytes.
mechanism · pending
This actin-buffering capacity is essential for the regulation of the cytoskeleton, which in turn governs cell shape, motility, and division.
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Within cells, Thymosin Beta-4 maintains a large reservoir of unpolymerized actin that can be rapidly mobilized when the cell needs to migrate, divide, or change shape in response to extracellular signals.
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When released from damaged cells or secreted by platelets at sites of injury, it acts as a paracrine signaling molecule that promotes wound healing, angiogenesis, and anti-inflammatory responses.
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Mechanism of Ac
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When a cell receives a migration or proliferation signal, signaling pathways trigger the release of G-actin from the Tβ4 complex, allowing profilin to facilitate actin polymerization at the leading edge of the cell.
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Cell Migration and Angiogenesis # TB500 promotes the migration of multiple cell types critical to tissue repair, including endothelial cells, keratinocytes, and cardiac progenitor cells.
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In wound healing models, topical or systemic administration of Thymosin Beta-4 increased keratinocyte migration 2- to 3-fold over controls in Boyden chamber assays (Goldstein AL et al., Expert Opin Biol Ther 2012; PMID 22074294) 1 .
mechanism · pending
The pro-migratory effect is mediated through activation of integrin-linked kinase (ILK), which in turn activates the Akt/protein kinase B survival pathway 1 .
mechanism · pending
The peptide promotes endothelial cell differentiation, tubule formation, and sprouting angiogenesis in both in vitro and in vivo models 1 .
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Anti-Inflammatory and Anti-Fibrotic Activity # Thymosin Beta-4 exerts anti-inflammatory effects through multiple mechanisms.
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It inhibits TNF-alpha-stimulated NF-kB binding activity through its interaction with PINCH-1 and ILK signaling partners, independently of its actin-sequestering function.
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In corneal injury models, Thymosin Beta-4 treatment reduced polymorphonuclear leukocyte infiltration and decreased mRNA transcript levels of interleukin-1 beta, MIP-1alpha, MIP-2, and MCP-1 by several fold compared to controls.
outcome · pending
In dermal wound models, Thymosin Beta-4 reduces the number of myofibroblasts in healing wounds, which results in decreased scar formation.
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This anti-fibrotic effect has been observed in cardiac tissue as well, where Tβ4 treatment reduced fibrosis following myocardial infarction in animal models.
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Cardioprotective Mechanisms # Thymosin Beta-4 has demonstrated remarkable cardioprotective properties in preclinical models.
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In mouse models of coronary artery ligation, systemic administration of Tβ4 resulted in upregulation of ILK and Akt phosphorylation in the heart, enhanced early myocyte survival, and significantly improved cardiac function.
mechanism · pending
This regenerative capacity represents a novel mechanism for cardiac repair that is distinct from conventional stem cell therapies.
outcome · pending
In the foundational 1999 study by Malinda and colleagues (PMID 10469335 [animal model]) 2 , topical or intraperitoneal administration of Tβ4 increased re-epithelialization by 42% over saline controls at 4 days and by 61% at 7 days post-wounding in a rat full-thickness wound model 2 .
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Treated wounds also showed increased collagen deposition, enhanced angiogenesis, and accelerated wound contraction 2 .
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The peptide demonstrated efficacy across multiple wound types, including diabetic wounds, aged-animal wounds, and steroid-impaired healing models 3 .
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Studies by Sosne and colleagues demonstrated that topical Tβ4 accelerated corneal re-epithelialization, decreased inflammation, and reduced polymorphonuclear leukocyte infiltration after alkali injury in mouse models.
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In a randomized, double-blind phase II trial (NCT01387347), RGN-259 demonstrated a 35.1% reduction in ocular discomfort and a 59.1% reduction in total corneal fluorescein staining compared to vehicle control.
outcome · pending
Following coronary artery ligation in mice, systemic Tβ4 administration improved left ventricular function, reduced infarct size, and decreased cardiac fibrosi
mechanism · pending
These effects were mediated through ILK-Akt survival signaling and mobilization of epicardial progenitor cells 1 .
safety · pending
Clinical translation of these findings has been slower, with early-phase human studies focusing on safety and tolerability.
dosing · pending
A first-in-human Phase I trial in healthy Chinese volunteers reported no dose-limiting toxicities or serious adverse events (Wang X et al., 2021; PMID 34346165) 5 .
dosing · pending
Earlier Allan-led work reported tolerability at IV doses up to 1260 mg with no dose-limiting toxicities.
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Pharmacokinetics # Following intravenous administration in healthy volunteers, Thymosin Beta-4 exhibited dose-proportional pharmacokinetics across the tested range of 42 to 1260 mg (Wang X et al., 2021; PMID 34346165) 5 .
dosing · pending
The half-life increased with increasing dose, suggesting non-linear elimination kinetics at higher concentrations 5 .
outcome · pending
Tβ4 is naturally present in serum at concentrations of approximately 12-18 ng/mL in healthy individuals, and endogenous levels increase at sites of injury due to platelet degranulation and cellular release.
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