Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline, also called goralatide or seraspenide) is a naturally occurring tetrapeptide made in the body from thymosin beta-4 and normally broken down by angiotensin-converting enzyme (ACE). It is best known as a natural anti-fibrotic signal: it appears to suppress the abnormal collagen buildup (“fibrosis”) linked to heart, kidney, lung, and liver injury in animal studies, and it may explain part of why ACE-inhibitor blood pressure medications also reduce organ fibrosis. Human clinical trial data on administering Ac-SDKP itself as a treatment are essentially absent; almost all direct dosing evidence comes from animal research.
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Research snapshot
| Category | Current information |
|---|---|
| Peptide category | Naturally occurring tetrapeptide, ACE-regulated (thymosin beta-4 fragment) |
| Primary research interest | Anti-fibrotic effects in the heart, kidney, lung, and liver |
| Highest available evidence | Published animal research (rodent fibrosis models); human data limited to observational plasma-level measurements |
| Human research available | No interventional trial administering Ac-SDKP itself; only observational measurements of endogenous plasma levels (e.g., during ACE-inhibitor therapy) |
| Development status | Not known to be in active pharmaceutical development; research/mechanistic-study compound |
| Regulatory status | Not FDA-approved |
| Last reviewed | September 27, 2026 |
Peptide category: naturally occurring, endogenous tetrapeptide (ACE substrate). Primary research interest: anti-fibrotic and anti-inflammatory effects in heart, kidney, lung, and liver injury models. Highest available evidence: published animal (rodent) research and laboratory/mechanistic studies; human evidence is limited to observational measurement of endogenous plasma Ac-SDKP levels (for example, during ACE-inhibitor therapy), not administered-dose clinical trials. Human research available: no identified completed clinical trial administering Ac-SDKP as a drug to treat a fibrotic condition. Development status: not in active pharmaceutical development as a marketed drug candidate as far as could be verified; remains a basic-science and translational research molecule. Regulatory status: not FDA-approved; not a marketed drug. Last reviewed: 2026-09-20.
Technical identity
| Technical property | Information |
|---|---|
| Primary name | Ac-SDKP |
| Alternative names | Goralatide, Seraspenide (brand names), N-acetyl-seryl-aspartyl-lysyl-proline, thymosin beta-4 fragment (1-4) |
| Peptide sequence | Ac-Ser-Asp-Lys-Pro (N-acetyl-Ser-Asp-Lys-Pro) |
| Amino-acid length | 4 residues |
| Molecular formula | C20H33N5O9 |
| Molecular weight | Approximately 487.51 g/mol |
| CAS Registry Number | 120081-14-3 |
| PubChem CID | 65938 |
| Chemical modifications | N-terminal acetylation |
| Peptide class | Natural ACE substrate tetrapeptide, fragment of thymosin beta-4 |
| Primary biological target | No single, confirmed human cell-surface receptor definitively established; degraded by angiotensin-converting enzyme (ACE) |
| Developer or originator | Naturally occurring peptide, first characterized as a hematopoietic stem cell inhibitory factor; not a single-company pharmaceutical candidate as far as could be verified |
| Development status | Research/mechanistic-study compound; no known active clinical development |
Primary name: Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline). Alternative names: goralatide (INN), seraspenide, thymosin beta-4 fragment (1-4)-related tetrapeptide (Ac-SDKP is derived from the N-terminal region of thymosin beta-4, whose first four residues are Ser-Asp-Lys-Pro, acetylated at the N-terminus). Peptide sequence: Ac-Ser-Asp-Lys-Pro (4 amino acids). Amino-acid length: 4. Molecular formula: C20H33N5O9. Molecular weight: approximately 487.51 g/mol. CAS Registry Number: 120081-14-3. PubChem CID: 65938 (listed under “Goralatide”). Peptide class: acetylated linear tetrapeptide. Primary biological target: functions as a physiological substrate of the N-terminal catalytic domain of angiotensin-converting enzyme (ACE), which degrades it; its own downstream anti-fibrotic signaling has been linked in animal/mechanistic research to reduced TGF-beta/Smad signaling and altered collagen turnover, though a single confirmed human receptor has not been established. Developer/originator: naturally occurring peptide first characterized as a hematopoietic stem cell inhibitory factor; not a single-company pharmaceutical candidate as far as could be verified from the sources reviewed.
What is Ac-SDKP?
