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TB-500 Fragment 1-4

Ac-SDKP · TB-500 Fragment 1-4

C
Animal replicated
Research chemicalTB-4 FragmentTetrapeptideAnti-Fibrotic Peptide
RouteInjectableGray-market only
C
Evidence grade: Animal replicated

Effect demonstrated in multiple animal studies; human data sparse or extrapolated. Grades summarize evidence quality, not whether a compound is appropriate, legal, or risk-free.

At a glance
What it is
Ac-SDKP — N-Acetyl-Seryl-Aspartyl-Lysyl-Proline — Anti-Fibrotic Tetrapeptide — ACE Substrate — TB-4 Fragment, Tetrapeptide, Anti-Fibrotic Peptide.
Why people use it
Used primarily for muscle and performance and skin, hair, and cosmetic use.
What the evidence supports
No human RCT for community use of exogenous Ac-SDKP. Extensive animal model evidence: cardiac fibrosis prevention and reversal in hypertensive and post-infarction rat models; renal fibrosis inhibition in multiple models; bone marrow progenitor cell regulation. Evidence grade: C (animal replicated) for anti-fibrotic effects; D (mechanistic/observational) for the ACE inhibitor connection; E (community) for community injection protocols.
If you only read one thing

Ac-SDKP may be part of the reason ACE inhibitors protect the heart and kidneys in ways that exceed their blood pressure lowering effects. This hypothesis has been building in the cardiovascular research literature for two decades. The direct experimental support: in animal models, the anti-fibrotic effects of ACE inhibitors are attenuated when Ac-SDKP levels are normalized (i.e., when the Ac-SDKP elevation from ACE inhibition is blocked). This implicates Ac-SDKP as a functional mediator of ACE inhibitor benefit. The community is injecting Ac-SDKP to directly deliver the fragment without requiring ACE inhibitor co-administration. The hypothesis is compelling. The human clinical trial evidence for direct Ac-SDKP supplementation is zero.

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Evidence reality check
Evidence snapshot
No human RCT for community use of exogenous Ac-SDKP. Extensive animal model evidence: cardiac fibrosis prevention and reversal in hypertensive and post-infarction rat models; renal fibrosis inhibition in multiple models; bone marrow progenitor cell regulation. Evidence grade: C (animal replicated) for anti-fibrotic effects; D (mechanistic/observational) for the ACE inhibitor connection; E (community) for community injection protocols.
From the chapter quick-reference block.
Risk posture
No major flags listed
Review route-specific cautions before use.
Categories
Muscle & PerformanceSkin, Hair & Beauty
Properties
Not injectable
Evidence
CAnimal replicated
Why This Is Not the Actin Story
TB-500 Fragment 17-23 (LKKTETQ) is the actin-binding domain of Thymosin Beta-4 — the cell migration mechanism. Ac-SDKP (Fragment 1-4) has nothing to do with actin. Its mechanism is entirely different: anti-fibrotic (prevents fibroblast-to-myofibroblast differentiation; reduces TGF-β1 signaling; prevents collagen accumulation); anti-inflammatory (reduces macrophage infiltration; inhibits bone marrow-derived haematopoietic progenitor proliferation). The two fragments from the same parent peptide do completely different things in the body.
The ACE Inhibitor Connection
ACE (angiotensin-converting enzyme) degrades Ac-SDKP via its N-domain. When ACE is inhibited (by drugs like enalapril, lisinopril, ramipril), Ac-SDKP accumulates in blood. Plasma Ac-SDKP levels increase 4-5-fold on ACE inhibitor therapy. This is now recognized as a potential contributor to the anti-fibrotic effects of ACE inhibitors beyond blood pressure lowering. The implication: some of the cardiac and renal protective effects attributed to ACE inhibitors may be partly mediated by elevated Ac-SDKP levels. Direct Ac-SDKP administration in animal models produces fibrosis reduction consistent with this hypothesis.
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