Recovery ⏱ Half-life: Short plasma half-life (degraded by ACE). Functional anti-fibrotic effects persist with consistent dosing. Experimental

TB4-FRAG

TB4-FRAG (Ac-SDKP / Thymosin Beta-4 Fragment)

Updated March 15, 2026

Evidence at a Glance

Regulatory statusExperimental
Thymosin beta-4 fragment; research-use peptide, no human trials of the fragment itself
Human evidenceNone
Animal evidenceLimited

A fragment of thymosin beta-4 studied in vitro and in animals for actin-binding and tissue-repair mechanisms; the human clinical data that exist belong to full-length thymosin beta-4, not this fragment.

What the research does not support

  • No human clinical trials have tested this fragment for any indication.
  • It is not FDA-approved and is sold only as a research chemical.
  • Healing and regeneration claims are extrapolated from full-length thymosin beta-4 and animal work, not fragment-specific human data.
Half-Life
Short plasma half-life (degraded by ACE). Functional anti-fibrotic effects persist with consistent dosing.
Mol. Weight
487.51 g/mol

What is TB4-FRAG?

TB4-FRAG (Ac-SDKP) is the naturally occurring active fragment of thymosin beta-4, released by normal enzymatic processing in the body. While TB-500 provides the full range of thymosin beta-4 effects, this fragment concentrates specifically on anti-fibrotic and stem cell regulatory activity.

Research Applications

Key research areas include:

  • Cardiac fibrosis: Inhibits collagen I and III deposition in cardiac tissue
  • Renal fibrosis: Reduces tubulointerstitial fibrosis in kidney models
  • Pulmonary fibrosis: Anti-fibrotic activity in lung tissue
  • Hematopoiesis: Maintains stem cell pluripotency
  • Inflammation: Reduces macrophage infiltration and inflammatory cytokines

Dosage Information (Research Use)

Research protocols: 100-750 mcg/day subcutaneously. Continuous administration studied in most models (not course-based like some peptides). Research use only.

Reconstitution & Handling

Standard BAC water reconstitution. Small tetrapeptide dissolves instantly.

Half-Life & Pharmacokinetics

Short plasma half-life (degraded by ACE). Functional anti-fibrotic effects persist with consistent dosing.

Reported Observations in Literature

Naturally occurring peptide with good safety profile in animal studies. No significant adverse effects reported at research doses. Endogenous levels are elevated by ACE inhibitor therapy without apparent harm.

Key Research References

  • Peng H, et al. “Ac-SDKP reverses cardiac fibrosis in rats with renovascular hypertension.” Hypertension. 2003
  • Rasoul S, et al. “Antifibrotic effect of Ac-SDKP and angiotensin-converting enzyme inhibition in hypertension.” J Hypertens. 2004

How TB4-FRAG Works

Ac-SDKP (TB4-FRAG) is the N-terminal tetrapeptide fragment of thymosin beta-4, released by prolyl oligopeptidase (POP) cleavage. It is naturally present in human plasma and is a substrate of ACE (angiotensin-converting enzyme) — ACE inhibitors increase endogenous Ac-SDKP levels. Primary mechanisms include potent anti-fibrotic activity (inhibits collagen deposition by cardiac fibroblasts), anti-inflammatory signaling (reduces macrophage infiltration), and hematopoietic stem cell regulation (prevents premature differentiation of pluripotent stem cells).

Research Findings

Endogenously produced — every person has circulating Ac-SDKP. Levels are elevated 4-5x by ACE inhibitor therapy, which may partially explain the anti-fibrotic benefits of ACE inhibitors beyond blood pressure reduction. Studied for cardiac fibrosis, renal fibrosis, and pulmonary fibrosis with promising results. Smaller and more stable than full TB-500, with more focused anti-fibrotic activity.

Dosage & Administration

Research protocols: 100-750 mcg/day subcutaneously. Continuous administration studied in most models (not course-based like some peptides). Research use only.

Safety & Side Effects

Naturally occurring peptide with good safety profile in animal studies. No significant adverse effects reported at research doses. Endogenous levels are elevated by ACE inhibitor therapy without apparent harm.

Important: All safety information is derived from published research, primarily animal studies. No controlled human clinical trial data exists unless explicitly noted. This compound is sold for research purposes only.

Quick Facts

Sequence Ac-Ser-Asp-Lys-Pro
Molecular Weight 487.51 g/mol
Half-Life Short plasma half-life (degraded by ACE). Functional anti-fibrotic effects persist with consistent dosing.
Available Sizes 5mg
Storage Lyophilized: -20°C. Reconstituted: 2-8°C.

Key Research References

  • Peng H, et al. "Ac-SDKP reverses cardiac fibrosis in rats with renovascular hypertension." Hypertension. 2003
  • Rasoul S, et al. "Antifibrotic effect of Ac-SDKP and angiotensin-converting enzyme inhibition in hypertension." J Hypertens. 2004

Related Peptides

View all →
Thymosin Beta-4
Recovery
The complete 43-amino acid protein behind TB-500's regenerative properties — orchestrates tissue repair, cell migration, and wound healing.
View Profile → Buy Now
LL-37
Recovery
Human host defense peptide (cathelicidin) with antimicrobial, immunomodulatory, and wound healing properties.
View Profile →
Teriparatide
Recovery
FDA-approved parathyroid hormone analog that stimulates new bone formation rather than just preventing bone loss.
View Profile →