Ac-SDKP: what the studies show, status and safety
Summary
Ac-SDKP is a tiny peptide of four building blocks that the body cuts from the protein thymosin β4 and that the enzyme ACE breaks down again. It is sold online as a TB-500 fragment, but that name is wrong. TB-500 copies a different stretch of the same protein, and the two do not overlap. In people, Ac-SDKP has mainly been studied as a blood marker that rises about 5.5-fold when ACE is blocked. Every effect of giving it comes from animals and cells, and no country has approved it.
Key findings at a glance
- Positions 1 to 4, not 17 to 23. Ac-SDKP is the first four building blocks of thymosin β4, and TB-500 copies positions 17 to 23. The two pieces share not a single building block [1], [2].
- About 5.5 times higher after one blood pressure tablet. In eight healthy people, a single dose of the ACE inhibitor captopril raised the blood level about 5.5-fold, with a range of 4- to 8.5-fold [3].
- Gone from the blood within minutes. After an infusion in six healthy volunteers, half of it had disappeared from the blood in about 4.5 minutes [4].
- No registered trial found that gives Ac-SDKP itself. The one registered study that gives anything uses a chemically altered version to measure kidney function, and it has posted no results [5].
- Less heart scarring in rats, but no better pumping. In rats with high blood pressure, scar tissue took up 5.4% of the left heart chamber with Ac-SDKP against 10.1% on dummy treatment [6]. After a heart attack in rats, pumping got worse in one group [7].
- One key lung paper is under an expression of concern. The journal published that notice in 2025 [8].
- Banned in sport at all times. It is not named on the 2026 list, and the stricter reading places it under S2.3 as a derivative of thymosin β4 [9].
What it is
Ac-SDKP is a peptide of four building blocks, serine, aspartic acid, lysine and proline, with a small acetyl cap at the front. It is not an invention. French researchers isolated it in 1989 from the bone marrow of calves, worked out its structure and then made it in the laboratory to confirm it [10]. A year later it was shown to come from thymosin β4 [11].
Every person carries it in their blood at a steady level of about 1.7 to 3.2 nM [4].
Made in a laboratory, the molecule is chemically identical and carries the international non-proprietary name goralatide; an older name in the literature is seraspenide [12]. Under the name goralatide it went through early clinical studies in the 1990s, and development was not continued [4], [12].
Quick facts
| Field | Value | Ref |
|---|---|---|
| Common names | Ac-SDKP, AcSDKP, goralatide, seraspenide | [12] |
| Class | Peptide the body makes itself, four building blocks | [1] |
| Sequence | Ac-Ser-Asp-Lys-Pro | [10] |
| Place in thymosin β4 | Positions 1–4 | [1] |
| Formula and mass | C20H33N5O9, 487.5 g/mol | [13] |
| Half-life in the blood | About 4.5 minutes after an infusion, healthy volunteers | [4] |
| Normal blood level | 1.7–3.2 nM | [4] |
| Status | Approved nowhere; development as goralatide not continued | [14], [15] |
| CAS registry number | 120081-14-3 | [12] |
| PubChem CID | 65938 | [13] |
| UNII | H041538E9P | [12] |
| ChEMBL | CHEMBL2104460 | [12] |
| InChIKey | HJDRXEQUFWLOGJ-AJNGGQMLSA-N | [13] |
How it works
The body cuts Ac-SDKP from a larger protein and removes it again quickly, and that is the best-established fact about it. What it does in between is known only from cells and animals, and no receptor has been found [16], [17].
Where it sits. Thymosin β4 is a chain of 43 building blocks found in almost every cell. Written out, the first part of the chain looks like this [1]:
| Positions | Building blocks | What it is |
|---|---|---|
| 1–4 | S D K P | Ac-SDKP |
| 5–16 | D M A E I E K F D K S K | Not part of either peptide |
| 17–23 | L K K T E T Q | The stretch TB-500 copies |
| 24–43 | E K N P L P S K E T I E Q E K Q A G E S | Rest of the protein |
Twelve building blocks separate the two pieces. Both are cut from the same chain, but from different places, so neither can be a piece of the other. Calling Ac-SDKP a TB-500 fragment is like calling the first word of a sentence part of a phrase that only starts later in the same sentence.
