Levcromakalim

94535-50-9

C16H18N2O3

DMSO : >= 50 mg/mL (174.62 mM); H2O : < 0.1 mg/mL (insoluble)

Membrane Transporter/Ion Channel

Levcromakalim ((-)-Cromakalim) is an ATP-sensitive K⁺ channel (K_ATP) activator. IC50 & Target: K⁺ channel^[1] In Vitro: Levcromakalim ((-)-Cromakalim) inhibits spontaneous contractions completely in a glibenclamide-sensitive manner. LevCromakalim (5 uM) inhibits spontaneous contractions, which are recovered by glibenclamide. Levcromakalim (1, 5 and 10 uM) inhibits phasic contractions to 34+/-21.1%, 20.1+/-20.0% and 0% of the control (n=5, respectively; P<0.05). Glibenclamide reverses the inhibition of spontaneous isometric contractions caused by LevCromakalim (5 uM) to 84+/-1.5% of the control (n=5; P<0.05). Levcromakalim (20 and 100 uM) also inhibits oxytocin (OXT) (10 nM)-induced phasic contractions to 34+/-21.4% and 14+/-12.6% of the control (n=6 and 4, respectively; P<0.05). Glibenclamide reverses the inhibition of spontaneous isometric contractions by LevCromakalim (100 uM) to 79+/-3.5% of the control (n=4; P<0.05). Tonic contraction by OXT is also suppressed by Cromakalim in a glibenclamide-sensitive manner^[2].The function of the K_ATP channels is examined with the specific channel opener LevCromakalim (Cromakalim). LevCromakalim induces dose-dependent relaxation in both the young and old mesenteric artery (MAs); and there is no difference in relaxation with age. However, the relaxation is markedly reduced in response to the high-salt (HS) diet in the old MAs (P<0.05). Maximum dilations to Levcromakalim (10^-4 M) are 97 +/- 3% in the young MAs versus 98 +/- 1% in the young salt arteries, while dilations are 99+/-0.7% in the old MAs when compared with 85 +/- 5% in the old salt arteries (P<0.05)^[3].