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Aspirin
| Product Name | Aspirin |
| Price: | $15 / 20mg |
| Catalog No.: | CN03300 |
| CAS No.: | 50-78-2 |
| Molecular Formula: | C9H8O4 |
| Molecular Weight: | 180.16 g/mol |
| Purity: | >=98% |
| Type of Compound: | Phenols |
| Physical Desc.: | Powder |
| Source: | |
| Solvent: | Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc. |
| SMILES: | CC(=O)Oc1ccccc1C(=O)O |
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| Description | Aspirin is a non-selective and irreversible inhibitor of COX-1 and COX-2 with IC50s of 5 and 210 μg/mL. |
| Target | COX-1:27.75 μM (IC50) COX-2:1.17 mM (IC50) |
| In Vitro | Aspirin and other non-steroid anti-inflammatory drugs inhibit the activity of cyclooxygenase (COX) which leads to the formation of prostaglandins (PGs) that cause inflammation, swelling, pain and fever[2]. Aspirin acetylates serine-530 of cyclooxygenase-1 (COX-1), thereby blocking thromboxane A synthesis in platelets and reducing platelet aggregation. This mechanism of action accounts for the effect of aspirin on prevention of coronary artery and cerebrovascular thrombosis. Aspirin is less effective in inhibiting COX-2 activity. Aspirin and salicylate inhibit 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 the activation of NF-κB. This inhibition prevents the degradation of the NF-κB inhibitor, 1κB, and therefore NF-κB is retained in the cytosol. Aspirin also 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 inhibits COX-1 and COX-2 with IC50 values of 3.57 μM and 29.3 μM, respectively in human articular chondrocytes[5]. |
| Cell Assay | Chondrocytes are isolated from articular cartilage of donors with no articular disease. Unstimulated and interleukin 1 (IL-1) stimulated chondrocytes are used as models to study the effects of drugs on COX-1 and COX-2. Cells are incubated with vehicle or drugs (Asprin); supernatants are removed and the level of prostaglandin E2 (PGE2) in each sample is determined by enzyme immunoassay. IC50s are calculated from the reduction in PGE2 content by different concentrations of the test substance by linear regression analysis[5]. |
| Density | 1.3±0.1 g/cm3 |
| Boiling Point | 321.4±25.0 °C at 760 mmHg |
| Flash Point | 131.2±16.7 °C |
| Exact Mass | 180.042252 |
| PSA | 63.60000 |
| LogP | 1.19 |
| Vapour Pressure | 0.0±0.7 mmHg at 25°C |