How it is released. Two enzymes work one after the other [16]:
- Meprin-α first cuts thymosin β4 into shorter pieces that still carry the front end.
- Prolyl oligopeptidase then snips Ac-SDKP free from those pieces. On its own, it cannot cut the whole protein [16], [18].
- ACE, the enzyme that blood pressure tablets called ACE inhibitors block, breaks Ac-SDKP down again. That is why those tablets raise its level [17], [3].
What it may do. These are hypotheses from cells and animals:
- A brake on blood-forming stem cells. It was first described as a substance that slows the division of early blood-forming cells in mice [10].
- Damping a scarring signal. In heart cells from rats and from human fetal tissue, it weakened the signal chain that turns connective tissue cells into scar-forming cells [19], [20].
- New blood vessels. At nanomolar amounts it made blood vessel cells migrate and form tubes, and it caused new vessels to grow in chick embryos and rats [21].
TB-500 is linked in the literature to a different job: the stretch at 17 to 23 grips actin, the building material of the cell scaffold. Ac-SDKP is assigned to the part of thymosin β4 that calms inflammation and scarring [22].
What the studies found
No study has tested whether Ac-SDKP given from outside helps people with any condition. The human data describe how the body clears it and how its own level changes under ACE inhibitors; all effect data come from animals and cells.
The body's own level under ACE inhibitors
Human data In a placebo-controlled crossover study in eight healthy people, one 50 mg dose of captopril raised the blood level about 5.5-fold, with a range of 4- to 8.5-fold, and the rise lasted [3]. In an observational comparison of people treated long term for high blood pressure, 27 with and 23 without an ACE inhibitor, the average level was 3.78 pmol/ml with an ACE inhibitor against 0.75 pmol/ml without one. The ranges did not overlap at all (p < 0.0001), and the authors called it the best marker of long-term ACE inhibition [23].
Geometric means in people treated long term for high blood pressure; ranges 1.48–14.5 against 0.36–1.22, p < 0.0001. The peptide was measured, not given. Source [23].
Observational The DIABHYCAR trial used urine levels to check whether 1,871 participants took their tablets. Among 597 people meant to take ramipril, 27.3% fell below 4 nmol/mmol, a sign they were not taking it. Among 621 on dummy tablets, 9.7% were above it, a sign they took another ACE inhibitor [24].
Meta-analysis A review pooled 4 studies with 206 people. In the 3 studies of healthy people, with 106 participants, ACE inhibitors raised the level by 5.07 pmol/ml on average (95% confidence interval 0.64 to 9.51). In the 2 studies of people with kidney failure, with 100 participants, the rise was 8.94 pmol/ml (2.55 to 15.33; I² = 44%, a measure of how much the studies disagreed). The review did not test whether the rise does anything useful [25].
How the body handles a dose
Human data Six healthy volunteers received the peptide once, by a 12-hour infusion into a vein or by an injection under the skin or into a muscle. After the infusion ended, half of it was gone in about 4.5 minutes on average. Peak levels came after 0.26 hours under the skin and 0.28 hours in the muscle, and 100% and 81% reached the blood [4]. In human plasma in a test tube, the half-life was 80 minutes [17].
The only registered study tests a different molecule
No results A Paris hospital study from 2010 to 2015 enrolled 100 people, healthy men and patients with kidney disease [5]. It gave AcSDKP-NH2, a chemically altered version that the body does not break down, as a test of kidney filtration. No results are posted, and the only linked paper describes the laboratory test method alone [26]. Two further registered entries only measure the body's own level [27], [28].
Heart scarring in rats
Animal data In rats with high blood pressure caused by a clamped kidney artery, scar tissue took up 10.1% of the left heart chamber on dummy treatment and 5.3% in sham-operated animals. With 400 µg/kg a day of Ac-SDKP it was 5.4% (p < 0.001). Blood pressure, heart weight and heart muscle cell size did not change [6].
Rats with high blood pressure from a clamped kidney artery, long-term treatment at 400 µg/kg a day; group sizes are not given in the abstract. Source [6].
Kidneys and lungs
Animal data In mice with a tied-off ureter, Ac-SDKP reduced scar proteins and scar-forming cells, early and late. Thymosin β4 given with a blocker of the releasing enzyme increased scarring instead [29]. In two kinds of diabetic mice, Ac-SDKP by mouth reduced kidney scarring; the dose is not in the abstract [30].
