The mechanism of gabapentin's anticonvulsant effect is still unclear, but animal studies suggest that gabapentin can inhibit epileptic seizures, similar to other marketed anticonvulsant drugs. Results from the maximum electric shock test in mice and rats, the benzotetrazolyl epilepsy seizure test, and other animal studies (such as genetic epilepsy models) suggest that gabapentin has antiepileptic effects, but the relevance of these epilepsy models to humans is unclear. Gabapentin is structurally related to the neurotransmitter GABA, but does not interact with GABA receptors. It can neither be metabolized into GABA or GABA agonists, nor is it an inhibitor of GABA uptake or degradation. Radioligand binding experiments have found that gabapentin has no affinity for many common receptor sites, including benzodiazepine receptors, at concentrations of 100 μM.

Telmisartan is an oral specific non-peptide angiotensin II receptor (AT1 type) antagonist. Telmisartan selectively binds to the AT1 receptor site with high affinity, persistently antagonizes angiotensin II, and causes a decrease in blood aldosterone levels, thereby reducing blood pressure. Telmisartan does not inhibit human plasma renin, nor does it block ion channels, nor does it inhibit angiotensin converting enzyme (kinase II), nor does it affect the degradation of bradykinin by the enzyme, so there will be no adverse reactions caused by the enhanced effect of bradykinin. For patients with hypertension, telmisartan can reduce systolic and diastolic blood pressure without affecting heart rate. Rebound hypertension does not occur after discontinuation of telmisartan.

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