It is oxidized in the body to phenobarbital and phenethyl malonamide, which have anti-epileptic activity. Its anti-epileptic effect is similar to that of phenobarbital, but its intensity and toxicity are lower. It is rapidly and completely absorbed orally, reaching the peak plasma concentration in about 3 hours. The half-life is about 8 hours, and the plasma protein binding rate is 20%. It can easily penetrate the blood-brain barrier, the placenta, and appear in breast milk. It reduces the excitatory effect of glutamate, strengthens the inhibitory effect of gamma-aminobutyric acid, inhibits monosynaptic and polysynaptic transmission in the central nervous system, leads to a decrease in the excitability of the entire nerve cell, and increases the electrical stimulation threshold of the motor cortex. It can increase the threshold of seizures and inhibit the spread of discharges of epileptic foci.

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This product is a central antihypertensive drug that selectively stimulates the I1 imidazoline receptors in the rostral ventrolateral nucleus of the medulla oblongata (RVLM). By stimulating the medullary imidazoline receptors, peripheral sympathetic nerve activity is reduced, vasodilation occurs, and peripheral vascular resistance decreases, thereby lowering blood pressure. The affinity of this product for α2A receptors is weaker than that for I1 imidazoline receptors, so this product does not slow down the heart rate when lowering blood pressure, and has no obvious central sedative effect.

Nimodipine is a Ca2 channel blocker that inhibits smooth muscle contraction and relieves vascular spasm by preventing Ca2 from entering cells. It has a strong effect on cerebral arteries, can pass through the blood-brain barrier, increase cerebral blood flow, reduce ischemic brain damage, and also has the effect of protecting and promoting memory and promoting intellectual recovery.