Acetylsalicylic acid - for plant cell cultrure, ≥99.0%, high purity , CAS No.50-78-2, Channel blocker of ASIC3;Inhibitor of COX-1;Inhibitor of COX-2

Item Number

A118582

• Synonyms: aspirin|ACETYLSALICYLIC ACID|50-78-2|2-Acetoxybenzoic acid|2-(Acetyloxy)benzoic acid|Acetylsalicylate|O-Acetylsalicylic acid|o-Acetoxybenzoic acid|Acenterine|Acetophen|Acetosal|Acylpyrin|Easprin|Ecotrin|Salicylic acid acetate|Acetosalin|Aspirdrops|Polopir
• Specifications & Purity: Moligand™, for plant cell culture, ≥99%
• Biochemical and Physiological Mechanisms: Blocks the production of prostaglandins by inhibiting cyclooxygenase (prostaglandin H synthase), with greater selectivity toward the COX-1 isoform. The antithrombotic effect is due to the inhibition of COX-1 in platelets that blocks thromboxane production
• Shipped In: Normal
• Grade: for plant cell culture, Moligand™
• Action Type: CHANNEL BLOCKER, INHIBITOR
• Mechanism of action: Channel blocker of ASIC3;Inhibitor of COX-1;Inhibitor of COX-2

Product Description

Aspirin is an antiinflammatory compound that inhibits NFκB, cylooxygenase-1 (Cox-1), and cyclooxygenase-2 (Cox-2). NFκB is a transcription factor that plays an important role in the expression of cellular and viral genes, which regulate the inflammatory response and infection. Adhesion molecules IL-1 and IL-6 are genes regulated by NFκB. Along with sodium salicylate, aspirin has been shown to block the long terminal repeat from the human immunodeficiency virus and the Ig κ enhancer from NFκB dependent transcription. Research indicates that aspirin acts at a site downstream of glutamate receptors and blocks induction of NFκB mediated by glutamate. Additional studies suggest that aspirin and sodium salicylate specifically inhibit IKKβ, which results in the blocking of NFκB genes responsible for the inflammatory response. Aspirin has also been described to elevate extracellular adenosine levels, downregulate the expression and activity of inducible NOS, decrease the levels of adenosine triphosphate, act on multiple mitogen-activated protein kinase activities, and block the uncoupling of oxidative phosphorylation. Studies reveal that aspirin alters the equilibrium of Mcl-1/Noxa, giving rise to apoptosis of leukemia cells, independent of NFκB and MAPKs.
An inhibitor of COX-1 (cylooxygenase) and NFκB.