EC50: 2.9 μM (KCa2.1), 1.9 μM (KCa2.2), 2.9 μM (KCa2.3), 260 nM (KCa3.1)

SKA-31 activates KCa2/3 channels more potently than PK 26124, and is more selective over other Ion channels.
SKA-31 reduces cell viability with IC _50s of 5.3 μM , 46.9 μM in HCT-116 cells and HCT-8 cells, respectively.
SKA-31 (5.3 μM; 0-96 hours) reduces HCT-116 cells proliferation when added at time zero at 5.3 μM.
SKA-31 triggers apoptosis in HCT-116 cells at 5 μM, and the effect is smaller in HCT-8 cells at 45 μM.
SKA-31 increases the percentage of cells in G0/G1 phase in HCT-116 and HCT-8 cell lines at 5 μM and 45 μM, respectively.
SKA-31 further activates Caspase 3 and reduces Akt phosphorylation induced by CDDP.
SKA-31 has a synergic effect with CDDP also on the inhibition of HCT-116 cell proliferation.

SKA-31 is not acutely toxic and has good pharmacokinetic properties.
SKA-31 potentiates native KCa3.1 and KCa2.3 in murine carotid endothelium with EC ₅₀ values of 225 nM and 1.6 μM for KCa3.1 and KCa2.3, respectively.
SKA-31 stimulates KCa3.1 and KCa2.3 in vascular endothelial cells and increases acetylcholine-induced endothelium-derived hyperpolarizing factor (EDHF) -mediated vasodilation.
SKA-31 potentiates EDHF-type vasodilations and lowers blood pressure in mice. Injections of SKA-31 (1-30 mg/kg; i.p.) lower MAP over 24 hours in normotensive wild-type mice but not in KCa3.1(-/-) mice (-/-).