Animal data In mice given bleomycin to scar the lungs, 0.6 mg/kg into the belly reduced deaths, weight loss, inflammation and scarring up to day 21. The abstract gives no exact numbers [31]. A 2015 paper on lung cells from patients found less scar-protein production, but it has carried an expression of concern since 2025 [8].
The body's own supply
Animal data When a blocker of prolyl oligopeptidase lowered natural Ac-SDKP in rats from 1.76 ± 0.2 to 1.01 ± 0.1 nM [18], scarring around vessels in heart and kidney increased [32]. That suggests the body's own supply matters, at least in rats.
Brain, tested next to TB-500
Animal data A 2026 study gave both Ac-SDKP and TB-500 to mice bred to develop Alzheimer-like changes. Both improved maze and recognition tests and calmed the brain's support cells, while the amyloid deposits stayed the same [33]. It is the only paper that tests the two side by side, and it shows no shared mechanism.
Negative findings
- Heart pumping did not improve. After a heart attack in rats, total collagen fell from 23.7 ± 0.9 to 15.0 ± 0.7 µg/mg in the prevention group and from 22.6 ± 2.2 to 14.4 ± 1.6 µg/mg in the reversal group (p < 0.01). Pumping worsened in the prevention group and stayed the same in the other, "not accompanied by an improvement in cardiac function" [7].
- Fewer inflammatory cells, same function. Macrophages in the same study fell from 264.7 ± 8.1 to 170.2 ± 9.2 per mm² (p < 0.001) [7].
- More growth of vessel muscle cells. In cell culture, Ac-SDKP lowered a laboratory read-out of a scarring signal by 55 ± 9.7% (p = 0.01), but it increased the growth of smooth muscle cells from vessel walls [19].
What is still unknown
- Whether any effect seen in rats and mice happens in people. No study has tested this [5].
- Whether a dose given from outside matters, when the body clears it in minutes and the rat studies used continuous delivery [4], [6].
- Whether it is absorbed when swallowed. Only a mouse study has given it by mouth [30].
- Whether other teams can repeat the results. Much of the heart and kidney work comes from a single hospital group in Detroit [6], [7], [32].
Side effects and safety
No modern safety study of Ac-SDKP given from outside could be found. No side-effect rates are published, and no warning about it from a regulator could be found [34].
- It slows blood formation by design. The body uses it as a brake on early blood-forming cells [10]. Among 98 heart failure patients on ACE inhibitors, 10 had unexplained anaemia. Their ACE activity was 73% lower (p = 0.018), and their Ac-SDKP was higher. The higher the level, the slower red blood cell precursors grew (r = −0.64, p = 0.001) [35].
- Kidney disease multiplies the level. In a study of 176 kidney patients, 39 of whom took ACE inhibitors, the level was four times higher in those on the tablets [36]. With poor kidney function, levels on ACE inhibitors were 22 times higher (95% confidence interval 15 to 33) [37].
- It grows new vessels in animals. What long-term use would mean for tissue changes that have not yet been noticed has never been studied [21].
- Vessel wall cells grew faster. In culture, smooth muscle cells from vessel walls multiplied more quickly [19].
Data gaps:
- No studies found on repeated dosing, damage to genetic material or long-term effects in people.
- No data on taking it by mouth, although capsules are sold.
- No data on immune reactions, or on combining it with ACE inhibitors.
- No independent quality tests of the products sold online.
Doses used in studies
The doses below are simply what the cited studies gave, listed so that the results can be understood. They are not advice on how to use anything. Only the third line describes Ac-SDKP given to people: a single dose in healthy volunteers, given only to measure how fast the body clears it. The last line concerns a different molecule.
| Study | Substance | Model | Dose | Route | Duration | Ref |
|---|---|---|---|---|---|---|
| Rhaleb 2001, heart scarring | Ac-SDKP | Rat with high blood pressure | 400 µg/kg a day | Not given in the abstract | Long-term | [6] |
| Conte 2016, lung scarring | Ac-SDKP | Mouse | 0.6 mg/kg | Into the belly | 1 to 3 weeks | [31] |
| Ezan 1994, uptake and clearance | Ac-SDKP | 6 healthy volunteers, clearance measurement only | 128 nmol/kg | Into a vein over 12 hours, or under the skin or into a muscle | Once | [4] |
| NCT01588756, kidney test | AcSDKP-NH2, a different molecule | Healthy men and kidney patients | 100 µg or less | Into a vein | Once | [5] |
The animal doses mostly came from continuous delivery, while the body clears the peptide within minutes. They cannot be scaled to people [4].
