Ac-SDKP

N-acetyl-seryl-aspartyl-lysyl-proline, AcSDKP, Goralatide, Seraspenide, "thymosin β4 metabolite"

Recovery, repair & tissue

Awaiting medical reviewEN ES DE FR PT ZH+ Follow for updates

Summary

Class: Naturally occurring tetrapeptide (4 amino acids), released from the N-terminus of thymosin β4
Mechanism: Slows the division of blood-forming stem cells and dampens TGF-β-driven scarring; broken down by ACE, so ACE inhibitors raise its level several-fold
Routes studied: Intravenous infusion (human); subcutaneous and intraperitoneal injection, osmotic minipump (animal); community: subcutaneous
Dose range reported: Human: continuous IV infusion in chemotherapy-support studies (µg/kg/h range). Animal anti-fibrosis: roughly 400–800 µg/kg/day by minipump. Community: scattered reports, no consistent protocol. No validated human dose for any fibrosis use
Half-life: Very short — about 4–5 minutes in human plasma; cleared mainly by ACE, with some renal clearance
Storage: Lyophilised: refrigerate, protect from light. Reconstituted: refrigerate; community practice is use within ~2–4 weeks
Regulatory status: Not approved anywhere. Studied clinically in the 1990s and shelved

Doses are as reported in studies or by the community — never recommendations.

1What it is

Ac-SDKP is a four-amino-acid peptide that your body makes all the time. The enzyme prolyl oligopeptidase clips it from the front end of thymosin β4 (the full protein behind TB-500), and angiotensin-converting enzyme (ACE) destroys it. It was first purified in 1989 from fetal calf bone marrow as a factor that keeps blood-forming stem cells resting (Lenfant 1989, PNAS). Normal plasma levels are in the low nanomolar range.

Two things make it interesting beyond its origin. First, anyone taking an ACE inhibitor for blood pressure has roughly four to five times the normal level, which has led to the idea that part of the ACE-inhibitor benefit on heart and kidney scarring runs through this peptide (Azizi 1996, J Clin Invest). Second, it was developed in the 1990s under the names Seraspenide and Goralatide as a way to protect bone marrow during chemotherapy; that programme reached early-phase human trials and then stopped.

In the peptide community it appears mainly as "the anti-fibrotic part of TB-500", a framing that is reasonable in rodents and untested in humans.

2How it's thought to work

Stem-cell quiescence. keeps haematopoietic stem cells out of the S phase of the cell cycle, which is why it was tested to shield marrow from cycle-specific chemotherapy.

Anti-fibrosis. in rodent heart, kidney and lung models it reduces fibroblast proliferation, collagen deposition and TGF-β1/Smad signalling, and lowers infiltration of macrophages and other inflammatory cells (Peng 2001; Rhaleb 2001; Pokharel 2002).

Endothelial-to-mesenchymal transition. in diabetic mouse kidneys it blocks the conversion of blood-vessel cells into scar-forming cells; DPP-4 inhibitors may act partly by raising Ac-SDKP (Nagai 2014, Diabetes).

Angiogenesis. it promotes blood-vessel growth in cell and animal models (Wang 2004, Am J Physiol Heart Circ Physiol), which may help repair but carries the usual theoretical caution.

Galectin-3. reported to bind and inhibit galectin-3, a pro-fibrotic lectin, in rodent work.

A natural tetrapeptide that holds fibroblasts back from becoming the scarring kind, limiting collagen deposition. It is broken down by ACE, which is why ACE inhibitors raise its level — thought to contribute to their anti-fibrotic effects.Schematic — not to scale

3What the research shows

Pharmacology and plasma levels in humans

Human studies have measured endogenous Ac-SDKP, shown the ~4–5-fold rise under ACE inhibition, and characterised the minutes-long after intravenous administration (Azizi 1996, J Clin Invest; Azizi 1997, Hypertension). These are mechanistic studies, not treatment trials. [2][3]

Protection of bone marrow during chemotherapy

Early-phase trials of Seraspenide/Goralatide given by infusion around chemotherapy in cancer patients reported reduced neutrophil and platelet dips in small numbers of patients (Carde 1992, C R Acad Sci III; Bogden 1998, Ann N Y Acad Sci review). Numbers were small and the programme did not progress to approval. [9]

Cardiac fibrosis and hypertension-related damage

In rat models of aldosterone-salt, angiotensin II and renovascular hypertension, Ac-SDKP infusion prevented or reversed left-ventricular collagen deposition and inflammatory cell infiltration, often without lowering blood pressure (Peng 2001, Hypertension; Rhaleb 2001, Hypertension; Pokharel 2002, Circulation). Independent groups have replicated the core finding. [4][5][6]

Kidney fibrosis, including diabetic

Reduced glomerulosclerosis and interstitial fibrosis in rat and mouse models of kidney disease (Nagai 2014, Diabetes; several Carretero-group papers). [7]

Lung fibrosis

Reduced collagen and improved lung histology in rodent silica- and bleomycin-induced fibrosis models.

