N-(p-amylcinnamoyl) Anthranilic Acid (ACA; 20 μM) completely blocks ADPR-induced whole-cell currents and H2O2-induced Ca2+ signals (IC50=1.7 μM) in HEK293cells transfected with human TRPM2[1]. N-(p-amylcinnamoyl) Anthranilic Acid (ACA; 20 μM) also blocks currents through human TRPM8 and TRPC6 expressed in HEK293 cells[1]. N-(p-amylcinnamoyl) Anthranilic Acid (ACA) modulates the activity of different TRP channels independent of PLA22 inhibition[1].
Kinase Assay
Cell Assay
Animal Administration
References
[1]. Kraft R, et al. Inhibition of TRPM2 cation channels by N-(p-amylcinnamoyl)anthranilic acid. Br J Pharmacol. 2006 Jun;148(3):264-73.
[2]. Harteneck C, et al. N-(p-amylcinnamoyl)anthranilic acid (ACA): a phospholipase A(2) inhibitor and TRP channel blocker. Cardiovasc Drug Rev. 2007 Spring;25(1):61-75.
[3]. Gwanyanya A, et al. Inhibition of the calcium-activated chloride current in cardiac ventricular myocytes by N-(p-amylcinnamoyl)anthranilic acid (ACA). Biochem Biophys Res Commun. 2010 Nov 19;402(3):531-6.
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