Ac-SDKP: research

An experimental repair peptide with old human studies, but no proven healing dose.

Also called: AcSDKP, Goralatide, Seraspenide, N-acetyl-seryl-aspartyl-lysyl-proline, Thymosin beta-4 fragment 1–4, TB4-Frag.

Healing and repair peptides · Endogenous tetrapeptide; thymosin beta-4 N-terminal fragment.

Four direct-dose records in the reviewed corpus. Biomarker studies, analogue studies, registries and reviews are excluded from that count. Cohorts may overlap.

Studies

• Early chemotherapy trial. crossover-rct, n=53, 53 cancer patients receiving single-drug cytarabine or ifosfamide. The abstract reports better peripheral blood-cell protection; no per-arm counts or effect sizes are given. (source)
• Chemotherapy trial: no clear protection. rct, n=84, Locally advanced, nonmetastatic head/neck or esophageal squamous cancer. Across 221 chemotherapy cycles, no significant difference in blood-count nadirs or duration of low counts was reported. (source)
• Human uptake and clearance. pk-study, n=11, Six healthy volunteers and five patients receiving chemotherapy. After IV infusion, mean half-life was 4.5 minutes. SC uptake was 100%; IM uptake was 81%. (source)
• Brief infusion and ACE genotype. pk-study, n=24, 12 DD and 12 II ACE-genotype normotensive adults. Exogenous Ac-SDKP broke down slightly faster in DD subjects only without captopril; baseline peptide levels did not differ. (source)
• Captopril raises natural Ac-SDKP. crossover-rct, n=8, Healthy adults. Plasma Ac-SDKP rose 5.5-fold, range 4–8.5-fold; hydrolysis was inhibited 90–99%. (source)
• ACE inhibition and renal clearance. cohort, Healthy adults and people with impaired kidney function. Plasma rose 4-fold after one dose and 4.8-fold after 7 days. With kidney failure, chronic ACE-I levels were 22 times controls. (source)
• Kidney disease and anemia risk. cohort, n=176, 120 hemodialysis and 56 nondialysis patients; 39 used ACE inhibitors. Without ACE-I: 10.3 ± 3.9 pmol/mL on dialysis, 3.1 ± 1.8 off dialysis, versus 1.8 ± 0.2 in controls. ACE-I increased levels fourfold. (source)
• Heart failure and low red cells. cohort, n=98, Advanced stable heart failure on ACE inhibitors; 10 anemic matched to 10 nonanemic patients. Anemic patients had higher Ac-SDKP and 73% lower ACE activity. Their serum inhibited red-cell progenitor growth by 17%. (source)
• Perindopril dose-response marker. crossover-rct, n=32, Healthy male volunteers with mild sodium depletion. Urinary Ac-SDKP rose with dose: median differences over 48 hours were 49.1 nmol for 14 vs 10 mg and 73.2 nmol for 20 vs 14 mg. (source)
• Lisinopril and fibrosis markers. cohort, n=66, African American adults with hypertension and left ventricular thickening. Ac-SDKP was higher with detectable lisinopril; the adjusted association had P<0.001. This did not test Ac-SDKP therapy. (source)
• Urine test for ACE-I adherence. cohort, Healthy volunteers and a prospective hypertensive outpatient cohort. Urine Ac-SDKP detected ACE-I adherence with sensitivity 92.2% and specificity 100% versus active metabolites. (source)
• Kidney-function marker in diabetes. cohort, n=21, Normoalbuminuric diabetes with eGFR at least 30 mL/min/1.73 m². The higher urinary Ac-SDKP group had more stable eGFR over about 4 years, P=0.003. Association does not establish benefit from dosing. (source)
• Ac-SDKP after kidney transplant. cohort, n=40, Japanese recipients more than 90 days after kidney transplant. Peptide levels correlated with creatinine clearance and differed between recipients with and without renal anemia. (source)
• Kidney recovery lowers peptide levels. cohort, n=14, First kidney-transplant recipients with end-stage kidney disease. Ac-SDKP fell significantly from day 3 after transplant. Creatinine clearance was the only independent associated factor. (source)
• Salt restriction changes Ac-SDKP. crossover-rct, n=46, Nondiabetic proteinuric chronic kidney disease. Lower sodium increased Ac-SDKP during single and dual blockade, P=0.032 and P=0.042. (source)
• Ac-SDKP in pericardial fluid. cohort, Patients with tuberculous pericardial effusion. Clinical biomarker letter; the accessible PubMed record has no abstract. Numerical results were not extracted. (source)
• Blood assay in kidney failure. cohort, Healthy subjects and patients with chronic renal failure. Plasma immunoreactive Ac-SDKP was 0.92 ± 0.39 pmol/mL in renal failure versus 0.29 ± 0.07 in healthy subjects. (source)
• Dialysis lowers blood Ac-SDKP. cohort, n=9, Hemodialysis patients. Concentrations were 0.59 ± 0.23 ng/mL before versus 0.44 ± 0.19 after dialysis. All nine decreased. (source)
• ACE-I levels in dialysis patients. cohort, n=69, 7 healthy adults; 34 dialysis controls; 10 enalapril and 18 trandolapril users. Ac-SDKP: 27.3 ± 24.6 ng/mL with enalapril; 12.3 ± 16.9 with trandolapril; 0.6 ± 0.2 in dialysis controls; 0.4 ± 0.2 healthy. (source)
• Blood levels in blood cancers. cohort, People with hematologic malignancies. The title reports elevated plasma levels in some patients. No abstract or numerical findings were available. (source)
