Se-Aspirin (Se-NSAID-8) has anticancer activity and gastroprotective effects, inhibits activation of proinflammatory and pro-survival NF-ĸB pathways, and inhibits the expression of anti-apoptotic targets downstream of NF-ĸB (e.g., Bcl-xL, Mcl-1, and survivin).Se-Aspirin induces Cell cycle arrest and activation of apoptosis accelerates ulcer healing and can be used to study pancreatic and colorectal cancer.

Aspirin inhibits COX-1 and COX-2 in human articular chondrocytes with IC50 values ​​of 3.57 μM and 29.3 μM, respectively[1]; Aspirin acetylates serine 530 of COX-1, thereby blocking the synthesis of thromboxane A in platelets and reducing platelet aggregation; Aspirin inhibits COX-2 protein expression by interfering with the binding of CCAAT/enhancer protein beta (C/EBPbeta) to its homologous sites on the COX-2 promoter/enhancer[2]; Aspirin inhibits NF-κB-dependent transcription from the lgκ enhancer and long terminal repeat (LTR) in human immunodeficiency virus (HIV)-transfected T cells[3]; Aspirin inhibits mitochondrial cytochrome c release, activation of p38 MAP kinase, and activation of the ceramide pathway[4].

Aspirin (5-150 mg/kg, PO, once) displays significant antipyretic activity in adult yeast-fever male rats. [5]