(17R,18S)-Epoxyeicosatetraenoic acid

(17R,18S)-Epoxyeicosatetraenoic acid (17(R),18(S)-EETeTr) (100 nM; 40 min) stimulates BK channel-mediated outward K⁺ currents by up to 2.6-fold at +60 mV in freshly isolated rat cerebral artery VSMC, independent of intracellular or extracellular Ca²⁺ changes, L-type Ca²⁺ channels, or EET receptors targeted by 14,15-epoxyeicosa-5(Z)-enoic acid^[1].
(17R,18S)-Epoxyeicosatetraenoic acid (100 nmol l⁻¹; 40 min) stimulates BK channel-mediated outward K⁺ currents by up to 3.5-fold at +60 mV in wild-type, BKβ1^(-/-), and RyR3^(-/-) mouse cerebral artery VSMC, but has no effect in BKα^(-/-) mouse cerebral artery VSMC, demonstrating dependence on the BKα subunit^[1].
(17R,18S)-Epoxyeicosatetraenoic acid (1 μmol l⁻¹; 40 min) stimulates BK channel-mediated outward K⁺ currents by 2.2-fold at +100 mV in freshly isolated wild-type mouse mesenteric artery VSMC^[1].
(17R,18S)-Epoxyeicosatetraenoic acid exerts immediate negative chronotropic effects and protects neonatal rat cardiomyocytes against calcium overload with an EC₅₀ of 1-2 nM, and reduces beating rate by -21.3 beats/min when incubated at 30 nM for 5 min^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.