Peptide Profile
Ac-SDKP
N-acetyl-seryl-aspartyl-lysyl-proline · AcSDKP
Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline) is an endogenous tetrapeptide generated from the N-terminus of thymosin beta-4 by the enzyme prolyl oligopeptidase, with further regulation by angiotensin-converting enzyme (ACE),…
- Routes
- subcutaneous, intravenous
Educational research information — not medical advice. Review primary sources and consult a qualified professional before any decision.
Educational research tools — not medical advice.
What Ac-SDKP is
About Ac-SDKP
Inhibits hematopoietic stem cell entry into S-phase. Blocks TGF-β1-mediated fibroblast activation, reducing collagen deposition. Promotes angiogenesis via VEGF upregulation. Regulated in vivo by ACE enzyme.
Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline) is an endogenous tetrapeptide generated from the N-terminus of thymosin beta-4 by the enzyme prolyl oligopeptidase, with further regulation by angiotensin-converting enzyme (ACE), and is characterized by roles in hematopoietic progenitor regulation and anti-fibrotic signaling in renal, cardiac, and vascular tissue. Ac-SDKP inhibits collagen synthesis and fibroblast proliferation, reduces TGF-beta-1-mediated fibrotic signaling, and promotes anti-inflammatory macrophage polarization in preclinical models, suggesting a role in tissue homeostasis downstream of the thymosin beta-4 pathway. Preclinical studies in rodent models of renal fibrosis and systemic lupus erythematosus — predominantly from the NIH-funded Rhaleb and Carretero laboratory at Henry Ford Health — have demonstrated that exogenous Ac-SDKP reduces collagen deposition and inflammatory infiltrate; no human clinical trials have been completed or indexed in PubMed. Ac-SDKP has no FDA approval and no approved indication in any jurisdiction; it is studied as a research compound with a plausible anti-fibrotic mechanism and consistent preclinical evidence, but extrapolation of rodent findings to human therapeutic outcomes has not been validated by any clinical investigation.
Ac-SDKP Benefits & Research Areas
What the evidence says about Ac-SDKP
Research Evidence
based on 4 studies · most recent 2026
Regulatory Status
- Availability Status
- Research Only
- FDA Status
- Not Evaluated
Regulatory status reflects publicly available information and may change. This is not legal or medical advice.
Research Sources
4 sources cited · 4 moderate
2 Cohorts · 2 Animals
Device surface-functionalized ac-SDKP nanoassemblies accelerate endothelial recovery through dual anti-inflammatory and endothelial homeostatic mechanisms.
Biomater Adv · 2026
# Summary Research found that Ac-SDKP nanoassemblies incorporated into stent surface coatings promoted endothelial cell recovery and repair through dual mechanisms: reducing inflammatory responses (by suppressing macrophage and neutrophil activity) while simultaneously protecting endothelial cells from apoptosis and dysfunction. This study demonstrated that the modified stent surface reduced neointimal hyperplasia and inflammatory infiltration in animal models, suggesting a potential strategy to address in-stent restenosis complications.
Ac-SDKP Attenuates Silica-Induced Pulmonary Fibrosis by Inhibiting ALKBH1-Mediated m(6)A Demethylation of miR-129-5p.
FASEB J · 2026
# Summary Research found that Ac-SDKP inhibits the development of silica-induced pulmonary fibrosis by blocking ALKBH1, an enzyme that removes chemical modifications from microRNA precursors, thereby restoring miR-129-5p levels and suppressing the inflammatory activation of macrophages. This study identified the Ac-SDKP-ALKBH1-miR-129-5p regulatory pathway as a critical mechanism in silicosis progression and a potential therapeutic target for this occupational lung disease.
N-Acetyl-Seryl-Aspartyl-Lysyl-Proline: mechanisms of renal protection in mouse model of systemic lupus erythematosus
American Journal of Physiology: Renal Physiology · 2015
Research in a lupus mouse model found that Ac-SDKP treatment significantly reduced macrophage and T cell infiltration, decreased proinflammatory cytokine levels, prevented complement C5-9 upregulation, and preserved glomerular filtration rate, identifying anti-inflammatory and complement-modulating mechanisms underlying its renoprotective effects.
Show 1 more source ↓
Thymosin β4 and its degradation product, Ac-SDKP, are novel reparative factors in renal fibrosis
Kidney International · 2013
Research in mouse models of renal fibrosis found that Ac-SDKP, the tetrapeptide degradation product of thymosin β4, consistently reduced collagen and fibronectin deposition, decreased myofibroblast and macrophage infiltration, and suppressed profibrotic signaling in both early and late stages of kidney injury.
Ac-SDKP Side Effects & Safety Considerations
Research-use compound with limited human data. Evidence strength varies — see the Evidence section.
No established clinical contraindications. This is an investigational compound with limited human data and has not been evaluated by the FDA for safety in this context. Consult a qualified clinician.
Consult a qualified healthcare professional before making any health decisions. This information is educational only and does not constitute medical advice.
Compare
VSAc-SDKP
Frequently Asked Questions — Ac-SDKP
Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline) is an endogenous tetrapeptide generated from the N-terminus of thymosin beta-4 by the enzyme prolyl oligopeptidase, with further regulation by angiotensin-converting enzyme (ACE), and is characterized by roles in hematopoietic progenitor regulation and anti-fibrotic signaling in renal, cardiac, and vascular tissue. Ac-SDKP inhibits collagen synthesis and fibroblast proliferation, reduces TGF-beta-1-mediated fibrotic signaling, and promotes anti-inflammatory macrophage polarization in preclinical models, suggesting a role in tissue homeostasis downstream of the thymosin beta-4 pathway.
anti-fibrotic, cardiac repair, wound healing, kidney protection.
Research on Ac-SDKP primarily documents effects related to anti-fibrotic and cardiac repair and wound healing and kidney protection. These are areas covered in preclinical and clinical literature — individual response varies and effects depend on context of use.
For Ac-SDKP, its FDA status is not evaluated by the FDA, and it is designated for research use only. Regulatory status reflects publicly available information and may change. This is not legal or medical advice.
# Summary Research found that Ac-SDKP nanoassemblies incorporated into stent surface coatings promoted endothelial cell recovery and repair through dual mechanisms: reducing inflammatory responses (by suppressing macrophage and neutrophil activity) while simultaneously protecting endothelial cells from apoptosis and dysfunction. This study demonstrated that the modified stent surface reduced neointimal hyperplasia and inflammatory infiltration in animal models, suggesting a potential strategy to address in-stent restenosis complications.
How to get Ac-SDKP
Where to buy Ac-SDKP
Coverage expanding
No verified providers currently list Ac-SDKP. Get notified when one does, or explore providers carrying similar peptides in the Recovery category.
Questions to ask your provider
Stay updated on verified Ac-SDKP providers
New verified providers added weekly — delivered to your inbox.
Last updated
Keep exploring
Tools & Guides
Reconstitution Calculator
Convert vial size + BAC water volume into draw volume.
How to Reconstitute Peptides
Step-by-step guide: BAC water, vial prep, and storage after mixing.
Peptide Dosage Guide
Key factors that determine dosing in clinical practice.
Peptide Storage Guide
How to store lyophilized and reconstituted peptides.