Ac-SDKP (Goralatide) — Safety, Research, Risks & Legal Status

Not medical advice. Ac-SDKP (Goralatide) is discussed here for informational and harm-reduction purposes only. We do not endorse use, and any dosing context is informational, not a protocol.

Also known as	Goralatide; Seraspenide; Thymosin Beta-4 Fragment (1-4); TB4 Fragment (1-4); N-acetyl-seryl-aspartyl-lysyl-proline
Category	Peptide (research chemical)
CAS Number	120081-14-3
Structure	Tetrapeptide: N-acetyl-Ser-Asp-Lys-Pro
Endogenous source	Cleaved from thymosin beta-4 by meprin-alpha and prolyl oligopeptidase (POP)
IV half-life	Approximately 4.5 minutes; degraded by angiotensin-converting enzyme (ACE)
Developer	Ipsen SA; INN designation: goralatide
Development stage	Investigational; Phase II documented in limited context; no published human therapeutic trial results
US legal status	Not FDA-approved for any indication. Ac-SDKP (goralatide) is an investigational peptide with no approved therapeutic use in the United States. It is not classified as a dietary supplement under DSHEA. It is commercially available as a research reagent and is sold by some vendors as a "wellness peptide," but these sales are not regulated under a pharmaceutical framework. It is not a DEA-controlled substance. Any human use outside a clinical trial would occur outside regulated channels. Development is ongoing under Ipsen SA.

What is Ac-SDKP (Goralatide)?

Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline; CAS 120081-14-3) is an endogenous tetrapeptide produced in the body via enzymatic cleavage of thymosin beta-4 by meprin-alpha and prolyl oligopeptidase (POP). It is a natural substrate for angiotensin-converting enzyme (ACE), which rapidly degrades it. Preclinical evidence positions it as an anti-fibrotic, anti-inflammatory, and pro-angiogenic agent with a possible role in regulating hematopoietic stem cell proliferation. It has an INN designation (goralatide) and is under development by Ipsen SA, though no human therapeutic efficacy data have been published as of the knowledge cutoff.

How it works

Ac-SDKP is generated endogenously from thymosin beta-4 via sequential cleavage by meprin-alpha (at the kidney) and prolyl oligopeptidase, establishing the Tbeta4-POP-Ac-SDKP axis. Its primary pharmacological actions in preclinical models include: (1) blockade of TGF-beta/Smad signaling, the central pathway driving organ fibrosis and myofibroblast differentiation; (2) suppression of fibroblast proliferation and collagen deposition; (3) attenuation of endoplasmic reticulum (ER) stress-stimulated collagen production in cardiac fibroblasts; (4) inhibition of NF-kappaB-mediated inflammatory signaling; (5) promotion of angiogenesis and tissue remodeling; and (6) negative regulation of hematopoietic stem cell cycling. Because ACE degrades Ac-SDKP, ACE inhibitor drugs elevate circulating Ac-SDKP levels, which may contribute to some of the organ-protective effects observed with ACE inhibition beyond blood pressure control.

Background & history

Ac-SDKP was first characterized as an endogenous hematopoietic inhibitor, identified as a regulator of stem cell proliferation in bone marrow. Its connection to thymosin beta-4 as a precursor peptide and to ACE as a degrading enzyme was established through work in the 1990s and 2000s. The observation that ACE inhibitors increase systemic Ac-SDKP levels prompted investigation of its anti-fibrotic properties across multiple organ systems. Ipsen SA acquired or developed the compound under the INN goralatide. As of available records, the compound has reached Phase II status in at least one context (a diagnostic application in chronic kidney disease for glomerular filtration rate testing), though published therapeutic trial results are not available in the open literature. The compound remains investigational.

What the research says

Preclinical evidence is substantial across multiple fibrosis models but human clinical data are essentially absent from the public literature. In animal models: bleomycin-induced pulmonary fibrosis in mice showed decreased mortality, inflammation, lung damage, and fibrosis with Ac-SDKP treatment (PMC5085123); cardiac fibrosis models including post-MI, renovascular hypertension, and radiation injury in rats demonstrated fibrosis reversal and improved cardiac function; kidney fibrosis models in renovascular hypertension showed reduced glomerular fibrosis and proteinuria; liver fibrosis preclinical models showed antifibrotic effects; a spinal cord injury model showed improved functional recovery. Mechanistic studies support ER stress attenuation in cardiac fibroblasts as an additional pathway. The Tbeta4-POP-Ac-SDKP axis has been reviewed as a unifying framework for organ fibrosis (PMC9655242). No published human clinical efficacy trial results have been located. Phase II documentation exists for a diagnostic (GFR testing) context. Human tolerability data are described as early-phase and limited. The gap between extensive preclinical data and the near-complete absence of published human evidence is notable and means all claimed therapeutic effects should be treated as unconfirmed in humans.

Reported effects

Anti-fibrotic in multiple organ systems in animal models (lung, heart, kidney, liver) - not confirmed in human trials
Suppression of TGF-beta/Smad-driven myofibroblast differentiation and collagen synthesis (preclinical)
Reduction of NF-kappaB-mediated inflammatory signaling (preclinical)
Attenuation of ER stress-stimulated collagen production in cardiac fibroblasts (preclinical, in vitro)
Pro-angiogenic and tissue remodeling effects (preclinical)
Negative regulation of hematopoietic stem cell proliferation (endogenous role, preclinical characterization)
Improved functional recovery in spinal cord injury model (single preclinical study)

Dosing & administration (informational)

Published animal studies use a range of doses administered by infusion or injection, reflecting the compound's very short IV half-life (approximately 4.5 minutes) and the impracticality of oral administration. These figures are reported here as literature context only and do not constitute a protocol or recommendation. No human dosing regimen has been established or validated in published clinical trials. Formulation for human use presents significant challenges due to rapid enzymatic degradation. Anyone considering Ac-SDKP for any purpose should consult a licensed clinician and, where applicable, enroll in a controlled clinical trial.

