TY 11223
TY 11223 is an orally active, long-acting platelet aggregation inhibitor belonging to prostaglandin analogs. TY-11223 inhibits ADP (HY-W010918)- and Collagen-induced aggregation of washed rabbit platelets, with IC50 values of 2.6 nM and 8.6 nM, respectively. TY 11223 exerts hypotensive effects and alleviates ethanol-induced gastric ulcers, with an ED50 of 15.3 μg/kg when administered orally 30 minutes before ethanol exposure. TY 11223 can be used in research related to cardiovascular diseases and gastric ulcers.
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- CAS. Nr.: 140694-43-5
- Formel: C24H34O5
- Molecular Weight:402.52
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
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Help & FAQs
Biologische Aktivität
TY 11223 (compound 3) potently inhibits ADP (HY-W010918)-induced aggregation of washed rabbit platelets, with an IC50 of 2.6 nM[1].
TY 11223 exhibits extremely high stability in acidic ethanol aqueous solution (pH 1.2) at 40°C[1].
TY 11223 (compound 74b) potently inhibits collagen-induced aggregation of washed rabbit platelets, with an IC50 of 8.6 nM[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
TY 11223 (compound 74b) (1.0-10.0 μg/kg/min; i.v.; infusion over 20 min) inhibits collagen-induced platelet aggregation by up to 100% and reduces mean blood pressure by up to 57.9 mmHg in rabbits following intravenous infusion, with dose-dependent activity[2].
TY 11223 (0.1-1.0 mg/kg; p.o.) provides sustained, dose-dependent inhibition of ADP-induced platelet aggregation in rabbits for up to 6 hours following oral administration, with peak inhibition reaching 79.4% at the 1.0 mg/kg dose[2].
TY 11223 (15.3 μg/kg; p.o.; 30 minutes prior to ethanol exposure) inhibits ethanol-induced gastric lesions in rats with an ED50 of 15.3 μg/kg when administered orally 30 minutes prior to ethanol exposure[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:The Japanese white rabbits were anesthetized with sodium pentobarbital
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Dosage:10.0 μg/kg/min; 3.0 μg/kg/min; 1.0 μg/kg/min; 1 mg/kg
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Administration:i.v.; continuous infusion; 20 minutes; p.o.; single dose
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Result:Achieved 100% inhibition of ex vivo ADP-induced platelet aggregation, and a maximum arterial blood pressure reduction of -57.9 mmHg at 10.0 μg/kg/min i.v..
Achieved 91.3% inhibition of ex vivo ADP-induced platelet aggregation, and a maximum arterial blood pressure reduction of -36.1 mmHg at 3.0 μg/kg/min i.v..
Achieved 80.5% inhibition of ex vivo ADP-induced platelet aggregation, and a maximum arterial blood pressure reduction of -8.8 mmHg at 1.0 μg/kg/min i.v..
Maintained ex vivo platelet aggregation inhibition above 50% for >15 minutes after 20-minute i.v. infusion at 3.0 μg/kg/min.
Maintained >60% inhibition of ex vivo ADP-induced platelet aggregation for 6 hours post-dose at 1 mg/kg p.o..
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Animal Model:Male Japanese white rabbits (2.5-3.0 kg) were anesthetized with pentobarbital (60 mg/kg, i.m.), and the carotid artery was cannulated for blood pressure monitoring and blood sampling, while the femoral vein was cannulated for intravenous infusion.[2]
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Dosage:10.0 μg/kg/min; 3.0 μg/kg/min; 1.0 μg/kg/min
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Administration:i.v.; infusion over 20 min
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Result:Inhibited collagen-induced platelet aggregation by 100% and reduced mean blood pressure by 57.9 mmHg at 10.0 μg/kg/min.
Inhibited collagen-induced platelet aggregation by 91.3% and reduced mean blood pressure by 36.1 mmHg at 3.0 μg/kg/min.
Inhibited collagen-induced platelet aggregation by 80.5% and reduced mean blood pressure by 8.8 mmHg at 1.0 μg/kg/min.
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Animal Model:Male Japanese white rabbits (2.5-3.5 kg) were fasted for 24 hours, anesthetized with pentobarbital (60 mg/kg, i.m.), and the carotid artery was cannulated with a polyethylene tube for blood sampling.[2]
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Dosage:1.0 mg/kg; 0.3 mg/kg; 0.1 mg/kg
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Administration:p.o.
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Result:Inhibited ADP-induced platelet aggregation at rates of 56.2% (30 min), 60.1% (60 min), 54.4% (120 min), 65.9% (180 min), 79.4% (300 min), and 66.4% (360 min) at 1.0 mg/kg.
Inhibited ADP-induced platelet aggregation at rates of 30.2% (30 min), 42.9% (60 min), 59.1% (120 min), 48.2% (180 min), 49.6% (300 min), and 49.5% (360 min) at 0.3 mg/kg.
Inhibited ADP-induced platelet aggregation at rates of 8.7% (30 min), 9.0% (60 min), 7.4% (120 min), and 0.8% (180 min) at 0.1 mg/kg.
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Animal Model:Male Wistar rats (170-270 g) were fasted for 24 hours, then administered 1 mL of 99.5% ethanol orally to induce gastric lesions.[2]
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Dosage:1mg/kg, 3 mg/kg,10 mg/kg, 30 mg/kg
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Administration:p.o.; 0.5 or 3.5 h prior to ethanol exposure
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Result:Exhibited an ED50 of 15.3 μg/kg for inhibition of ethanol-induced gastric lesions 30 minutes post-administration.
Chemical Information
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CAS. Nr. 140694-43-5
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Molecular Weight 402.52
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Formel C24H34O5
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SMILES
CCC#CCC(C)(C)[C@H](O)C#C[C@@H]1[C@]2([H])[C@@](C[C@H]1O)([H])C=C(CC2)CCOCC(O)=O
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
[1]. Shibasaki M, et al. A novel homoisocarbacyclin analog with potent and long-lasting activity. Chemical & pharmaceutical bulletin. 1992 Jan;40(1):279-81. [Content Brief]
[2]. Narita S, et al. Syntheses and biological activities of chemically stable prostacyclin mimics with cis-bicyclo[4.3.0]nonene ring system: the novel homoisocarbacyclin analogues. Bioorg Med Chem. 1993 Aug;1(2):77-118. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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