97781-16-3
97781-16-3
Chemical Structure
Aspirin-d4
Synonym(s): Acetylsalicylic acid-d4;ASA-d4
- CAS No.: 97781-16-3
- Formula:C9H4D4O4
- Molecular Weight:184.18
IUPAC Name: 2-acetoxybenzoic-3,4,5,6-d4 acid
InChIKey: BSYNRYMUTXBXSQ-QFFDRWTDSA-N
SMILES: OC(C1=C(C([2H])=C([2H])C([2H])=C1[2H])OC(C)=O)=O
Biological Activity: Aspirin-d4 is the deuterium labeled Aspirin (HY-14654). Aspirin (Acetylsalicylic acid) is an orally active, potent and irreversible inhibitor of cyclooxygenase COX-1 and COX-2, with IC50 values of 5 and 210 μg/mL, respectively. Aspirin induces apoptosis. Aspirin inhibits the activation of NF-κB. Aspirin also inhibits platelet prostaglandin synthetase, and can prevent coronary artery and cerebrovascular thrombosis[1][2][3][4][5][6].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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Aspirin-d4 | 98.41% | Aspirin-d4 is the deuterium labeled Aspirin (HY-14654). Aspirin (Acetylsalicylic acid) is an orally active, potent and irreversible inhibitor of cyclooxygenase COX-1 and COX-2, with IC50 values of 5 and 210 μg/mL, respectively. Aspirin induces apoptosis. Aspirin inhibits the activation of NF-κB. Aspirin also inhibits platelet prostaglandin synthetase, and can prevent coronary artery and cerebrovascular thrombosis. | ||||||||||||||||||||
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Aspirin (Standard) | 99.92% | Aspirin (Standard) is the analytical standard of Aspirin. This product is intended for research and analytical applications. Aspirin (Acetylsalicylic acid) is an orally active, potent and irreversible inhibitor of cyclooxygenase COX-1 and COX-2, with IC50 values of 5 and 210 μg/mL, respectively. Aspirin induces apoptosis. Aspirin inhibits the activation of NF-κB. Aspirin also inhibits platelet prostaglandin synthetase, and can prevent coronary artery and cerebrovascular thrombosis. | ||||||||||||||||||||
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Aspirin-d7 | Aspirin-d7 is the deuterium labeled Aspirin (HY-14654). Aspirin (Acetylsalicylic acid) is an orally active, potent and irreversible inhibitor of cyclooxygenase COX-1 and COX-2, with IC50 values of 5 and 210 μg/mL, respectively. Aspirin induces apoptosis. Aspirin inhibits the activation of NF-κB. Aspirin also inhibits platelet prostaglandin synthetase, and can prevent coronary artery and cerebrovascular thrombosis. | |||||||||||||||||||||
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Aspirin-d3 | 99.84% | Aspirin-d3 is the deuterium labeled Aspirin (HY-14654). Aspirin (Acetylsalicylic acid) is an orally active, potent and irreversible inhibitor of cyclooxygenase COX-1 and COX-2, with IC50 values of 5 and 210 μg/mL, respectively. Aspirin induces apoptosis. Aspirin inhibits the activation of NF-κB. Aspirin also inhibits platelet prostaglandin synthetase, and can prevent coronary artery and cerebrovascular thrombosis. | ||||||||||||||||||||
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Aspirin | 99.67% | Aspirin (Acetylsalicylic acid) is an orally active, potent and irreversible inhibitor of cyclooxygenase COX-1 and COX-2, with IC50 values of 5 and 210 μg/mL, respectively. Aspirin induces apoptosis. Aspirin inhibits the activation of NF-κB. Aspirin also inhibits platelet prostaglandin synthetase, and can prevent coronary artery and cerebrovascular thrombosis. | ||||||||||||||||||||
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References
- [1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216. [Content Brief]
- [2]. Mitchell JA, et al. Selectivity of nonsteroidal antiinflammatory drugs as inhibitors of constitutive and induciblecyclooxygenase. Proc Natl Acad Sci U S A. 1993 Dec 15;90(24):11693-7. [Content Brief]
- [3]. Vane JR, et al. The mechanism of action of aspirin. Thromb Res. 2003 Jun 15;110(5-6):255-8. [Content Brief]
- [4]. Wu KK, et al. Aspirin and other cyclooxygenase inhibitors: new therapeutic insights. Semin Vasc Med. 2003 May;3(2):107-12. [Content Brief]
- [5]. Kopp E, et al. Inhibition of NF-kappa B by sodium salicylate and aspirin. Science. 1994 Aug 12;265(5174):956-9. [Content Brief]
- [6]. Blanco FJ, et al. Effect of antiinflammatory drugs on COX-1 and COX-2 activity in human articular chondrocytes. J Rheumatol. 1999 Jun;26(6):1366-73. [Content Brief]
