TB4-Frag
Also known as: Thymosin Beta-4 Fragment · Ac-SDKP · N-acetyl-seryl-aspartyl-lysyl-proline · TB4 Fragment 17-23
Ac-SDKP (TB4-Frag) is produced in vivo from Thymosin Beta-4 and circulates as an independent endogenous peptide. Its primary mechanisms are: (1) Anti-fibrotic — inhibits differentiation of fibroblasts into myofibroblasts (the key step in pathological fibrosis); reduces TGF-β1-driven collagen synthesis and...
What It Is
Ac-SDKP (TB4-Frag) is produced in vivo from Thymosin Beta-4 and circulates as an independent endogenous peptide. Its primary mechanisms are: (1) Anti-fibrotic — inhibits differentiation of fibroblasts into myofibroblasts (the key step in pathological fibrosis); reduces TGF-β1-driven collagen synthesis and collagen deposition in cardiac, renal, and pulmonary fibrosis. (2) Cardioprotective — inhibits cardiomyocyte apoptosis after ischemia; promotes cardiac angiogenesis via VEGF. (3) Anti-inflammatory — inhibits NF-κB activation and reduces macrophage-driven inflammation. (4) Hematopoietic — ACE (angiotensin-converting enzyme) is the enzyme that inactivates Ac-SDKP; ACE inhibitors (lisinopril, enalapril) dramatically raise Ac-SDKP levels, which is thought to partly explain their cardioprotective effects beyond blood pressure lowering. This makes Ac-SDKP distinct from TB-500 and BPC-157 — it is specifically anti-fibrotic rather than primarily pro-regenerative.
Supplies Needed
Reconstitution
Subcutaneous injection
Sterilization
Storage
Store at -20°C; stable 2+ years
Refrigerate at 2–8°C; use within 30 days
This information is provided for educational and research purposes only. Not approved for human consumption by the FDA or any regulatory body. Always consult a qualified medical professional.
Dosing Protocols
Timing: Morning. Used for anti-fibrotic and cardiac/renal protective purposes. Very limited human data u2014 dose extrapolated from animal research.
↓ Apply these values to the reconstitution calculatorTiming: Morning. Stack with BPC-157 for complementary healing (BPC-157 repairs; TB4-Frag prevents fibrotic scarring)
↓ Apply these values to the reconstitution calculatorTiming: Morning. Advanced fibrosis prevention protocol; combine with BPC-157 and TB-500 for comprehensive tissue protection
↓ Apply these values to the reconstitution calculatorWeekly Timeline
| Week | Expected Effects |
|---|---|
| Week 1 | Anti-inflammatory effects beginning; reduced fibrotic signaling in chronic conditions |
| Week 2 | Improved tissue quality in injury recovery; reduced scar tissue formation |
| Week 4 | Anti-fibrotic benefits accumulating; improved cardiac/renal markers in affected individuals |
| Week 8 | Sustained fibrosis prevention; comprehensive tissue repair without pathological scarring; improved cardiac function markers |
Reconstitution Calculator
1 unit on U-100 syringe = 0.01 mL · Always label your vial after reconstitution
Injection Technique & Reconstitution
- Wipe vial stopper with alcohol swab
- Draw 2 mL bacteriostatic water
- Inject slowly along vial wall
- Gently swirl until dissolved
- Refrigerate at 2u20138u00b0C
Use our free peptide calculator to get the exact syringe units for your vial size and dose.
Mechanism of Action
Ac-SDKP (TB4-Frag) is produced in vivo from Thymosin Beta-4 and circulates as an independent endogenous peptide. Its primary mechanisms are: (1) Anti-fibrotic — inhibits differentiation of fibroblasts into myofibroblasts (the key step in pathological fibrosis); reduces TGF-β1-driven collagen synthesis and collagen deposition in cardiac, renal, and pulmonary fibrosis. (2) Cardioprotective — inhibits cardiomyocyte apoptosis after ischemia; promotes cardiac angiogenesis via VEGF. (3) Anti-inflammatory — inhibits NF-κB activation and reduces macrophage-driven inflammation. (4) Hematopoietic — ACE (angiotensin-converting enzyme) is the enzyme that inactivates Ac-SDKP; ACE inhibitors (lisinopril, enalapril) dramatically raise Ac-SDKP levels, which is thought to partly explain their cardioprotective effects beyond blood pressure lowering. This makes Ac-SDKP distinct from TB-500 and BPC-157 — it is specifically anti-fibrotic rather than primarily pro-regenerative.
Key Research Papers
Demonstrated Ac-SDKP directly inhibited TGF-u03b21-driven cardiac fibroblast differentiation into myofibroblasts and reduced collagen synthesis, providing a cellular mechanism for its anti-fibrotic effects.
View on PubMed →Identified the enzymatic pathway by which endogenous Ac-SDKP is generated from Thymosin Beta-4 and how ACE inhibitors elevate its circulating levels.
View on PubMed →Stacks Well With
BPC-157 accelerates tissue repair; TB4-Frag prevents pathological fibrotic scarring during that repair u2014 ideal combination for injury recovery without excessive scar tissue
TB-500 provides systemic angiogenesis and full-length TB4 effects; TB4-Frag provides specific anti-fibrotic action u2014 together cover the full Thymosin Beta-4 biological spectrum
SS-31 protects mitochondria in cardiac tissue; TB4-Frag prevents cardiac fibrosis u2014 comprehensive cardiac protection and repair protocol
Frequently Asked Questions
TB-500 is the synthetic form of Thymosin Beta-4 fragment (aa 17-23 u2014 the actin-binding sequence), primarily known for systemic angiogenesis, cell migration, and wound healing. TB4-Frag (Ac-SDKP) is the N-terminal tetrapeptide of TB4, specifically anti-fibrotic and cardioprotective. They come from the same parent protein (Thymosin Beta-4) but have distinct biological roles.
Angiotensin-converting enzyme (ACE) is the primary enzyme responsible for degrading Ac-SDKP in the body. When ACE is inhibited (by drugs like lisinopril), Ac-SDKP accumulates u2014 raising its plasma levels 4u20135 fold. This anti-fibrotic effect of elevated Ac-SDKP is thought to contribute to the cardioprotective effects of ACE inhibitors beyond blood pressure control.
Animal studies show Ac-SDKP can both prevent and partially reverse established cardiac, renal, and pulmonary fibrosis. It reduces myofibroblast numbers and promotes ECM remodeling away from fibrotic collagen deposition.
Legal Status by Region
This information is provided for educational and research purposes only. Not approved for human consumption by the FDA or any regulatory body. Always consult a qualified medical professional.