The nonproprietary name is derived from the cinnamyl substituent on the free nitrogen atom of the benzhydrylpiperazine core, combined with the generic ending "-rizine" for "antihistaminics/cerebral (or peripheral) vasodilators".

[13] The disparity of signal processing between inner ear motion receptors and the visual senses is abolished, so that the confusion of brain whether the individual is moving or standing is reduced.

Vomiting in motion sickness could be a physiological compensatory mechanism of the brain to keep the individual from moving so that it can adjust to the signal perception, but the true evolutionary reason for this malady is currently unknown.

[18] Beyond an anti-vertigo treatment, cinnarizine could be also viewed as a nootropic drug because of its vasorelaxating abilities (due to calcium channel blockade), which happen mostly in brain, and the fact that it is also used as a labyrinthine sedative.

[15] Because cinnarizine can cause drowsiness and blurred vision, it is important that users make sure their reactions are normal before driving, operating machinery, or doing any other jobs which could be dangerous if they are not fully alert or able to see well.

[6] Cinnarizine causes acute and chronic parkinsonism due to its affinity for D2 receptors,[22] which strongly counter-suggests its actual usefulness for improving neurological health.

Cinnarizine's antagonistic effects of D2 dopamine receptors in the striatum leads to symptoms of depression, tremor, muscle rigidity, tardive dyskinesia, and akathisia.

[5] Chronic treatment with cinnarizine builds the drug concentrations high enough that they interfere with the proton electrochemical gradient necessary for packaging dopamine into vesicles.

[5] Several cases of pediatric and adult cinnarizine overdose have been reported, with effects including a range of symptoms such as somnolence, coma, vomiting, hypotonia, stupor, and convulsions.

[32] The lipid emulsion administration had a higher AUC and lower clearance than the solution form, which meant that there was an increased bioavailability of cinnarizine, allowing for an improved therapeutic effect.

[4] The IC50 (half-maximal inhibitory concentration) of cinnarizine for smooth muscle contraction inhibition is 60 mM[34] and it has been shown that this drug preferentially binds to its target calcium channels when they are in an open, as opposed to closed conformation.

[35] In treatment of nausea and motion sickness it was previously hypothesized that cinnarizine exerts its effects by inhibiting the calcium currents in voltage gated channels in type II vestibular hair cells within the inner ear.

[9] However, more recent evidence supports the idea that at pharmacologically relevant levels (0.3–0.5 μM), cinnarizine is not lessening vestibular vertigo by blocking calcium channels, but rather by inhibiting potassium (K+) currents that are activated by heightened hydrostatic pressure on the hair cells.

[13] The inhibition of these currents works to lessen the vertigo and motion-induced nausea by dampening the over-reactivity of the vestibular hair cells, which send information about balance and motion to the brain.