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.
For research use only. We do not sell to patients.
- CAS No.: 140694-43-5
- Formula: C24H34O5
- Molecular Weight:402.52
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
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 No. 140694-43-5
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Molecular Weight 402.52
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Formula 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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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.
Purity & Documentation
References
[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
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)