In vitro activity: Quinine exhibits concentration-dependent and reversible blocking of Cx36 and Cx50 junctional currents, with half maximal blocking concentrations of 32 mM and 73 mM, respectively. Quinine causes the channel's open probability to decrease by causing gradual transitions between the open and fully closed states. Quinine thus provides a potentially helpful way to block specific kinds of gap junction channels, such as those formed by Cx36 between neurons.[1] Quinine is a K+ channel blocker that stops the hepatic DNA from fragmenting and leaking liver enzymes by preventing the formation of tumor necrosis factor (TNF).[2] The medial third of the nucleus is where quinine causes Fos-like immunoreactivity (FLI) to be concentrated, whereas the lateral region is where acid causes FLI to be more widely distributed. In resistant cells, quinine fully restored doxorubicin sensitivity while having a negligible impact on doxorubicin accumulation[3]. Quinine has the ability to alter the distribution of drugs within cells as evidenced by its modification of the intracellular tolerance to doxorubicin. [4] In general, quinine inhibits voltage-dependently the whole cell potassium currents (IK). While largely unaffected by quinine, calcium currents (ICa) are likewise diminished in a use-dependent manner.[5]