| Bioactivity | 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]. | ||||||||||||
| Invitro | Aspirin inhibits COX-1 and COX-2 in human articular chondrocytes, with IC50 values of 3.57 μM and 29.3 μM, respectively[2].Aspirin acetylates serine-530 of COX-1, thereby blocking thromboxane A synthesis in platelets and reducing platelet aggregation[3]. Aspirin inhibits COX-2 protein expression through interference with binding of CCAAT/enhancer binding protein beta (C/EBPbeta) to its cognate site on COX-2 promoter/enhancer[3]. Aspirin inhibits NF-κB-dependent transcription from the lgκ enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells[4]. Aspirin induces apoptosis by the activation of caspases, the activation of p38 MAP kinase, release of mitochondrial cytochrome c, and activation of the ceramide pathway[6]. | ||||||||||||
| Name | Aspirin | ||||||||||||
| CAS | 50-78-2 | ||||||||||||
| Formula | C9H8O4 | ||||||||||||
| Molar Mass | 180.16 | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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