Development and approval status
Ac-SDKP is not approved as a medicine in any of the seven markets checked, and it never was. Its development as goralatide in the 1990s was not continued, and no approval was ever granted.
From calf bone marrow to marker of ACE inhibition
- 1989Isolated from calf bone marrow and its structure determinedRef [10]
- 1990Shown to be cut from thymosin β4Ref [11]
- 1993ACE identified as the enzyme that breaks it downRef [17]
- 1994Uptake and clearance measured in six healthy volunteersHalf-life about 4.5 minutes, ref [4]
- 1990sEarly clinical studies as goralatide, not continuedNever approved, ref [12]
- 1996-1997Recognised as a marker of ACE inhibitionAbout 5.5-fold rise after captopril, refs [3], [23]
- 2001-2004Rat studies on heart scarringLess scarring, no better pumping, refs [6], [7]
- 2016Two-step release by meprin-α and prolyl oligopeptidaseRef [16]
- 2025Expression of concern on a 2015 lung paperRef [8]
- 2026Not approved in any of seven markets checkedRegisters searched on 23 September 2026
- 1989 to 1993 — discovery, origin in thymosin β4 and breakdown by ACE [10], [11], [17].
- 1990s — early clinical studies as goralatide, then no further development [4], [12].
- 1996 onwards — use as a marker of ACE inhibitor treatment [3], [24].
- 2001 onwards — animal work on scarring in heart, kidney and lung [6], [29], [31].
| Market | Status | Note | Ref |
|---|---|---|---|
| United States | Not approved | Not on compounding lists | [14], [38] |
| European Union | Not approved | Substance code only | [15] |
| Germany | Not approved | No authorisation found | [15] |
| United Kingdom | Not approved | No listing | [39] |
| Australia | Unclear | Possibly Schedule 4 | [40] |
| Canada | Not approved | No listing | [41] |
| Switzerland | Not approved | No listing | [42] |
In Australia, thymosin β4 and its derivatives sit in Schedule 4 and in the appendix that restricts possession. Whether the authority would count Ac-SDKP as such a derivative has not been decided [40]. All registers were searched on 23 September 2026.
Anti-doping
Ac-SDKP is banned in sport at all times, but not by name. Section S2.3 of the 2026 Prohibited List covers "Thymosin-ß4 and its derivatives e.g. TB-500" [9]. Ac-SDKP is a natural piece of thymosin β4, just as TB-500 copies one, so the stricter reading places it there, among the non-specified substances.
That is an interpretation, not an official ruling; no statement from WADA on Ac-SDKP could be found. If S2.3 did not apply, class S0 would catch it as a substance with no approval anywhere. Either way the result is the same: banned in and out of competition [9].
German anti-doping law lists "Thymosin-beta-4 und seine Derivate" and states that derivatives are included [43]. Whether a natural piece of the protein counts as a derivative under criminal law has not been tested in court. More on the rules is under peptides banned in sport.
Compared with related peptides
| Peptide | Place in thymosin β4 | Made by the body | Human data | Sport |
|---|---|---|---|---|
| Ac-SDKP | Positions 1–4 [1] | Yes, cut by two enzymes [16] | Clearance in 6 volunteers; marker studies [4], [23] | Not named; S2.3 by stricter reading [9] |
| TB-500 | Positions 17–23, with a cap [2] | No, lab-made [2] | See its own page | Named in S2.3 [9] |
| TB-500 Fragment 17-23 | Positions 17–23 [1] | No, lab-made | Not assessed on this page | Not assessed on this page |
| Thymosin β4 | The whole protein, 43 building blocks [1] | Yes | See the TB-500 page | Named in S2.3 [9] |
All four come from the same protein, but Ac-SDKP comes from its front end and the other fragments from the actin-gripping middle. Results for TB-500 or the whole protein say nothing about Ac-SDKP, and the reverse is also true [22].