Ac-SDKP is a very short, four-amino-acid peptide that the body makes naturally by clipping it off the front end of a larger protein called thymosin beta-4. It circulates at low but measurable levels in blood and tissue, and it is normally broken down fairly quickly by angiotensin-converting enzyme (ACE) — the same enzyme targeted by ACE-inhibitor blood pressure medications like lisinopril or enalapril. Because ACE inhibitors block the enzyme that normally destroys Ac-SDKP, they cause plasma Ac-SDKP levels to rise several-fold, a finding that has been directly measured in human blood samples during ACE-inhibitor therapy.
Ac-SDKP was first identified for its ability to keep blood-forming stem cells in a resting (non-dividing) state, an original research interest tied to protecting bone marrow cells during chemotherapy. Over subsequent decades, research attention shifted substantially toward a different property: its apparent ability to reduce or prevent fibrosis (excess scar-tissue-like collagen deposition) in multiple organs after injury, including the heart after a heart attack, the kidney after obstruction or hypertension-related damage, the lungs after silica exposure, and the liver after bile duct injury.
This anti-fibrotic research interest connects directly to why ACE inhibitors are already used clinically: part of their benefit in protecting the heart and kidneys during chronic disease is thought to come not only from lowering blood pressure but potentially also from allowing natural Ac-SDKP levels to rise, since Ac-SDKP is one of the natural substrates ACE would otherwise degrade. Researchers have studied whether directly administering Ac-SDKP (rather than relying on ACE inhibition to raise it indirectly) could reproduce or enhance this anti-fibrotic effect — but this work has been conducted almost entirely in animal models, not in human clinical trials.
Ac-SDKP has no approved therapeutic use and is not in active late-stage pharmaceutical development as far as could be verified; it remains primarily a subject of translational and mechanistic research into fibrosis biology.
How does it work?
Plain-English explanation
Ac-SDKP appears to act like a natural “brake” on the process that lays down excess scar tissue after organ injury. In animal studies, giving extra Ac-SDKP reduces the amount of collagen (the main scar-tissue protein) that builds up in damaged hearts, kidneys, lungs, and livers, and it also appears to calm some of the inflammation and cell-death signals that drive that scarring in the first place.
Technical explanation
Ac-SDKP is a physiological substrate of the N-domain active site of angiotensin-converting enzyme (ACE), which hydrolyzes and inactivates it; ACE inhibition (or genetic ACE N-domain modification) raises circulating and tissue Ac-SDKP concentrations. In animal fibrosis models, Ac-SDKP administration has been reported to reduce transforming growth factor-beta (TGF-beta)/Smad2/3 signaling, reduce collagen I/III deposition and myofibroblast (fibroblast-to-myofibroblast) transformation, and in some models reduce apoptosis of epithelial cells (for example, alveolar type II cells in silicotic lung injury) via effects on endoplasmic reticulum stress pathways. It has also been reported to have pro-angiogenic (new blood vessel-promoting) activity and to interact with components of the ACE2-angiotensin-(1-7)-Mas receptor axis in some pulmonary fibrosis models, an axis generally considered counter-regulatory to the classical, pro-fibrotic renin-angiotensin pathway. These mechanisms are derived from cell-culture and animal-model research; a single, confirmed cell-surface receptor mediating Ac-SDKP’s anti-fibrotic signaling in humans has not been definitively established in the sources reviewed.
Potential benefits and research applications
Cardiac fibrosis after myocardial infarction
What is being investigated: whether Ac-SDKP reduces pathological scarring (fibrosis) and improves healing in the heart after a heart attack. How the effect might occur: reduced TGF-beta-driven collagen deposition and myofibroblast activity, and reduced cardiac rupture risk in some models. Evidence: a published review (Cavasin, 2006, PMID 17083265) summarizing preclinical data reports that Ac-SDKP reduced left ventricular fibrosis in hypertensive rats, reduced fibrosis and inflammation after myocardial infarction in rats, and reduced cardiac rupture rate in mice post-infarction — but this same review explicitly states that “there are no data available from a clinical trial supporting the use of thymosin-beta4 or Ac-SDKP” for cardiac healing in patients. Strength: Tier 3 (published animal research) for the anti-fibrotic effect; no human interventional evidence exists. Limitation: rodent-model findings on cardiac remodeling do not automatically translate to human infarct healing, and no human dosing trial has tested this application.
