Product Details
Place of Origin: China
Brand Name: Sunshine
Certification: ISO,COA
Model Number: 58-32-2
Payment & Shipping Terms
Minimum Order Quantity: Negotiation
Price: Negotiation
Packaging Details: Bag,Drum
Delivery Time: 7-15 days
Payment Terms: L/C, D/A, T/T, Western Union
Supply Ability: TON
CAS NO:: |
58-32-2 |
Appearance:: |
Yellow Powder |
Molecular Formula:: |
C24H40N8O4 |
Molecular Weight:: |
504.62600 |
EINECS NO:: |
200-374-7 |
MDL NO:: |
MFCD00010555 |
CAS NO:: |
58-32-2 |
Appearance:: |
Yellow Powder |
Molecular Formula:: |
C24H40N8O4 |
Molecular Weight:: |
504.62600 |
EINECS NO:: |
200-374-7 |
MDL NO:: |
MFCD00010555 |
Product Description:
Product Name: Dipyridamole CAS NO: 58-32-2
Synonyms:
2,2',2'',2'''-((4,8-Di(piperidin-1-yl)pyrimido[5,4-d]-pyrimidine-2,6-diyl)bis(azanetriyl))tetraet;
Corosan;
Coroxin;
Chemical & Physical Properties:
Appearance: Yellow Powder
Assay :≥99.0%
Density: 1.352 g/cm3
Boiling Point: 806.5℃ at 760 mmHg
Melting Point: 165-166℃
Flash Point: 441.5℃
Refractive Index: 1.666
Stability: Stable at normal temperatures and pressures. Sensitive to light.
Storage Condition: -20℃
Safety Information:
Safety Statements: S26-S36
HS Code: 2933990090
WGK Germany: 2
Risk Statements: R36/37/38
Hazard Code: Xi
Signal Word: Warning
Caution Statement: P261; P305 + P351 + P338
Hazard Declaration: H315; H319; H335
Symbol: GHS07
Dipyridamole (trademarked as Persantine) is a medication that inhibits blood clot formation when given chronically and causes blood vessel dilation when given at high doses over a short time. Dipyridamole (Persantine) is a phosphodiesterase inhibitor that blocks uptake and metabolism of adenosine by erythrocytes and vascular endothelial cells.Target: Phosphodiesterase (PDE)Dipyridamole concentrations of 1 nmol/ml blood caused 90% inhibition of adenosine metabolism. Dipyridamole at therapeutic concentrations causes significant inhibition of adenosine metabolism in whole blood. Dipyridamole has a dose-dependent inhibitory effect on thromboxane synthesis which was independent of aggregation. Dipyridamole also inhibited malonyldialdehyde production in response to both thrombin and arachidonic acid. Dipyridamole enhances platelet inhibition by amplifying the signaling of the NO donor sodium nitroprusside. These data support the concept that enhancement of endothelium-dependent NO/cGMP-mediated signaling may be an important in vivo component of dipyridamole action.
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