The TB-500 page reaches the same conclusion from the other side. There, the calming effect of thymosin β4 on inflammation belongs to a piece that TB-500 does not contain. That piece is Ac-SDKP [22].
Common misconceptions
- "Ac-SDKP is TB-500 fragment 1-4." TB-500 is itself a fragment, positions 17 to 23 of thymosin β4. Ac-SDKP is positions 1 to 4 of the same protein and cannot come from TB-500 [1], [2].
- "Ac-SDKP and TB-500 do the same thing." The literature links them to different parts of the protein: Ac-SDKP to inflammation and scarring, TB-500's stretch to gripping actin and cell movement [22].
- "It is a designer peptide." The body makes it all the time, and every person has a measurable level [4], [16].
- "ACE inhibitors have nothing to do with it." ACE inhibitors are the best-known way the level rises, which is why it serves as a check on tablet taking. Whether this matters for their benefit in people is unproven [23], [24].
- "There is a clinical trial of Ac-SDKP." The registered study gives a different, altered molecule to measure kidney function, and has no results [5].
- "Goralatide is an approved medicine." It is the drug name of the same molecule, and its development ended without approval [12], [15].
Frequently asked questions
Is Ac-SDKP a fragment of TB-500?
No. Ac-SDKP is positions 1 to 4 of the protein thymosin β4, while TB-500 copies positions 17 to 23 of the same protein. The two stretches do not overlap, so Ac-SDKP is not contained in TB-500 and cannot be made from it. The correct description is thymosin β4 fragment 1 to 4.
Does the body make Ac-SDKP itself?
Yes. Two enzymes cut it from thymosin β4 in two steps, first meprin-α and then prolyl oligopeptidase, and the enzyme ACE breaks it down again. Healthy people carry a steady level of about 1.7 to 3.2 nM in their blood.
Has Ac-SDKP ever been tested in people?
Only in a narrow sense. A study from the 1990s measured how six healthy volunteers took up and cleared a single dose. Most human data since then measure the body's own level as a marker of ACE inhibitor treatment, without giving any Ac-SDKP at all.
Why do ACE inhibitors raise Ac-SDKP levels?
ACE is the enzyme that breaks Ac-SDKP down, so blocking it lets the peptide build up. A single dose of captopril raised the blood level about 5.5-fold in eight healthy people, and the rise was large enough to check in a trial whether patients were taking their tablets.
What is goralatide, and how does it relate to Ac-SDKP?
Goralatide is the international non-proprietary name of Ac-SDKP made in a laboratory, and the molecule is identical to the natural one. In the 1990s it went through early clinical studies under that name. Development was not continued, and it was never approved anywhere.
What did the animal studies of Ac-SDKP find?
In rats and mice, it reduced scar tissue in the heart, kidneys and lungs across several models. In rats after a heart attack, the scarring fell but heart pumping did not improve, and in one group it got worse. None of this has been tested in people.
Is there a registered clinical trial of Ac-SDKP?
None could be found that gives the peptide itself. The only registered study found that gives anything tests a chemically altered version, the amide, as a way of measuring kidney function, and it has published no results. Two further entries only measure the body's own level.
What are the side effects of Ac-SDKP?
No proper study of that could be found. The body uses Ac-SDKP to slow the division of blood-forming stem cells, and higher levels in heart failure patients on ACE inhibitors went along with unexplained anaemia. There are no data on repeated use, on capsules or on product quality.
Is Ac-SDKP banned in sport?
Yes, at all times. It is not named on the 2026 Prohibited List. Under the stricter reading it falls under S2.3 as a derivative of thymosin β4, and even otherwise the catch-all class S0 would ban it.
Sources
- UniProt Consortium. UniProtKB P62328, Thymosin beta-4 (human); feature "Hemoregulatory peptide AcSDKP". Retrieved 23 September 2026. https://rest.uniprot.org/uniprotkb/P62328.json
- Esposito S, Deventer K, Goeman J, Van der Eycken J, Van Eenoo P (2012). Synthesis and characterization of the N-terminal acetylated 17-23 fragment of thymosin beta 4 identified in TB-500, a product suspected to possess doping potential. Drug Testing and Analysis 4(9):733-738. PMID 22962027. DOI 10.1002/dta.1402
- Azizi M, Rousseau A, Ezan E, et al. (1996). Acute angiotensin-converting enzyme inhibition increases the plasma level of the natural stem cell regulator N-acetyl-seryl-aspartyl-lysyl-proline. Journal of Clinical Investigation 97(3):839-844. PMID 8609242. DOI 10.1172/JCI118484
- Ezan E, Carde P, Le Kerneau J, et al. (1994). Pharmacokinetics in healthy volunteers and patients of NAc-SDKP (seraspenide), a negative regulator of hematopoiesis. Drug Metabolism and Disposition 22(6):843-848. PMID 7895600. Only the healthy-volunteer part is used on this page.
