Goralatide
The stem-cell brake hidden inside thymosin beta-4
Goralatide is the international name for Ac-SDKP, a four-amino-acid peptide the body cuts from thymosin beta-4 and that the enzyme ACE breaks down. It keeps blood stem cells from dividing, so it was tested in the 1990s as a way to shield bone marrow from chemotherapy; a randomized trial found no benefit. Animal studies since cast it as an antifibrotic.
What is it?
Ac-SDKP was found as a natural inhibitor of blood stem cell division: it stops stem cells and early progenitors from entering the S-phase, when DNA is copied. Since chemotherapy kills dividing cells, keeping marrow stem cells resting might spare them. In the lab it slowed normal human marrow progenitors but not leukaemia cells, and in mice it reduced deaths from doxorubicin.
The human test did not bear this out. In a French double-blind trial, 84 patients with head and neck or oesophageal cancer receiving carboplatin and fluorouracil were given goralatide (12.5 or 62.5 micrograms per kg a day for four days) or placebo. Across 221 chemotherapy cycles, there was no difference in white cell, granulocyte or platelet nadirs or in the length of blood toxicity; anaemia and lymphopenia were more frequent with goralatide. It was well tolerated.
A second story then took over. ACE, the enzyme that blood pressure drugs such as captopril block, breaks Ac-SDKP down, so those drugs raise its levels several-fold in people. In hypertensive rats, Ac-SDKP at matching levels reduced heart inflammation and collagen as much as captopril did, without lowering blood pressure, suggesting the peptide carries part of the drugs' antifibrotic effect.
Rodent studies have since reported benefits in radiation heart damage and in kidney, liver and lung fibrosis. Reviews describe a thymosin beta-4 to Ac-SDKP axis in repair, the link to TB-500, which is based on another part of that protein. No antifibrotic human trial appears in what we read, and goralatide is approved nowhere.
At a Glance
Every value in this table is printed from the Grey Peptides dataset, the same record the compound explorer and comparison tool read, so the three can never disagree.
Educational information, not medical advice. The doses on this page come from approved labels, published studies and, where no study exists, amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
Published Research
Studies of goralatide (Ac-SDKP), from their PubMed abstracts.
Randomized myeloprotection trial
In 84 patients on carboplatin and fluorouracil, goralatide (12.5 or 62.5 micrograms/kg/day, days 1-4) did not change blood count nadirs or the duration of blood toxicity versus placebo; anaemia and lymphopenia were more frequent with it.
Captopril raises Ac-SDKP
In 8 healthy volunteers in a double-blind crossover study, one 50 mg dose of captopril blocked 90-99% of Ac-SDKP breakdown and raised plasma levels a long-lasting 5.5-fold (range 4-8.5).
Clearance during ACE inhibition
Captopril raised plasma AcSDKP 4- to 4.8-fold in healthy subjects; in chronic renal failure, plasma levels were 22 times higher with ACE inhibitors than without (95% CI 15 to 33).
Heart fibrosis in hypertensive rats
At 400 micrograms/kg/day, Ac-SDKP raised plasma levels to those seen with captopril and, like captopril, reduced angiotensin II-induced cell proliferation, macrophage infiltration and collagen in the left ventricle without lowering blood pressure.
Radiation damage to the heart
In rats given cardiac irradiation, 18 weeks of Ac-SDKP strongly inhibited loss of contractile function, macrophage infiltration, fibrosis and galectin-3 release.
Doxorubicin toxicity in mice
Ac-SDKP for 3 days starting 48 hours before doxorubicin reduced mouse deaths and protected long-term reconstituting stem cells and progenitors; G-CSF afterwards improved recovery.
Normal versus leukaemic cells
AcSDKP inhibited normal human marrow progenitors at nanomolar concentrations but did not change proliferation of HL-60, AML or CML cells at any dose.
The thymosin beta-4 axis in fibrosis
Prolyl oligopeptidase cleaves thymosin beta-4 to release Ac-SDKP, and this axis is reviewed as protective against liver, kidney, heart and lung fibrosis.
Side Effects & Contraindications
Reported Side Effects
From the one randomized human trial.
Contraindications & Cautions
There is no label.
Legal Status
Goralatide is not approved anywhere we could find.
Frequently Asked Questions
?What is goralatide?
The international name for Ac-SDKP, a natural tetrapeptide (acetyl-Ser-Asp-Lys-Pro) cut from thymosin beta-4. It holds blood stem cells in a resting state and is broken down by ACE.
?Did goralatide protect bone marrow during chemotherapy?
Not in people. It worked in mice, but a 1995 randomized, double-blind trial in 84 patients found no difference from placebo in blood count nadirs, and anaemia and lymphopenia were more common with it.
?Is goralatide related to TB-500?
Yes, through thymosin beta-4. Ac-SDKP is released from that protein by prolyl oligopeptidase, while TB-500 is based on a different part of it. They are separate molecules with separate evidence.
References
- [other] PubChem CID 65938, Goralatide: formula C20H33N5O9, molecular weight 487.5. Read October 3, 2026. https://pubchem.ncbi.nlm.nih.gov/compound/65938
- [fda] FDA. Drugs@FDA (openFDA): no application on record for goralatide. Read October 3, 2026.
- [clinical-trial] Cappelaere P, et al. "[Randomized placebo trial of myeloprotection with goralatide in patients with squamous cell carcinoma of the upper respiratory and digestive tracts or esophagus, treated with a carboplatin-fluorouracil combination]." Bull Cancer, 1995;82(9):732-7. PMID: 8535033.
- [pubmed] Azizi M, et al. "Acute angiotensin-converting enzyme inhibition increases the plasma level of the natural stem cell regulator N-acetyl-seryl-aspartyl-lysyl-proline." J Clin Invest, 1996;97(3):839-44. PMID: 8609242.
- [pubmed] Azizi M, et al. "Renal and metabolic clearance of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) during angiotensin-converting enzyme inhibition in humans." Hypertension, 1999;33(3):879-86. PMID: 10082503.
- [pubmed] Rasoul S, et al. "Antifibrotic effect of Ac-SDKP and angiotensin-converting enzyme inhibition in hypertension." J Hypertens, 2004;22(3):593-603. PMID: 15076166.
- [pubmed] Sharma UC, et al. "A Small Peptide Ac-SDKP Inhibits Radiation-Induced Cardiomyopathy." Circ Heart Fail, 2018;11(8):e004867. PMID: 30354563.
- [pubmed] Massé A, et al. "The tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (Goralatide) protects from doxorubicin-induced toxicity: improvement in mice survival and protection of bone marrow stem cells and progenitors." Blood, 1998;91(2):441-9. PMID: 9427696.
- [pubmed] Bonnet D, et al. "The tetrapeptide AcSDKP, an inhibitor of the cell-cycle status for normal human hematopoietic progenitors, has no effect on leukemic cells." Exp Hematol, 1992;20(2):251-5. PMID: 1544396.
- [pubmed] Wang W, et al. "The Role of Tβ4-POP-Ac-SDKP Axis in Organ Fibrosis." Int J Mol Sci, 2022;23(21). PMID: 36362069.
Sources & Citations
Studies were read from their PubMed records, October 3, 2026. The 1995 trial is a French-language article read from its English abstract.
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