ATP-dependen potassium (KATP) channels are cellular metabolic sensors linking potassium transport to changes in concentration of nucleotide phosphates, lipids and glycolysis metabolites. Cardiac KATP channels mainly open under hypoxic and ischemic conditions and take part in decreasing intracellular calcium concentration and cardiac excitability.Fluorine-containing analogue of pinacidil is an effective, nontoxic and stable hypotensive preparation that opens KATP channels (with EC50=8.1±0.4 µM on heterologously expressed cardiac channels). At submicromolar concentrations flocalin decreases cardiac excitability by hyperpolarizing plasma membrane, shortening action potential (AP) duration and decreasing rate of spontaneous contractions.Here using patch clamp method we found that flocalin blocks sodium current of neonatal cardiomyocytes with IC50=17.0±1.6 µM and maximal block of 70±18% and shifts stationary inactivation curve by −5.8±1.8 mV. High-voltage actived calcium current is also inhibited with IC50=21.7±2.1 µM and maximal block of 52±16% not changing inactivation properties and voltage dependency. Flocalin significantly changed intracellular calcium signal. 5 µM flocalin reduced amount of Ca2+ released during contraction, amplitude of [Ca2+]i transients and rate by 2-3-fold and decreased resting calcium level.Described effects explain decrease of AP amplitude and upstroke velocity observed earlier. Inhibition of sodium currents was in part due to hyperpolarizing shift of inactivation curve. Block of sodium and calcium channels in addition to KATP opening accounts for complex effect of flocalin on cardiac activity reduction.