- ClinicalTrials.gov. NCT01588756, a new non-radioactive test of kidney filtration using AcSDKP-NH2 (Assistance Publique – Hôpitaux de Paris); no results posted. API v2, retrieved 23 September 2026. https://clinicaltrials.gov/study/NCT01588756
- Rhaleb NE, Peng H, Yang XP, et al. (2001). Long-term effect of N-acetyl-seryl-aspartyl-lysyl-proline on left ventricular collagen deposition in rats with 2-kidney, 1-clip hypertension. Circulation 103(25):3136-3141. PMID 11425781. DOI 10.1161/01.cir.103.25.3136
- Yang F, Yang XP, Liu YH, et al. (2004). Ac-SDKP reverses inflammation and fibrosis in rats with heart failure after myocardial infarction. Hypertension 43(2):229-236. PMID 14691195. DOI 10.1161/01.HYP.0000107777.91185.89
- Conte E, Iemmolo M, Fruciano M, et al. (2015). Effects of thymosin β4 and its N-terminal fragment Ac-SDKP on TGF-β-treated human lung fibroblasts and in the mouse model of bleomycin-induced lung fibrosis. Expert Opinion on Biological Therapy 15 Suppl 1:S211-S221. PMID 26098610. DOI 10.1517/14712598.2015.1026804. Expression of concern: Expert Opinion on Biological Therapy 2025;25(11):1269, DOI 10.1080/14712598.2025.2596474
- World Anti-Doping Agency. The 2026 Prohibited List, classes S0 and S2.3; full text searched for SDKP, goralatide and seraspenide with no match. https://www.wada-ama.org/en/prohibited-list
- Lenfant M, Wdzieczak-Bakala J, Guittet E, Prome JC, Sotty D, Frindel E (1989). Inhibitor of hematopoietic pluripotent stem cell proliferation: purification and determination of its structure. Proceedings of the National Academy of Sciences USA 86(3):779-782. PMID 2915977. DOI 10.1073/pnas.86.3.779
- Grillon C, Rieger K, Bakala J, et al. (1990). Involvement of thymosin beta 4 and endoproteinase Asp-N in the biosynthesis of the tetrapeptide AcSerAspLysPro, a regulator of the hematopoietic system. FEBS Letters 274(1-2):30-34. PMID 2253778. DOI 10.1016/0014-5793(90)81322-f
- US FDA / NCATS. Global Substance Registration System, GORALATIDE, UNII H041538E9P; INN 7149, CAS 120081-14-3, ChEMBL2104460; seraspenide listed as a common name. Retrieved 23 September 2026. https://gsrs.ncats.nih.gov/ginas/app/beta/substances/f69fcec4-e8b1-4d88-b4b9-9198ba1cb321
- PubChem. Compound CID 65938 (Goralatide), properties. Retrieved 23 September 2026. https://pubchem.ncbi.nlm.nih.gov/compound/65938
- openFDA (Drugs@FDA, labels, NDC directory, enforcement reports) and DailyMed, searched for goralatide, seraspenide and SDKP with no match; control search for captopril returned results. Retrieved 23 September 2026. https://api.fda.gov/drug/drugsfda.json?search=openfda.generic_name:goralatide
- European Medicines Agency. Medicines output – medicines report (xlsx, 23 September 2026); no match for goralatide, seraspenide or SDKP. https://www.ema.europa.eu/en/documents/report/medicines-output-medicines-report_en.xlsx
- Kumar N, Nakagawa P, Janic B, et al. (2016). The anti-inflammatory peptide Ac-SDKP is released from thymosin-β4 by renal meprin-α and prolyl oligopeptidase. American Journal of Physiology – Renal Physiology 310(10):F1026-F1034. PMID 26962108. DOI 10.1152/ajprenal.00562.2015
- Rieger KJ, Saez-Servent N, Papet MP, et al. (1993). Involvement of human plasma angiotensin I-converting enzyme in the degradation of the haemoregulatory peptide N-acetyl-seryl-aspartyl-lysyl-proline. Biochemical Journal 296(Pt 2):373-378. PMID 8257427. DOI 10.1042/bj2960373
