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Aspirin-d7

CAT: 0804-HY-W707656Size: 1 EachDry Ice: NoHazardous: No
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CAT#:0804-HY-W707656Size:1 Each
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24/48H Stock Items & 2 to 6 Weeks non Stock Items.
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Description
Aspirin-d7 is the deuterium labeled Aspirin. 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].
UNSPSC
12352005
Target
Apoptosis; Autophagy; Caspase; COX; Isotope-Labeled Compounds; Mitophagy; NF-κB; p38 MAPK; Virus Protease
Related Pathways
Anti-infection; Apoptosis; Autophagy; Immunology/Inflammation; MAPK/ERK Pathway; NF-κB; Others
Applications
Metabolism-protein/nucleotide metabolism
Field of Research
Cancer; Infection; Metabolic Disease; Inflammation/Immunology; Cardiovascular Disease
Smiles
O=C(OC1=C(C([2H])=C(C([2H])=C1[2H])[2H])C(O)=O)C([2H])([2H])[2H]
Molecular Formula
C9HD7O4
Molecular Weight
187.20
References & Citations
[1]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. |[2]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. |[3]Wu KK, et al. Aspirin and other cyclooxygenase inhibitors: new therapeutic insights. Semin Vasc Med. 2003 May;3 (2) :107-12. |[4]Kopp E, et al. Inhibition of NF-kappa B by sodium salicylate and aspirin. Science. 1994 Aug 12;265 (5174) :956-9. |[5]Burch JW, et al. Inhibition of platelet prostaglandin synthetase by oral aspirin. J Clin Invest. 1978 Feb;61 (2) :314-9.|[6]Elwood PC, et al. Aspirin, salicylates, and cancer. Lancet. 2009 Apr 11;373 (9671) :1301-9.
Shipping Conditions
Room temperature
Scientific Category
Isotope-Labeled Compounds
Clinical Information
No Development Reported

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