Remacemide is a drug which acts as a low-affinity NMDA antagonist with sodium channel blocking properties.

[17] The median toxic dose of remacemide for neural impairment tests in mice is 5.6 mg/kg.

[22] Remacemide binds weakly and noncompetitively to the ionic channel site of the NMDA receptor complex.

[7] That is, remacemide may actually act as a prodrug to deliver the active metabolite FPL 12495 to the central nervous system.

[24] In a well validated and described genetic model of absence epilepsy, rats of the WAG/Rij strain, remacemide and its metabolite FPL 12495 were found to have a common for glutamate antagonist usual effect on the number of spike/wave dischargesEEG, the drugs decrease spike/wave discharges dose dependently.

[25] The brain uptake index (BUI), a measure of a drug's ability to pass the blood–brain barrier that involves the injection of radiolabeled test and reference substances into the common carotid artery of anesthetized animals,[26][27] for remacemide is 51 ± 0.9 SD.

[7] Remacemide is an experimental drug most recently being developed by the British multinational pharmaceutical company AstraZeneca.

[33][34] Remacemide was one of the last drugs under development by the now-defunct English pharmaceutical company Fisons.

[34] In 1990, researchers at Fisons found that remacemide acted as an anticonvulsant in mice and rats[17][28] .

[40][42] By 1998, when Astra announced its merger with Zeneca, remacemide had progressed to Phase III trials for epilepsy and Phase II trials for Parkinson's disease, and Astra was also investigating its potential for treating neuropathic pain[43] In 1999, after the merger, AstraZeneca reported that they were investigating remacemide for its neuroprotective effects, and that they planned regulatory submissions for Huntington's disease in 2001 and for Parkinson's disease and epilepsy in 2003.

[44] Remacemide, under the trade name Ecovia, was designated an orphan drug for the treatment of Huntington's disease by the FDA in March 2000.