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Healing & Recovery
Preclinical

TB-500 Fragment (1-4)

Also known as: TB-500 Fragment 1-4, Thymosin Beta-4 Fragment 1-4, TB4 Frag 1-4

TB-500 Fragment 1-4 is the N-terminal tetrapeptide (Ac-SDKP) of thymosin beta-4, studied for anti-fibrotic and tissue-protective effects. This fragment is distinct from the actin-binding region and is associated with regulation of fibrosis and inflammation.

Last updated

Mechanism of Action

Fragment 1-4 corresponds to N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), a naturally occurring tetrapeptide released from thymosin beta-4 by prolyl oligopeptidase. Ac-SDKP exerts anti-fibrotic activity by inhibiting TGF-beta and Smad signaling, reducing collagen deposition and fibroblast-to-myofibroblast transition. It also displays anti-inflammatory and pro-angiogenic properties and helps regulate hematopoietic stem cell proliferation.

Half-life
Very short; Ac-SDKP is rapidly degraded by angiotensin-converting enzyme
Administration Routes
subcutaneous
Research Status
Preclinical

Reported Benefits

  • Anti-fibrotic activity through TGF-beta and Smad inhibition
  • Reduces excess collagen deposition in tissue
  • Supports angiogenesis and tissue protection
  • Modulates inflammatory responses
  • Studied for cardiac, renal, and pulmonary fibrosis models

Potential Side Effects

  • Limited human safety data
  • Possible injection-site reactions
  • Theoretical effects on blood pressure regulation
  • Unknown long-term effects

Common Dosing

No validated human protocols exist; preclinical work uses microgram-to-milligram ranges scaled to body weight. For research use only and not personal medical advice.

The dosing information above is aggregated from research literature and anecdotal community reports for educational purposes only. It is not a recommendation, prescription, or medical advice. Peptides are sold as research chemicals only and are not intended for human use.

Contraindications

  • Use with ACE inhibitors, which raise endogenous Ac-SDKP levels
  • Pregnancy or breastfeeding
  • Known hypersensitivity to thymosin-derived peptides
  • Thymosin β4 and its degradation product, Ac-SDKP, are novel reparative factors in renal fibrosis

    2013

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  • Prolyl oligopeptidase is involved in release of the antifibrotic peptide Ac-SDKP

    2004

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  • Decreased endogenous levels of Ac-SDKP promote organ fibrosis

    2007

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  • The Role of Tβ4-POP-Ac-SDKP Axis in Organ Fibrosis

    2022

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Fragment 1-4 (Ac-SDKP) comes from the N-terminus of thymosin beta-4 and is mainly studied for anti-fibrotic effects, whereas Fragment 17-23 contains the actin-binding motif tied to cell migration and repair.

Yes. Ac-SDKP is a naturally occurring peptide cleaved from thymosin beta-4 and is normally broken down by angiotensin-converting enzyme (ACE), which is why ACE inhibitors raise its levels.

PeptideChat is for educational and research purposes only. Nothing on this site constitutes medical advice. Peptides are sold as research chemicals only and are not intended for human use. These statements have not been evaluated by the FDA and are not intended to diagnose, treat, cure, or prevent any disease. PeptideChat is an independent educational resource — not a pharmacy, compounding, or 503A/503B outsourcing facility — and does not sell products or provide medical advice.