Like other calcium channel blockers of the dihydropyridine class, lercanidipine blocks L-type calcium channels in the smooth muscle cells of blood vessels. This relaxes them and allows better blood flow, which lowers blood pressure. Unlike the non-dihydropyridine calcium channel blockers verapamil and diltiazem, lercanidipine has no significant effect on calcium channels in the heart at usual therapeutic doses and therefore does not lower heart rate.
Lercanidipine is slowly but completely absorbed from the intestine. Bioavailability is only 10% due to an extensive first-pass effect, but can be as high as 40% when taken after a high-fat meal. Peak blood plasma levels are reached after 1.5 to 3 hours. Lercandipine is almost completely (>98%) bound to plasma proteins but in unbound form can be readily deposited in adipose tissue, resulting in a mild depot effect. It is completely metabolized in the liver, mainly via the enzyme CYP3A4. The elimination half-life is 8 to 10 hours. Due to the depot effect, the antihypertensive effect lasts for at least 24 hours. Lercandipine is excreted in the urine.
The substance is metabolized by the liver enzyme CYP3A4. This also metabolizes a number of other drugs. This results in a number of possible interactions.
CYP3A4-inhibiting drugs may increase the plasma level of lercandipine and thus enhance the effect and promote undesirable side effects. These include, for example, the agents ketoconazole and itraconazole, ciclosporin, erythromycin, and grapefruit juice. Conversely, CYP3A4 inducers such as carbamazepine, rifampicin, and St. John's wort likely lower plasma levels and thus reduce the efficacy of lercanidipine. Lercanidipine may increase plasma levels of ciclosporin and digoxin.