SRA-36 is a CLC-K chloride channel inhibitor with selectivity over CLC-5 and CLC-1 chloride channels. SRA-36 blocks CLC-Ka currents with an IC50 of 6.6 μM and a K d of 3.8 μM. SRA-36 blocks chloride currents mediated by targeted channels, and inhibits currents from hypertension-associated CLC-Ka A447T and CLC-Ka Y315F polymorphisms. SRA-36 can be used for the research of hypertension [1].
In Vitro, SRA-36 potently inhibits chloride currents from wild-type CLC-Ka channels heterologously expressed in HEK293 cells, with an IC50 of 6.6 μM[1]. SRA-36 potently inhibits chloride currents from wild-type CLC-Ka channels heterologously expressed in MDCK cells, with an apparent KD of 3.8 μM[1]. SRA-36 potently inhibits chloride currents from CLC-Kb and rat CLC-K1 channels heterologously expressed in HEK293 cells, reducing currents by ~90% at 50 μM[1]. SRA-36 (5 μM) does not inhibit chloride currents from CLC-5 or CLC-1 channels heterologously expressed in HEK293 cells at a concentration of 5 μM[1].
References:
[1]. Liantonio A, et al. Kidney CLC-K chloride channels inhibitors: structure-based studies and efficacy in hypertension and associated CLC-K polymorphisms. J Hypertens. 2016;34(5):981-992.
In Vitro, SRA-36 potently inhibits chloride currents from wild-type CLC-Ka channels heterologously expressed in HEK293 cells, with an IC50 of 6.6 μM[1]. SRA-36 potently inhibits chloride currents from wild-type CLC-Ka channels heterologously expressed in MDCK cells, with an apparent KD of 3.8 μM[1]. SRA-36 potently inhibits chloride currents from CLC-Kb and rat CLC-K1 channels heterologously expressed in HEK293 cells, reducing currents by ~90% at 50 μM[1]. SRA-36 (5 μM) does not inhibit chloride currents from CLC-5 or CLC-1 channels heterologously expressed in HEK293 cells at a concentration of 5 μM[1].
References:
[1]. Liantonio A, et al. Kidney CLC-K chloride channels inhibitors: structure-based studies and efficacy in hypertension and associated CLC-K polymorphisms. J Hypertens. 2016;34(5):981-992.