SKA-31 Is not acutely toxic and has good pharmacokinetic properties[1]. SKA-31 potentiates native KCa3.1 and KCa2.3 in murine carotid endothelium with EC50 values of 225 nM and 1.6 μM for KCa3.1 and KCa2.3, respectively[1]. SKA-31 stimulates KCa3.1 and KCa2.3 in vascular endothelial cells and increases acetylcholine-induced endothelium-derived hyperpolarizing factor (EDHF) -mediated vasodilation[1]. 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 (-/-)[1]. Animal Model: 16-25 weeks mice[1] Dosage: 1 mg/kg, 10 mg/kg, and 30 mg/kg Administration: Intraperitoneal injection Result: Lower MAP over 24 hours in normotensive wild-type mice but not in KCa3.1(-/-) mice (-/-).
In Vitro
SKA-31 activates KCa2/3 Channels more potently than Riluzole, and is more selective over other Ion channels[1]. SKA-31 reduces cell viability with IC50s of 5.3 μM , 46.9 μm in HCT-116 cells and HCT-8 cells, respectively[2]. SKA-31 (5.3 μM; 0-96 hours) reduces HCT-116 cells proliferation when added at time zero at IC50 value[2]. SKA-31 triggers apoptosis in HCT-116 cells at 5 μM, and the effect is smaller in HCT-8 cells at 45 μM[2]. 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[2]. SKA-31 further activates Caspase 3 and reduces Akt phosphorylation induced by Cisplatin[2]. SKA-31 has a synergic effect with Cisplatin also on the inhibition of HCT-116 cell proliferation[2]. Cell Viability Assay[2] Cell Line: HCT-116 cells, HCT-8 cells Concentration: Incubation Time: 24 hours Result: Reduced cell viability with IC50s of 5.3 μM , 46.9 μm in HCT-116 and HCT-8, respectively. Cell Proliferation Assay[2] Cell Line: HCT-116 cells Concentration: 5.3 μM Incubation Time: 0-96 hours Result: Reduced HCT-116 cells proliferation when added at time zero at IC50S value. Apoptosis Analysis[2] Cell Line: HCT-116 cells, HCT-8 cells Concentration: 5 μM (HCT-116 cells), 45 μM (HCT-8 cells) Incubation Time: 24 hours Result: Triggered apoptosis in HCT-116 cells, and the effect was smaller in HCT-8 cells. Cell Cycle Analysis[2] Cell Line: HCT-116cells, HCT-8 cells Concentration: 5 μM (HCT-116), 45 μM (HCT-8) Incubation Time: 24 hours Result: Increased the percentage of cells in G0/G1 phase in HCT-116 and HCT-8 cell lines. Western Blot Analysis[2] Cell Line: HCT-116 cells Concentration: Incubation Time: 24 hours Result: Further activated Caspase 3 and reduced Akt phosphorylation when co-treatment with Cisplatin in HCT-116 cells.
Kinase Assay
Cell Assay
Animal Administration
References
[1]. Sankaranarayanan A, et al. Naphtho[1,2-d]thiazol-2-ylamine (SKA-31), a new activator of KCa2 and KCa3.1 potassium channels, potentiates the endothelium-derived hyperpolarizing factor response and lowers blood pressure. Mol Pharmacol. 2009 Feb;75(2):281-95.
[2]. Serena Pillozzi, et al. The combined activation of KCa3.1 and inhibition of Kv11.1/hERG1 currents contribute to overcome Cisplatin resistance in colorectal cancer cells. Br J Cancer. 2018 Jan; 118(2): 200–212.
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