This is general research/context information, not medical advice or a recommended protocol.

Safety & side effects

No major toxicity or carcinogenicity signals identified in preclinical studies
As an endogenous peptide derived from thymosin beta-4, theoretical immunogenicity risk may be lower than fully synthetic peptides, though this is not formally characterized
IV half-life of approximately 4.5 minutes due to ACE degradation; rapid clearance may limit systemic accumulation but complicates administration
Oral bioavailability is expected to be very low due to peptide degradation in the GI tract - a general limitation of unprotected tetrapeptides
Potential pharmacokinetic interaction with ACE inhibitors: co-administration could substantially elevate Ac-SDKP levels by blocking its degradation; clinical implications unknown
No formal human adverse-event database exists; long-term safety profile is unknown
No published data on immunogenicity, hypersensitivity, or off-target effects in human subjects

Drug & supplement interactions

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Who should avoid it

Concurrent ACE inhibitor use without medical supervision due to unpredictable pharmacokinetic amplification
Use in individuals with active hematologic conditions given the compound's role as a hematopoietic stem cell proliferation inhibitor
Use during pregnancy or lactation - no safety data exist
Self-administration outside of a clinical trial context given the complete absence of human safety and efficacy data
Oral administration without validated formulation - peptide degradation renders unprotected oral peptides essentially inactive

How it is commonly combined

No clinical stacking data exist. In preclinical contexts, the compound's mechanism overlaps with TGF-beta pathway inhibitors and ACE inhibitors. Any combination would be speculative and should be considered only within a controlled research setting. The interaction with ACE inhibitors is mechanistically significant and likely not additive in a straightforward way - it represents a pharmacokinetic confound, not a complementary mechanism.

Legal & regulatory. Not FDA-approved for any indication. Ac-SDKP (goralatide) is an investigational peptide with no approved therapeutic use in the United States. It is not classified as a dietary supplement under DSHEA. It is commercially available as a research reagent and is sold by some vendors as a "wellness peptide," but these sales are not regulated under a pharmaceutical framework. It is not a DEA-controlled substance. Any human use outside a clinical trial would occur outside regulated channels. Development is ongoing under Ipsen SA.

Quality & harm reduction

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Frequently asked questions

What is Ac-SDKP and where does it come from?

Ac-SDKP is a naturally occurring tetrapeptide (four amino acids: serine, aspartate, lysine, proline, with an N-terminal acetyl group) produced in the body by enzymatic cleavage of a larger protein called thymosin beta-4. It is found endogenously in human plasma and urine. It is rapidly degraded by angiotensin-converting enzyme (ACE), which is why ACE inhibitor drugs are known to increase circulating Ac-SDKP levels.

What has research shown about Ac-SDKP's anti-fibrotic effects?

Preclinical animal studies have shown anti-fibrotic effects across multiple organ systems including the lungs, heart, kidneys, and liver. These studies demonstrate reduction in collagen deposition, suppression of TGF-beta signaling, and improved organ function in fibrosis models. However, no published human clinical trial has confirmed these effects in people. All therapeutic claims remain unvalidated in human subjects as of the current evidence base.

Is Ac-SDKP approved or legal to use?

Ac-SDKP is not approved by the FDA for any therapeutic indication. It has no supplement status under DSHEA. It is sold commercially as a research reagent and by some wellness peptide vendors, but these sales are unregulated from a pharmaceutical standpoint. It is not a controlled substance. Any human use outside an approved clinical trial falls outside established regulatory frameworks.

What is the recommended dose of Ac-SDKP?

No established human dosing protocol exists. Animal research doses are available in the literature but are not translatable to human use without formal pharmacokinetic and safety studies. The compound's very short half-life (approximately 4.5 minutes by IV) and poor oral bioavailability present substantial formulation challenges. Dosing questions should be directed to a licensed clinician or addressed only within the context of a clinical trial.

Does Ac-SDKP interact with other drugs?

The most significant known interaction is with ACE inhibitors such as lisinopril or enalapril. ACE is the enzyme that degrades Ac-SDKP, so ACE inhibitors substantially elevate endogenous Ac-SDKP levels. Taking exogenous Ac-SDKP alongside an ACE inhibitor could produce unpredictably elevated exposure. Interactions with other anti-fibrotic drugs, hematopoietic agents, or immunosuppressants have not been studied.

Is Ac-SDKP safe?

No major toxicity signals have emerged from preclinical studies, and its endogenous nature suggests some baseline compatibility with human biology. However, no formal human adverse-event data are published, long-term safety is unknown, and immunogenicity has not been characterized. The absence of reported toxicity in animal studies should not be interpreted as a human safety clearance. Self-administration outside clinical supervision is not supported by the available evidence.

References & further reading

PubMed: "Preventive and therapeutic effects of thymosin beta4 N-terminal fragment Ac-SDKP in the bleomycin model of pulmonary fibrosis" PMC5085123
PubMed: "The Role of Tbeta4-POP-Ac-SDKP Axis in Organ Fibrosis" International Journal of Molecular Sciences 23(21) PMC9655242
PubMed: "The anti-inflammatory peptide Ac-SDKP is released from thymosin-beta4 by renal meprin-alpha and prolyl oligopeptidase" American Journal of Physiology - Renal Physiology
PubMed: "Ac-SDKP attenuates ER stress-stimulated collagen production in cardiac fibroblasts" Frontiers in Pharmacology 2024
ClinicalTrials.gov: search goralatide OR Ac-SDKP for current trial status; NCATS Inxight Drugs entry GORALATIDE (H041538E9P) for regulatory summary