- Cavasin MA, Rhaleb NE, Yang XP, Carretero OA (2004). Prolyl oligopeptidase is involved in release of the antifibrotic peptide Ac-SDKP. Hypertension 43(5):1140-1145. PMID 15037553. DOI 10.1161/01.HYP.0000126172.01673.84
- Pokharel S, Rasoul S, Roks AJ, et al. (2002). N-acetyl-Ser-Asp-Lys-Pro inhibits phosphorylation of Smad2 in cardiac fibroblasts. Hypertension 40(2):155-161. PMID 12154106. DOI 10.1161/01.hyp.0000025880.56816.fa
- Peng H, Carretero OA, Peterson EL, Rhaleb NE (2010). Ac-SDKP inhibits transforming growth factor-beta1-induced differentiation of human cardiac fibroblasts into myofibroblasts. American Journal of Physiology – Heart and Circulatory Physiology 298(5):H1357-H1364. PMID 20154264. DOI 10.1152/ajpheart.00464.2009
- Liu JM, Lawrence F, Kovacevic M, et al. (2003). The tetrapeptide AcSDKP, an inhibitor of primitive hematopoietic cell proliferation, induces angiogenesis in vitro and in vivo. Blood 101(8):3014-3020. PMID 12480715. DOI 10.1182/blood-2002-07-2315
- Sosne G, Qiu P, Goldstein AL, Wheater M (2010). Biological activities of thymosin beta4 defined by active sites in short peptide sequences. FASEB Journal 24(7):2144-2151. PMID 20179146. DOI 10.1096/fj.09-142307
- Azizi M, Ezan E, Nicolet L, Grognet JM, Ménard J (1997). High plasma level of N-acetyl-seryl-aspartyl-lysyl-proline: a new marker of chronic angiotensin-converting enzyme inhibition. Hypertension 30(5):1015-1019. PMID 9369248. DOI 10.1161/01.hyp.30.5.1015
- Azizi M, Ménard J, Peyrard S, Lièvre M, Marre M, Chatellier G (2006). Assessment of patients' and physicians' compliance to an ACE inhibitor treatment based on urinary N-acetyl Ser-Asp-Lys-Pro determination in the DIABHYCAR study. Diabetes Care 29(6):1331-1336. PMID 16732017. DOI 10.2337/dc06-0255
- Mnguni AT, Engel ME, Borkum MS, Mayosi BM (2015). The effects of angiotensin converting enzyme inhibitors (ACE-I) on human N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) levels: a systematic review and meta-analysis. PLoS One 10(12):e0143338. PMID 26656271. DOI 10.1371/journal.pone.0143338
- Mesmin C, Cholet S, Blanchard A, Chambon Y, Azizi M, Ezan E (2012). Mass spectrometric quantification of AcSDKP-NH2 in human plasma and urine and comparison with an immunoassay. Rapid Communications in Mass Spectrometry 26(2):163-172. PMID 22173804. DOI 10.1002/rcm.5326
- ClinicalTrials.gov. NCT00224549, PHARES (Assistance Publique – Hôpitaux de Paris); Ac-SDKP measured only as a marker of tablet taking. Retrieved 23 September 2026. https://clinicaltrials.gov/study/NCT00224549
- ClinicalTrials.gov. NCT01485900, SAR407899A in kidney disease on ACE inhibitors (Sanofi); Ac-SDKP measured only as a marker of ACE inhibition. Retrieved 23 September 2026. https://clinicaltrials.gov/study/NCT01485900
- Zuo Y, Chun B, Potthoff SA, et al. (2013). Thymosin β4 and its degradation product, Ac-SDKP, are novel reparative factors in renal fibrosis. Kidney International 84(6):1166-1175. PMID 23739235. DOI 10.1038/ki.2013.209
- Nitta K, Shi S, Nagai T, et al. (2016). Oral administration of N-acetyl-seryl-aspartyl-lysyl-proline ameliorates kidney disease in both type 1 and type 2 diabetic mice via a therapeutic regimen. BioMed Research International 2016:9172157. PMID 27088094. DOI 10.1155/2016/9172157
- Conte E, Fagone E, Gili E, et al. (2016). Preventive and therapeutic effects of thymosin β4 N-terminal fragment Ac-SDKP in the bleomycin model of pulmonary fibrosis. Oncotarget 7(23):33841-33854. PMID 27029074. DOI 10.18632/oncotarget.8409
