Sepetaprost
Sepetaprost (ONO-9054) is a dual agonist of the prostaglandin E3 receptor and prostaglandin F receptor. Sepetaprost reduces intraocular pressure in animal models. Sepetaprost is applicable for research on ocular hypertension and open-angle glaucoma.
For research use only. We do not sell to patients.
- CAS No.: 1262873-06-2
- Formula: C26H36F2O6
- Molecular Weight:482.56
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
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EP3 |
FP Receptor |
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male cynomolgus monkeys[2]
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Dosage:0.002%
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Administration:topical ocular instillation; single dose
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Result:Significantly reduced IOP at 8, 10, 12, 26, and 28 h post-administration.
Showed consistently greater IOP-lowering effect than latanoprost at all measured time points.\nSignificantly enhanced outflow facility compared to vehicle.
Induced significant IOP reduction from baseline at 8, 24, and 26 h (IOP change from baseline: -1.3 mmHg at 8 h, -1.7 mmHg at 24 h, -1.4 mmHg at 26 h).
Had its IOP-lowering effect significantly attenuated at 26 h by pretreatment with an EP3 antagonist, with no significant differences observed at 8 or 24 h.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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CAS No. 1262873-06-2
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Molecular Weight 482.56
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Formula C26H36F2O6
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SMILES
O=C(OC(C)C)CCC[C@H]1CC[C@@]([C@@H](/C=C/[C@@H](O)COC2=CC(F)=CC=C2F)[C@H](O)C3)([H])[C@@]3([H])OC1
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Synonyms
ONO-9054
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Purity & Documentation
References
[1]. Suto F, et al. A Novel Dual Agonist of EP3 and FP Receptors for OAG and OHT: Safety, Pharmacokinetics, and Pharmacodynamics of ONO-9054 in Healthy Volunteers. Invest Ophthalmol Vis Sci. 2015;56(13):7963-7970. [Content Brief]
[2]. Maki K, et al. The Role of EP3 Agonism in Intraocular Pressure-Lowering by Sepetaprost, a Novel Dual Agonist of FP and EP3 Receptors, in Monkeys. J Ocul Pharmacol Ther. 2026;42(3):172-178. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Sepetaprost Related Classifications
HY-128538 Related Classifications
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