Aspirin

Category	Virus Protease
CAS	50-78-2
Description	Aspirin is a salicylate and irreversible COX1 and COX2 inhibitor. It can be used for the treatment of fever, rheumatism, nerve, muscle, joint pain, soft tissue inflammation and gout in animals.

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Synonyms	Acetylsalicylic acid; 1S/C9H8O4/c1-6(10)13-8-5-3-2-4-7(8)9(11)12/h2-5H,1H3,(H,11,12)
IUPAC Name	2-acetyloxybenzoic acid
Molecular Weight	180.16
Molecular Formula	C9H8O4
Canonical SMILES	CC(=O)OC1=CC=CC=C1C(=O)O
InChI	1S/C9H8O4/c1-6(10)13-8-5-3-2-4-7(8)9(11)12/h2-5H,1H3,(H,11,12)
InChIKey	BSYNRYMUTXBXSQ-UHFFFAOYSA-N
Boiling Point	140°C
Melting Point	134-136°C
Flash Point	131.2±16.7 °C
Purity	99.66%
Density	1.3±0.1 g/cm3
Solubility	Soluble in DMSO (36 mg/mL), Ethanol (36 mg/mL)
Appearance	White Solid
Storage	Store at -20°C
Complexity	212
Exact Mass	487.07428
Index Of Refraction	1.551
In Vivo	Aspirin inhibits NF-κB activation, prevents degradation of its inhibitor, IκB, so that NF-κB remains in the cytoplasm. In transfected T cells, Aspirin also inhibits transcription of NF-κB-dependent Igκ enhancers and HIV-long end repeats. Aspirin inhibits Ser307 phosphorylation and JNK, c-Jun phosphorylation of IRS-1, as well as degradation of IkappaBalpha in TNF-α-treated 3T3-L1 and Hep G2 cells. Aspirin inhibits Akt phosphorylation and inhibits the response of mammalian targets of rapamycin to TNF-α. In 3T3-L1 adipocytes pretreated with TNF-α, Aspirin reduces insulin-induced glucose uptake. In rat neuron primary cultures and hippocampal brain tablets, Aspirin reduces neurotoxicity triggered by the excitatory amino acid glutamate.
PSA	63.60000
Target	COX; Virus Protease; NF-κB; Autophagy; Apoptosis; Mitophagy; Caspase; p38 MAPK
Vapor Pressure	0.0±0.7 mmHg at 25°C
XLogP3-AA	1.2