Renal (kidney) fibrosis
What is being investigated: whether Ac-SDKP reduces fibrosis following kidney injury such as ureteric obstruction or hypertension-related damage. How the effect might occur: reduced TGF-beta/Smad signaling and collagen deposition in renal tissue. Evidence: published animal studies, including work on Ac-SDKP mediating some of the anti-fibrotic properties of the ACE inhibitor captopril in a mouse model of unilateral ureteric obstruction. Strength: Tier 3 (animal research); this connects mechanistically to why ACE inhibitors are already used clinically to slow kidney disease progression in humans, but that clinical benefit has not been directly attributed to Ac-SDKP levels in a human interventional trial. Limitation: human plasma Ac-SDKP elevation during ACE-inhibitor therapy has been measured (Tier 2, observational), but this documents a correlation, not proof that Ac-SDKP itself, apart from ACE inhibition’s other effects, drives the renal benefit.
Pulmonary (lung) fibrosis, including silicosis
What is being investigated: whether Ac-SDKP can reduce or reverse fibrotic lung scarring, including in silica-induced silicosis models. How the effect might occur: proposed suppression of alveolar epithelial cell apoptosis via reduced endoplasmic reticulum stress, and interaction with the protective ACE2-angiotensin-(1-7)-Mas signaling axis. Evidence: published rat silicosis studies report reduced fibrotic markers and epithelial cell death with Ac-SDKP administration. Strength: Tier 3 (animal research only). Limitation: no human silicosis or pulmonary fibrosis trial administering Ac-SDKP was identified.
Liver fibrosis
What is being investigated: whether Ac-SDKP reduces fibrosis following bile duct ligation or other liver injury models. How the effect might occur: reduced hepatic stellate cell activation and collagen deposition, and in more recent mechanistic work, modulation of an RNA methylation (m6A)/Hedgehog signaling pathway. Evidence: published rat bile-duct-ligation studies and cell-based mechanistic studies. Strength: Tier 3-4 (animal and laboratory/mechanistic research). Limitation: entirely preclinical; no human liver fibrosis trial of Ac-SDKP was identified.
What dosage information circulates?
Figures in this section summarize amounts and schedules reported in published research or circulating online. Their inclusion documents what is reported and does not establish that a regimen is verified, safe, effective, or appropriate.
| Reported use or research objective | Route reported | Amount reported | Frequency reported | Reported duration | Evidence or source category |
|---|---|---|---|---|---|
| Any administered human use | Not applicable | No established or reliably sourced dosing information was identified | Not applicable | Not applicable | Not established — no completed human clinical trial administering Ac-SDKP exists; human data are observational endogenous plasma-level measurements only |
| Cardiac, renal, pulmonary, and hepatic fibrosis models | Subcutaneous osmotic minipump infusion or injection | Microgram-per-kilogram-per-day to low-milligram-per-kilogram-per-day range; varies by study and organ system, no single standard reference figure | Continuous infusion or repeated injection | Days to several weeks, depending on the injury model | Published animal research (rodent) |
| General oral-capsule “research compound” framing, sometimes marketed as “thymosin beta-4 fragment 1-4” | Oral | Vendor-suggested amounts not derived from any published human clinical dosing study | Not established | Not established | Widely repeated online, but its original source could not be verified; oral bioavailability itself is unconfirmed, since the animal literature used injected or infused routes |
Amounts studied in human research
No established or reliably sourced dosing information was identified. No completed human clinical trial administering Ac-SDKP as a treatment (at any specified dose, route, or schedule) was identified in the sources reviewed for this entry. The human data that exist are observational measurements of naturally occurring plasma Ac-SDKP concentrations (for example, before and during ACE-inhibitor drug therapy), not interventional dosing of the peptide itself.
Amounts studied in animal research
Published rodent studies have administered Ac-SDKP by routes including subcutaneous osmotic minipump infusion and injection, at doses in the microgram-per-kilogram-per-day to low-milligram-per-kilogram-per-day range in various fibrosis models (cardiac, renal, pulmonary, hepatic), typically over days to several weeks depending on the injury model. Exact amounts, routes, and durations vary meaningfully across studies and organ systems, and no single dose has emerged as a standard reference figure across the literature; readers should consult the specific primary study for any given model rather than assuming one dose applies across all reported research.
Practitioner and community-reported protocols
Ac-SDKP (sometimes marketed under names referencing “thymosin beta-4 fragment 1-4”) is sold by some peptide and supplement vendors, including in oral capsule form, with vendor-suggested amounts that do not derive from any published human clinical dosing study identified in this review. Widely repeated online, but its original source could not be verified, particularly regarding oral bioavailability, since the animal research reviewed for this entry primarily used injected or infused routes rather than oral administration.
What circulates E5
Ac-SDKP (sometimes marketed under names referencing "thymosin beta-4 fragment 1-4") is sold by some peptide and supplement vendors, including in oral capsule form, with vendor-suggested amounts that do not derive from any published human clinical dosing study identified in this review. Widely repeated online, but its original source could not be verified.