- Cavasin MA, Liao TD, Yang XP, Yang JJ, Carretero OA (2007). Decreased endogenous levels of Ac-SDKP promote organ fibrosis. Hypertension 50(1):130-136. PMID 17470726. DOI 10.1161/HYPERTENSIONAHA.106.084103
- Ou H, Chen R, Zhou L, Zhang Y, Zhao S, Yang Z (2026). Thymosin β4-derived peptides alleviate neuroinflammation and neurite atrophy in both in vitro models and in vivo 5×FAD mice. International Immunopharmacology 170:116097. PMID 41443105. DOI 10.1016/j.intimp.2025.116097
- US Food and Drug Administration. Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks; Ac-SDKP not listed. Content current as of 22 April 2026. https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks
- van der Meer P, Lipsic E, Westenbrink BD, et al. (2005). Levels of hematopoiesis inhibitor N-acetyl-seryl-aspartyl-lysyl-proline partially explain the occurrence of anemia in heart failure. Circulation 112(12):1743-1747. PMID 16172283. DOI 10.1161/CIRCULATIONAHA.105.549121
- Le Meur Y, Lorgeot V, Comte L, et al. (2001). Plasma levels and metabolism of AcSDKP in patients with chronic renal failure: relationship with erythropoietin requirements. American Journal of Kidney Diseases 38(3):510-517. PMID 11532682. DOI 10.1053/ajkd.2001.26839
- Azizi M, Ezan E, Reny JL, Wdzieczak-Bakala J, Gerineau V, Ménard J (1999). Renal and metabolic clearance of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) during angiotensin-converting enzyme inhibition in humans. Hypertension 33(3):879-886. PMID 10082503. DOI 10.1161/01.hyp.33.3.879
- US Food and Drug Administration. Bulk drug substances nominated for use in compounding under section 503A (updated 14 May 2026) and 503B (updated 21 March 2025); Ac-SDKP not nominated. https://www.fda.gov/media/94155/download
- Electronic Medicines Compendium (UK). Search for goralatide: no results. Retrieved 23 September 2026. https://www.medicines.org.uk/emc/search?q=goralatide
- Therapeutic Goods (Poisons Standard—June 2026) Instrument 2026, F2026L00633, Australia. No match for goralatide or SDKP; thymosin beta-4 in Schedule 4 and Appendix D; rule that entries cover derivatives. https://www.legislation.gov.au/F2026L00633/latest/text
- Health Canada. Drug Product Database, active ingredient search for goralatide; empty result. Retrieved 23 September 2026. https://health-products.canada.ca/api/drug/activeingredient/?lang=en&type=json&ingredientname=goralatide
- Swissmedic. Extended list of medicinal products (HAM, xlsx); no match for goralatide, seraspenide or SDKP. Retrieved 23 September 2026. https://www.swissmedic.ch/dam/swissmedic/de/dokumente/internetlisten/erweiterte_ham_ind.xlsx.download.xlsx/Erweiterte_Arzneimittelliste%20HAM.xlsx
- Germany. Anti-Doping Act, annex to section 2(3), Federal Law Gazette 2023 I No. 67, section II.3. https://www.gesetze-im-internet.de/antidopg/anlage.html
Cite this page
The facts on this page were checked on 24 September 2026, and the register searches behind the status table were run on 23 September 2026. The anti-doping and Australian classifications rest on interpretation and may change if an authority rules on them.
myPeptides Research & Editing. (2026). Ac-SDKP: what the studies show, status and safety. Version 1.0, 24 September 2026. myPeptides Peptide Register. Retrieved from https://mypep.app/peptides/ac-sdkp
How pages in this register are compiled and graded is described under methodology; the full register is at peptides.
| Version | Date | Note |
|---|---|---|
| 1.0 | 24 September 2026 | Initial publication |