Norfluoxetine hydrochloride

Norfluoxetine (0.1-10 μM; 12-24 h) hydrochloride inhibits full-length human TREK-2 channels expressed in Xenopus laevis oocytes with an IC₅₀ of 2.7 μM at +40 mV; inhibition is reduced by TPA and ML335 but not by tetraethylammonium or 2-APB^[1].
Norfluoxetine (10-100 μM) hydrochloride reduces single-channel open probability, current amplitude, mean open time, and mean short closed time of truncated human TREK-2 channels reconstituted in lipid bilayers, with increased inhibitory efficacy at voltages above +60 mV, and exhibits similar inhibitory efficacy in high-P_o and standard gating modes^[1].
Norfluoxetine (10 μM) hydrochloride significantly attenuates nitric oxide and TNF release from lipopolysaccharide-activated primary rat microglia^[2].
Norfluoxetine (10-30 μM) hydrochloride reduces protein levels in non-activated primary rat microglia in a dose-dependent manner^[2].
Norfluoxetine (10-30 μM) hydrochloride reduces viability of non-activated primary rat microglia in a dose-dependent manner^[2].
Norfluoxetine (10 μM) hydrochloride significantly increases the number of dead non-activated primary rat microglia, as measured by live/dead nuclear staining^[2].
Norfluoxetine (10 μM) hydrochloride significantly increases the percentage of non-activated primary rat microglia expressing the apoptotic marker cleaved-caspase 3^[2].
Norfluoxetine (10-20 μM; 24 h) hydrochloride induces apoptosis in non-activated primary rat microglia by increasing cleaved-caspase 3 and decreasing full-length caspase 3, without altering caspase 8 levels^[2].
Norfluoxetine (1-100 μM; 30 s) hydrochloride concentration-dependently inhibits voltage-gated Ca²⁺ channel-mediated Ba²⁺ currents in isolated rat cochlear neurons with an EC₅₀ of 20.4 μM^[3].

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