This study was designed to determine whether remacemide hydrochloride, a no
ncompetitive N-methyl-D-aspartate-type glutamate receptor channel blocker,
has a significant impact on serum levodopa concentrations that could compli
cate the interpretation of future clinical trial results. We performed a mu
lticenter, open-label study of remacemide in 18 patients with mild to moder
ate Parkinson's disease (PD) who were taking stable dosages of levodopa. Le
vodopa pharmacokinetics were determined after administration of the patient
s' usual morning levodopa dose. Patients then took remacemide 300 mg twice
a day for 2 weeks, with levodopa pharmacokinetics determined again at an id
entical testing session, except that remacemide 300 mg was administered one
hour before levodopa. Clinical responses were also measured using the Unif
ied Parkinson's Disease Rating Scale (UPDRS). With remacemide treatment, th
e area-under-the-curve for levodopa did not change. The mean peak plasma le
vodopa concentration (Cmax) was reduced by 16% compared to baseline, and th
e mean time to achieve peak plasma levodopa concentration (Tmax) was delaye
d by 20%. Although remacemide delayed levodopa absorption, the magnitude of
the interaction suggests that is unlikely to be an important factor in pla
nning and interpreting future trials of remacemide in levodopa-treated pati
ents with PD.