Due to its lipophilic nature and small molecular size, lomerizine is able to cross the blood brain barrier.

Lomerizine was shown to have little affinity for NMDA or kainate receptors, so its protectivity against neurotoxicity in these cases is believed to be due to the blocking of Ca2+ influx through voltage-dependent calcium channels.

[7] Lomerizine also shows neuroprotective effects against secondary degeneration resulting from injury in retinal ganglion cells.

In this case, increased membrane depolarization, in conjunction with the inability of the sodium-calcium exchanger to function due to depleted ATP stores, causes the activation of calcium-dependent signal transduction.

[4] While some calcium-channel blockers, such as flunarizine, act on the dopaminergic system, lomerizine is ineffective in vivo at inhibiting the release of dopamine.

[8] While researchers are unsure of the reason for this difference, one hypothesis is that the doses administered cannot reach a high enough concentration in the brain to affect D2 receptors.

[12] When administered orally to healthy male subjects in 10, 20, and 40 mg doses, lomerizine produced peak plasma levels of ≈ 7.3, 15.7, and 31.3 ng/ml.

[10] In a group of 18 healthy adults, 10 mg of lomerizine administered orally had a half-life of 5.48 ± .90 hours, with a peak serum concentration (Cmax) of 9.06 ± 2.46 ng/mL.