• Peptide levels in tumor tissues. cohort, Human thyroid lesions, blood samples and cancer tissue arrays. Higher Ac-SDKP expression was found in several tumor tissues and tumor blood. This does not prove that dosing causes cancer. (source)
• DIABHYCAR adherence substudy. cohort, n=1871, Participants with type 2 diabetes and microalbuminuria/proteinuria. Median urine peptide/creatinine was six times higher with ramipril. Biomarkers suggested poor adherence in 27.3% of 597 eligible ramipril users. (source)
• Peptide levels in thyroid lesions. cohort, n=20, 10 benign nodular goiters and 10 papillary thyroid cancers. Ac-SDKP tissue levels were five times higher in malignant than benign lesions. This is an association. (source)
• Vasopeptidase inhibitor biomarker. crossover-rct, Normotensive adults on low- or high-sodium diets. 24-hour urine Ac-SDKP: AVE7688 25 mg, 919 nmol; 5 mg, 706 nmol; ramipril 10 mg, 511 nmol. (source)
• Omapatrilat biomarker comparison. crossover-rct, n=24, Normotensive volunteers with sodium depletion or repletion. Urine Ac-SDKP showed ACE inhibition lasted longer with omapatrilat than fosinopril. (source)
• Adherence testing in heart failure. rct, n=39, Chronic heart failure. For full nonadherence versus adherence, plasma Ac-SDKP was 89% sensitive and 100% specific; urine was 92% and 97%. (source)
• Natural peptide marks ACE inhibition. cohort, n=50, 27 hypertensive ACE-I users and 23 matched nonusers. Geometric mean Ac-SDKP: 3.78 pmol/mL, range 1.48–14.5, with ACE-I; 0.75, range 0.36–1.22, without. (source)
• Enalapril changes blood progenitors. open-label, n=12, Healthy volunteers. Ac-SDKP rose 2–5-fold; mixed progenitors rose 100%, while red-cell and granulocyte-monocyte progenitors fell 16% and 26%. (source)
• Natural peptide during 5-FU. cohort, n=14, Cancer patients on 5-fluorouracil. Ac-SDKP did not vary significantly during either course. (source)
• Natural peptide during AML therapy. cohort, n=20, Acute myeloid leukemia during high-dose cytoreduction. 12/20 had an early sharp peptide rise; nine peaked in the first 3 days. (source)
• Early survey of natural blood levels. cohort, Healthy controls, HIV patients and people with blood disorders. 34 healthy controls had serum levels of 0.7–2.5 pmol/mL. Levels were raised in about one-third of subjects with blood disorders. (source)
• Peptide marker in coronary disease. cohort, n=112, 72 adults with coronary disease/hypertension and 40 healthy controls. Cytokine and vascular-marker differences tracked ACE-inhibition strata. No direct Ac-SDKP treatment comparison. (source)
• Blood and marrow findings in AML. cohort, n=33, Acute myeloid leukemia patients providing serum and marrow stromal cells. Serum Ac-SDKP was higher than controls, P<0.05. In culture, added Ac-SDKP increased marrow stromal-cell proliferation. (source)
• PHARES adherence analysis. cohort, n=164, Adults with resistant hypertension. Natural Ac-SDKP helped assess medication adherence; it was not given as a treatment. (source)
• ACE inhibitors raise natural levels. meta-analysis, n=206, Four studies with 206 participants. Mean plasma increase: healthy adults 5.07 pmol/mL, 95% CI 0.64–9.51; renal failure 8.94 pmol/mL, 95% CI 2.55–15.33. (source)
• Kidney tracer: different molecule. open-label, n=100, Healthy adults and adults with chronic kidney disease. This studies AcSDKP-NH2 as a kidney-function marker, not Ac-SDKP for healing. (source)
• PHARES: biomarker only. rct, n=180, Resistant hypertension. Registry match reflects measurement of natural Ac-SDKP, not dosing it. (source)
• SAR407899A: biomarker only. rct, n=20, Moderate kidney disease on stable ACE-I. Registry match reflects measurement of natural Ac-SDKP, not dosing it. (source)
• New blood vessels in rats. animal, Rat cornea and heart models; mouse endothelial cells. Ac-SDKP increased cell migration, tube formation, corneal vessels and heart capillary density. (source)
• Less kidney scarring in mice. animal, Male BALB/C mice with unilateral ureter obstruction. Ac-SDKP reduced kidney scarring markers in an obstructed-kidney model. (source)
• Heart-injury repair in mice. animal, C57BL/6J mice after experimentally induced heart attack. Cardiac rupture and later scarring were reduced; heart structure and function improved. (source)
• Skin and hair experiments. in-vitro, Human cell cultures, skin explants and isolated hair follicles. Cultured skin and hair cells grew more; skin explants showed thicker epidermis and isolated follicles grew longer. (source)
• Gut inflammation in mice. animal, Experimental mouse colitis and intestinal cell cultures. Ac-SDKP reduced experimental gut inflammation through MEK-ERK signaling. (source)
• Repair and cell injury can coexist. animal, Aristolochic-acid kidney injury in mice; human tubular cells in culture. Early dosing protected kidney vessels and reduced scarring; in severely injured tubular cells, Ac-SDKP increased cell death. (source)

