F 15845 is a potent and persistent blocker of the sodium current. It possesses cardioprotective properties and exhibits both anti-ischemic activity and short- and long-term cardioprotection following myocardial infarction. Furthermore, F 15845 finds utility in the investigation of myocardial functional impairment [1].

F 15845, at concentrations ranging from 10 nM to 10 μM, has been shown to concentration-dependently mitigate veratrine-induced diastolic contracture in isolated atria, with an IC50 value of 0.14 μM [1]. Additionally, when administered at 0.1 to 10 μM, it effectively preserves the viability of isolated cardiomyocytes challenged with lysophosphatidylcholine (LPC) [1]. At a specific concentration of 0.3 μM, F 15845 significantly counteracts the increase in sodium levels ([Na+]) observed during no-flow ischemia, and when applied at the same concentration over a duration of 0-35 minutes, it not only delays the reduction in [Na+] but also prominently marks and sustains it upon reperfusion [1].

F 15845, administered intravenously at doses of 5 mg/kg, demonstrates significant cardioprotective effects in anesthetized rats. This includes a substantial reduction in infarct size, a decrease in troponin I levels, and the prevention of long-term infarct size expansion, underscoring its potential therapeutic benefits in cardiac injury models.