Tβ4 is a 43-amino acid peptide involved in actin regulation, wound healing, and tissue repair. Its active fragments (1–4, 1–15, 40–43) target fibrosis, oxidative stress, and organ-specific regeneration, especially in cardiac and fibrotic diseases.
Thymosin Beta-4
Also known as: Tβ4(1–4) / Ac-SDKP; Tβ4(1–15); Tβ4(40–43) / AGES
Overview
Benefits
- Reduces fibrosis and inflammation
- Protects cardiac tissue
- Prevents oxidative damage
- Improves vascular and mitochondrial function
- Promotes tissue regeneration
Consider This Peptide If You Want To
- Reduce fibrosis, inflammation, or oxidative damage
- Recover from organ or tissue injury
Dosage & Administration
Dosage Guidelines
Recommended Dosage
• Amount:300 mcg
• Frequency:daily
• Duration:2 weeks
• Rest Period:6 weeks
• Time of Day:morning
• Ingestion:subcutaneous
Do not co-administer with full-length Tβ4; use specific fragments based on therapeutic target
Administration Routes:OralSubcutaneous
Research Findings on Dosage:
Oral Administration (Fragments 1--4 & 1--15):
• Commonly Reported Dosage: 500 mcg per capsule, taken twice daily
• Duration: 4-12 weeks, depending on individual goals
Subcutaneous Injection (Fragments 1--15 & 40--43):
• Commonly Reported Dosage: 300 mcg to 1 g daily or 2.5 mg every other day (1--15); 100--500 mcg per injection (40--43)
• Duration: 2--4 week cycles for 40--43; up to 3 months for 1--15 followed by a 6-week break
Administration Notes:
• Do not co-administer with full-length Tβ4 simultaneously due to receptor competition
• Commonly stacked with BPC-157, Epitalon, or mitochondrial peptides for synergistic tissue repair
• Demonstrates oral bioavailability in animal models (Ac-SDKP)
Mechanism of Action
Mechanism of Action
How this peptide works in the body
Suppression of TGF-β1 Signaling and Fibrosis
Ac-SDKP binds to and inhibits the TGF-β1 receptor complex, reducing downstream phosphorylation of SMAD2 and SMAD3. This decreases transcription of pro-fibrotic genes (e.g., COL1A1, fibronectin, α-SMA), limiting myofibroblast activation and extracellular matrix deposition.
By preventing IκB degradation, Ac-SDKP reduces NF-κB nuclear translocation. This downregulates expression of inflammatory cytokines like TNF-α, IL-1β, and IL-6, lowering inflammation in fibrotic tissues.
Immune Cell Modulation
Endothelial Function Preservation
Ac-SDKP enhances endothelial nitric oxide synthase (eNOS) expression, supporting nitric oxide (NO) production, which improves microvascular perfusion and capillary density.
Inhibition of Intrinsic Apoptosis Pathways
Tβ4(1--15) modulates mitochondrial integrity by increasing Bcl-2 expression and reducing Bax, preventing mitochondrial outer membrane permeabilization and cytochrome c release. This reduces caspase-9 and caspase-3 activation.
Stimulates expression of antioxidant enzymes: superoxide dismutase (SOD), catalase, and glutathione peroxidase. Also boosts intracellular GSH:GSSG ratio to neutralize ROS.
Cytoskeletal and Membrane Stabilization
Preserves actin dynamics, stabilizes focal adhesions, and reduces lipid peroxidation during oxidative stress, supporting tissue integrity during repair.
Activates PI3K/Akt and ERK1/2 pathways, promoting stem cell proliferation and supporting regeneration in injured tissue environments.
Fragment 40--43 (AGES)
Attenuates TGF-β1-mediated fibroblast-to-myofibroblast transition. Reduces collagen I synthesis and α-SMA expression, limiting scar formation after ischemic injury.
Matrix Metalloproteinase Modulation
Promotion of Cardiomyocyte Survival
Enhances PI3K/Akt signaling in myocytes. Upregulates Bcl-2, downregulates Bax, mitigating apoptosis during ischemia/reperfusion injury.
Suppresses TNF-α and IL-6 production in infarct border zones. Supports anti-inflammatory cytokine balance and post-MI tissue healing.
Activation of Epicardial-Derived Progenitor Cells
Stimulates integrin-linked kinase (ILK) and focal adhesion kinase (FAK), recruiting EPDCs for neovascularization and cardiac regeneration.
Attenuates TGF-β1-mediated fibroblast-to-myofibroblast transition. Reduces collagen I synthesis and α-SMA expression, limiting scar formation after ischemic injury.
Matrix Metalloproteinase Modulation
Inhibits MMP-2/9 overactivity and maintains TIMP-1 equilibrium, reducing pathological ECM remodeling and preserving cardiac structure.
Promotion of Cardiomyocyte Survival
Enhances PI3K/Akt signaling in myocytes. Upregulates Bcl-2, downregulates Bax, mitigating apoptosis during ischemia/reperfusion injury.
Reduction of Pro-Inflammatory Cytokines
Suppresses TNF-α and IL-6 production in infarct border zones. Supports anti-inflammatory cytokine balance and post-MI tissue healing.
Activation of Epicardial-Derived Progenitor Cells
Stimulates integrin-linked kinase (ILK) and focal adhesion kinase (FAK), recruiting EPDCs for neovascularization and cardiac regeneration.
Consider Stacking With
- BPC-157
- Epitalon
- Thymosin Alpha-1
- MOTS-c
- SS-31
- FOXO4-DRI
Side Effects & Cautions
Common Side Effects
- Mild redness or irritation
Cautions
- Avoid in active cancer
- Avoid co-use with full-length Tβ4
- Caution in mast cell disorders
Rare Side Effects
- Allergic reactions (rare)
Research & References
Research Highlights
Ac-SDKP demonstrated significant reduction in organ fibrosis in multiple preclinical models
AGES fragment improves cardiac remodeling and EPDC activation in myocardial infarction models
Rhaleb NE et al. Am J Physiol Heart Circ Physiol. 2001
Yang F et al. Hypertension. 2004
Pokharel S et al. Cardiovasc Res. 2003
Bock-Marquette I et al. Nature. 2004
Smart N et al. Nature. 2007
Saxena A et al. Ann N Y Acad Sci. 2010
Bock-Marquette I et al. Nature. 2004
Smart N et al. Nature. 2007
Saxena A et al. Ann N Y Acad Sci. 2010