Gaps: No human repair, tendon-healing or antifibrotic efficacy trial was found. The old cancer-trial full texts were not obtained; exact route, arm sizes, titration and safety rates remain incomplete. No verified human oral absorption study or fully specified repeated SC regimen was found. Long-term, pregnancy, breastfeeding, fertility and pediatric safety are unknown. Anemia signals exist; cancer-risk implications of vessel growth and tumor associations remain unresolved. Community reports are sparse. Several posts are one repeat user with possible supplier interests, not independent confirmation. Oral blend amounts cannot reliably be assigned to Ac-SDKP alone; no oral protocol was created. No evidence-supported microdosing titration, maintenance schedule or stacking safety data were found. No validated home reconstitution, cold-chain or post-mixing stability instructions were found. No Ac-SDKP-specific market-testing survey, poison-center series or FDA warning letter was located. EU, UK and Australian authorization or scheduling conclusions are limited by incomplete product-level searches. No demonstrated insulin, sulfonylurea, anticoagulant or oral-drug absorption interaction was found; these remain uncharacterized. Human-study count is a record inventory, not independent trials or a pooled participant count. Biomarker cohorts and meta-analysis overlap. Safety blocks and monitoring are precautionary screens, not approved-label contraindications or validated follow-up schedules.

Related to Ac-SDKP

• BPC-157: An experimental repair peptide with mostly animal evidence and a few small human reports.
• TB-500: A short piece of thymosin beta-4 with no proven repair benefit in humans.
• GHK-Cu: A copper-binding skin peptide with small topical studies and untested systemic injections.
• AHK-Cu: A copper peptide used in scalp serums, with laboratory findings and weak patent-only human data.
• Thymosin beta-4: A peptide studied for eye conditions and skin wounds; tendon-repair injections lack controlled human evidence.
• ARA-290: Experimental peptide studied for small-fiber nerve damage, with uncertain pain relief and safety.

Ac-SDKP: the short version

Sources

• 503B Bulk Drug Substances List, FDA · FDA · 2026
• Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the Federal Food, Drug, and Cosmetic Act, FDA · FDA · 2026
• Bulk Drug Substances Used in Compounding Under Section 503A of the FD&C Act, FDA · FDA · 2026
• Concerns regarding the public health risks associated with unapproved peptide products, Therapeutic Goods Administration and Chief Medical Officer · Therapeutic Goods Administration · 2026
• July 23-24, 2026: Meeting of the Pharmacy Compounding Advisory Committee - 07/23/2026, FDA · FDA · 2026
• MHRA Products | Home, MHRA · MHRA · 2026
• TGA warning on the risks of importing unapproved peptide products, Therapeutic Goods Administration · 2026
• The 2026 Prohibited List, World Anti-Doping Agency · WADA · 2026
• Therapeutic Goods (Poisons Standard—October 2026) Instrument 2026, Australian Government · Australian Government · 2026
• Bulk Drug Substances Nominated for Use in Compounding Under Section 503B of the Federal Food, Drug, and Cosmetic Act, FDA · FDA · 2025
• Anaphylaxis: MedlinePlus Medical Encyclopedia, MedlinePlus · MedlinePlus
• Cellulitis: MedlinePlus Medical Encyclopedia, MedlinePlus
• GORALATIDE, NIH NCATS
• GORALATIDE, FDA
• Recognizing medical emergencies: MedlinePlus Medical Encyclopedia, MedlinePlus

Sources checked: 2026-10-18.

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