Not gradedno data

Human fibrosis of any kind

No trial of Ac-SDKP for scarring, injury recovery or any tissue-repair outcome in humans has been published.

4Reported side effects and interactions

Literature-reported

Infusion in chemotherapy patients was described as well tolerated at the doses used; the human safety file is small and short-term. Rodent studies at anti-fibrotic doses report few adverse effects.

Community-reported

very little; occasional injection-site reactions. Not enough volume of reports to characterise.

Theoretical. anti-proliferative effect on blood-forming cells could blunt marrow recovery in someone with low counts; action carries the standard caution around existing tumours; ACE inhibitors would be expected to raise exposure to exogenous peptide as well as endogenous.

Interactions. ACE inhibitors (reduce breakdown, raise levels several-fold); DPP-4 inhibitors may also raise levels; no clinical interaction studies exist.

Markers researchers commonly monitor

No compound-specific monitoring exists in human literature. Based on its known biology:

Marker	Why it's watched
CBC with differential, especially neutrophils and platelets	the compound's best-documented human action is slowing blood-cell production.
Blood pressure	the rodent benefit was largely independent of pressure, but ACE-inhibitor users are the natural comparison group and pressure is easy to log.
eGFR, creatinine, urine albumin	kidney fibrosis is a main preclinical target; these are the human equivalents.
hs-CRP	general inflammation marker relevant to the anti-inflammatory claims.
Plasma Ac-SDKP itself	measurable by research assays and used as a marker of ACE-inhibitor adherence in studies, but not available as a routine clinical test.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Where supplied, usually as a powder in low-milligram vials. with , swirl gently, protect from light. Because the is minutes, a single injection delivers a brief pulse; the rodent anti-fibrosis data mostly used continuous infusion, which no community protocol reproduces.

Open in calculator, pre-loaded →

6Commonly studied alongside

TB-500 / thymosin β4 (its parent molecule; see profile 2), BPC-157 (recovery context; no combined study). In the literature it is almost always discussed with ACE inhibitors and DPP-4 inhibitors rather than other peptides.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved. Not on the FDA Category 2 compounding list to our knowledge †
European Union	Not authorised
United Kingdom	Not licensed
Australia	Not approved
South Africa	Not registered
Sport	Not specifically named by WADA; as a non-approved substance it falls under S0 †

8Open questions

Does intermittent dosing of a 4-minute-half-life peptide produce any tissue effect in humans?
Would any anti-fibrotic benefit in humans add to what ACE inhibitors already deliver by raising endogenous levels?
Long-term effects of chronically suppressing haematopoietic stem-cell cycling.

9References

1Lenfant M et al. (1989). Inhibitor of hematopoietic pluripotent stem cell proliferation: purification and determination of its structure. Proc Natl Acad Sci USA. PubMed · DOI
2Azizi M et al. (1996). Acute angiotensin-converting enzyme inhibition increases the plasma level of the natural stem cell regulator N-acetyl-seryl-aspartyl-lysyl-proline. J Clin Invest. PubMed · DOI
3Azizi M et al. (1997). High plasma level of N-acetyl-seryl-aspartyl-lysyl-proline: a new marker of chronic angiotensin-converting enzyme inhibition. Hypertension. PubMed · DOI
4Peng H et al. (2001). Ac-SDKP reverses cardiac fibrosis in rats with renovascular hypertension. Hypertension. PubMed
5Rhaleb NE et al. (2001). Effect of N-acetyl-seryl-aspartyl-lysyl-proline on DNA and collagen synthesis in rat cardiac fibroblasts. Hypertension. PubMed · DOI
6Pokharel S et al. (2002). N-acetyl-Ser-Asp-Lys-Pro inhibits phosphorylation of Smad2 in cardiac fibroblasts. Circulation. PubMed · DOI
7Nagai T et al. (2014). N-acetyl-seryl-aspartyl-lysyl-proline inhibits diabetes-associated kidney fibrosis and endothelial-mesenchymal transition. Diabetes. PubMed · DOI
8Wang D et al. (2004). N-acetyl-seryl-aspartyl-lysyl-proline stimulates angiogenesis in vitro and in vivo. Am J Physiol Heart Circ Physiol. PubMed · DOI
9Bogden AE et al. (1998). Goralatide (AcSDKP), a negative growth regulator, protects the stem cell compartment during chemotherapy. Ann N Y Acad Sci. PubMed · DOI

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.

10Community

forum threads →

community protocols include this →

Threads and protocols are visible to members. Joining is free.

Self-reported side effects Phase 2

Not enough data yet. 0 of the 50 members needed have logged this compound for 4+ weeks. We don't show anything below 50, so no one can be identified.

11Page history

26 Oct 2026Profile published — awaiting medical review

Licensed CC BY-NC-SA 4.0. Found an error? Report it · Editorial standards — corrections are logged here.