Mechanism of Action
Ranolazine is believed to have its effects via altering the transcellular late sodium current. It affects the sodium-dependent calcium channels during myocardial ischemia in rabbits by altering the intracellular sodium level. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia in rats. The effects of ranolazine on the NaV 1.7 and NaV 1.8 sodium channels also make it potentially useful in the treatment of neuropathic pain.
Ranolazine, a partial fatty acid oxidation inhibitor, shifts ATP production from fatty acid to more oxygen-efficient carbohydrate oxidation.
Inhibition of fatty acid oxidation (e.g. with etomoxir or ranolazine) was also found to sensitize human leukemia cells to apoptosis induction.
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