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Voacangine is an antagonist for TRPV1 and TRPM8 but as an agonist for TRPA1 (EC₅₀=8 μM). Voacangine competitively blockes capsaicin binding to TRPV1 (IC₅₀=50 μM). Voacangine competitively inhibits the binding of menthol to TRPM8 (IC₅₀=9 μM) and it shows noncompetitive inhibition against icilin (IC₅₀=7 μM). Voacangine selectively abrogates chemical agonist-induced TRPM8 activation and did not affect cold-induced activation. Voacangine is an alkaloid isolated from the root bark of Voacanga africana.

Voacangine (100 μM; HEK cells) triggeres Ca₂₊ influx on TRPA1-expressing cells but not on the other TRPs. Voacangine not only suppresses capsaicin (CAP)-induced TRPV1 activation but also suppressed menthol- and icilin-induced TRPM8 activation. Voacangine attenuates CAP-induced TRPV1 activation. Voacangine shows a dose-dependent suppression of response by CAP. Voacangine competitively inhibits CAP on TRPV1. Voacangine is a competitive antagonist and that Voacangine and CAP act at the same recognition site on hTRPV1. Voacangine is an antagonist for TRPV1 and TRPM8 but an agonist for TRPA1. Voacangine selectively blocks CAP- and heat-induced activation of TRPV1. Voacangine is the first naturally occurring TRPM8 antagonist that competes with Menthol. Voacangine selectively blocks chemical agonist induced activation of TRPM8. Voacangine acts as an agonist for TRPA1. Voacangine inhibits the proliferation of HUVECs at an IC50 of 18 μM with no cytotoxic effects. Voacangine decreases the expression levels of hypoxia inducible factor-1α and its target gene, VEGF, in a dose-dependent manner.

Voacangine significantly suppresses in vitro angiogenesis, such as VEGF-induced tube formation and chemoinvasion.

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