This is a particular concern for Ac-SDKP because the animal research behind it used injected or infused routes, not oral dosing, so an oral vendor product's relationship to any studied amount is unclear rather than simply unconverted.
Recorded as an observation about what is published elsewhere. No figure here is a dose, a protocol, or a recommendation, and nothing in this section is evidence that any amount is safe or effective.
Side effects, risks, and limitations
Because no human clinical trial administering Ac-SDKP as a drug was identified, there is no established human safety or side-effect profile for the peptide when directly administered. Ac-SDKP is a normal, naturally occurring substance in the body, and animal studies reviewed did not report significant systemic toxicity at the doses studied, but this does not establish human safety at any given dose, route, or duration. Products sold as “Ac-SDKP” or related fragment names by supplement or peptide vendors carry the general risks of unregulated products: unverified purity and identity, uncertain and unverified oral bioavailability (a four-amino-acid peptide is generally expected to be poorly absorbed and rapidly degraded if swallowed, though this was not specifically confirmed for Ac-SDKP in the sources reviewed), inconsistent concentration, and no sterility assurance for injectable-labeled products not manufactured under pharmaceutical-grade controls.
Regulatory and developmental status
Ac-SDKP (goralatide) is not FDA-approved and is not, as far as could be verified from the sources reviewed, currently in active late-stage pharmaceutical development as a fibrosis treatment; it functions in the literature primarily as a research tool for understanding fibrosis biology and as a partial mechanistic explanation for some of the organ-protective effects of already-approved ACE-inhibitor drugs. No registered human clinical trial administering Ac-SDKP as an investigational drug was identified. Status verified: 2026-09-20.
Frequently asked questions
What is Ac-SDKP?
Ac-SDKP is a naturally occurring, four-amino-acid peptide made from thymosin beta-4 that is normally broken down by angiotensin-converting enzyme (ACE) and has been studied mainly in animals for its ability to reduce organ fibrosis (scarring).
How does Ac-SDKP work?
It is thought to reduce fibrotic signaling (particularly TGF-beta-driven collagen production) in injured tissue, and it naturally accumulates when ACE — the enzyme that normally degrades it — is inhibited, such as during ACE-inhibitor blood pressure medication use.
Has Ac-SDKP been studied in human clinical trials?
No completed human clinical trial administering Ac-SDKP itself was identified. Human data are limited to observational measurements of the body’s own Ac-SDKP levels, for example during ACE-inhibitor therapy.
What dosage has been studied for Ac-SDKP?
No established or reliably sourced human dosing information was identified. Animal studies have used a range of injected or infused doses that vary by organ system and injury model.
What dosage commonly circulates online for Ac-SDKP?
Some vendors sell oral or injectable “Ac-SDKP” products with suggested amounts, but these figures could not be traced to any published human clinical study and are widely repeated online without a verifiable original source.
Is Ac-SDKP the same as thymosin beta-4?
No. Ac-SDKP is a much smaller, four-amino-acid fragment derived from the N-terminal end of the larger thymosin beta-4 protein; the two molecules are related but distinct.
Does taking an ACE inhibitor raise Ac-SDKP levels?
Yes. Published research has directly measured several-fold increases in plasma Ac-SDKP in people taking ACE-inhibitor medications, since ACE is the enzyme that normally breaks Ac-SDKP down.
Is Ac-SDKP approved as a medicine?
No. It is not FDA-approved and is not known to be in active late-stage clinical development; it remains a research and mechanistic-study molecule.
What remains unknown about Ac-SDKP?
Whether directly administering Ac-SDKP to humans would be safe or effective for any fibrotic condition, what an appropriate human dose or route would be, and whether its oral bioavailability supports the oral products currently sold under its name are all unresolved.
Bottom line
Ac-SDKP is a well-documented, naturally occurring tetrapeptide with a substantial and consistent body of animal research supporting an anti-fibrotic role across the heart, kidney, lung, and liver, and a plausible mechanistic link to why ACE-inhibitor medications may help protect organs beyond their blood-pressure-lowering effect. What is genuinely published is this animal and mechanistic evidence, plus human observational data on endogenous Ac-SDKP levels rising during ACE-inhibitor therapy. What is not established, and should not be assumed, is any human clinical dosing, safety, or efficacy data for administering Ac-SDKP itself as a treatment — a 2006 published review explicitly noted the absence of clinical trial data for this purpose, and no evidence was found that this gap has since been closed. Any commercial “Ac-SDKP” product’s suggested human use is not supported by clinical evidence.
