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]}. IC50 & Target:IC50: 5 μg/mL (COX-1), 210 μg/mL (COX-2)^[1] In Vitro: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]. In Vivo:Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

Aspirin lithium (5-150 mg/kg, PO, once) shows significant antipyretic activity in adult yeast-fevered male rats^[7].
Aspirin can be used to induce gastrointestinal ulcer models^[8].