N-(p-Amylcinnamoyl)anthranilic acid - 96%, high purity , CAS No.110683-10-8, Channel blocker of TRPC3;Channel blocker of TRPC6;Channel blocker of TRPM2;Channel blocker of TRPM8

Item Number

A275778

• Synonyms: ACA - CAS 110683-10-8 | N-(4-Pentylcinnamoyl)anthranilic acid | N17081 | BRD-K77817104-001-01-3 | Benzoic acid, 2-((1-oxo-3-(4-pentylphenyl)-2-propenyl)amino)- | 2-(3-(4-Pentylphenyl)acrylamido)benzoic acid | Benzoic acid, 2-((1-oxo-3-(4-pentylphenyl)-2-p
• Specifications & Purity: Moligand™, ≥96%
• Biochemical and Physiological Mechanisms: Phospholipases A2 (PLA 2 ) inhibitor. Modulates TRP ion channels. Reversibly inhibits Ca 2+ activated chloride current in a concentration-dependent manner (IC 50 = 4.2 μM). Inhibits insulin secretion. Cell permeable. Active in vivo and in vitro .
• Storage Temp: Store at -20°C
• Shipped In: Ice chest + Ice pads
• Grade: Moligand™
• Action Type: CHANNEL BLOCKER
• Mechanism of action: Channel blocker of TRPC3;Channel blocker of TRPC6;Channel blocker of TRPM2;Channel blocker of TRPM8
• Note: Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20°C. Generally, these will be useable for up to one month. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour. Need more advice on solubility, usage and handling? Please visit our frequently asked questions (FAQ) page for more details.

Product Description

 N-(p-Amylcinnamoyl) anthranilic Acid (ACA), a cell permeable inhibitor of PLA2, has been reported to inhibit α-ketoisocaproic acid and glyceraldehyde-induced insulin secretion, as well as glucose-induced insulin secretion. Additionally, by inhibiting PLA2, ACA consequentially suppresses glucose-induced arachidonic acid formation in cells. Furthermore, research has shown ACA to modulate the activity of different transient receptor potential channels. In particular, ACA's blocking ability of diacylglycerol-activated TRP channels is of special interest since it offers the opportunity to interfere with receptor-induced Ca2+-dependent signaling processes in vascular smooth muscle cells and platelets.