OKY-1581
OKY-1581 is a potent, orally active and selective thromboxane A2 synthase inhibitor. OKY-1581 inhibits TXA2 synthesis and reduces the generation of its stable metabolite TXB2. OKY-1581 shifts arachidonic acid (MCE HY-109590) metabolism toward the production of prostaglandin E, prostaglandin F and 6-keto-prostaglandin F1α. OKY-1581 modulates the TXA2 / PGI2-related eicosanoid balance and inhibits arachidonic acid-induced platelet aggregation without directly inhibiting the cyclooxygenase step. At high oral doses, OKY-1581 also enhances hepatic peroxisomal β-oxidation and reduces serum triglyceride and cholesterol levels. OKY-1581 attenuates cerebral vasospasm after experimental subarachnoid hemorrhage by reducing TXA2-related vasoconstrictive signaling. OKY-1581 can be used in studies of atherosclerosis, cerebral vasospasm after subarachnoid hemorrhage and cardiovascular diseases.
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- CAS No.: 75987-18-7
- Formule: C16H14NNaO2
- Masse moléculaire:275.28
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Description
IC50 & Target
[3]|
Thromboxane A2 synthase |
In Vitro
OKY-1581 (43 μg/mL; at least 5 minutes) potently inhibits thromboxane synthesis in male New Zealand rabbit PRP with a TxB2 reduction to 3 ng/mL, while increasing PGE and PGF generation, without impairing collagen-induced platelet aggregation[1].
OKY-1581 (>8.3 mg/mL) inhibits thromboxane A2-induced aggregation in human platelets[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
OKY-1581 (160 mg; intravenous bolus, administered immediately after subarachnoid hemorrhage; 4 gm/50 mL/24 hours; continuous intravenous infusion until sacrifice at 4 days post-subarachnoid hemorrhage) potently and statistically significantly inhibits late cerebral vasospasm (88.1% reduction) and moderately inhibits early cerebral vasospasm (69.3% reduction) in a canine subarachnoid hemorrhage model, while preventing internal elastic lamina shrinkage without altering subarachnoid hemorrhage-induced endothelial or smooth muscle cell damage[2].
OKY-1581 (100-500 mg/kg; p.o.; daily; 14-30 days) dose-dependently increases the activities of peroxisomal and mitochondrial lipid metabolic enzymes in the liver of normal male Wistar rats, induces hepatomegaly, and reduces lipid levels in serum and liver, with the maximal effect observed at a daily dose of 500 mg/kg for consecutive 30 days[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:New Zealand rabbits (male, 3-5 kg)[1]
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Dosage:5.0 mg; 10 mg; 100 mg (s.c.); 25 mg; 50 mg; 100 mg (p.o.)
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Administration:s.c.; p.o.
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Result:Inhibited TXB2 generation within 2 h after administration, increased prostaglandin E and prostaglandin F production, and maintained TXB2 suppression for 24-48 h.
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Animal Model:Mongrel dogs (adult, 10 to 15 kg, intracisternal injection of autogenous arterial blood-induced cerebral vasospasm)[2]
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Dosage:160 mg (i.v. bolus); 4 gm/50 mL/24 hours (continuous i.v. infusion)
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Administration:i.v. bolus (immediately post-SAH); continuous i.v. infusion (until sacrifice at 4 days post-SAH)
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Result:Suppressed early and late basilar artery spasms by 69.3% and 88.1%, respectively, and almost completely abolished late spasm.
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Animal Model:Wistar rats (male, ~150 g body weight)[4]
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Dosage:100 or 500 mg/kg/day
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Administration:p.o., daily for 2 weeks
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Result:Enhanced hepatic peroxisomal β-oxidation and fatty acid-metabolizing enzyme activities, with serum cholesterol reduction at the high dose.
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Animal Model:Wistar rats (male, ~150 g body weight)[4]
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Dosage:500 mg/kg/day
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Administration:p.o., daily for 30 days
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Result:Reduced serum triglyceride and cholesterol levels.
Increased liver weight, and enhanced hepatic peroxisomal enzyme activities.
Chemical Information
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CAS No. 75987-18-7
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Masse moléculaire 275.28
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Formule C16H14NNaO2
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SMILES
O=C(O[Na])/C(C)=C/C(C=C1)=CC=C1CC2=CN=CC=C2
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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.
Pureté et documentation
Références
[2]. Sasaki T, et al. Prevention of cerebral vasospasm after SAH with a thromboxane synthetase inhibitor, OKY-1581. Journal of neurosurgery. 1982 Jul;57(1):74-82. [Content Brief]
[3]. Yui Y, et al. Intravenous infusion of a selective inhibitor of thromboxane A2 synthetase in man: influence on thromboxane B2 and 6-keto-prostaglandin F1 alpha levels and platelet aggregation. Circulation. 1984 Oct;70(4):599-605. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
OKY-1581 Related Classifications
HY-183483 Related Classifications
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