Nelonemdaz potassium (also known as Salfaprodil) is a potent NR2B-selective and uncompetitive antagonist of N-methyl-D-aspartate (NMDA). This compound exhibits remarkable neuroprotection against cell death induced by both NMDA and free radicals, in addition to its role as a free radical scavenger.

Nelonemdaz potassium (10-300 μM) shows apparent neuroprotection against 300 μM N-methyl-d-aspartate (NMDA) at doses as low as 30 μM[1]. Nelonemdaz potassium (10-500 μM) inhibits the electrophysiologic response of cultured cortical neurons to 300 μM NMDA in a concentration-dependent manner[1]. Nelonemdaz potassium (0.1-1 μM) produces a marked reduction of Fe 2+ -induced neurotoxicity, even at doses of 0.1 to 0.3 μM[1]. Nelonemdaz potassium (0.1-1 μM) blocks the degeneration of neurons and glia in cortical cell cultures[1]. Nelonemdaz potassium (0-350 μM) effectively scavenges superoxide radicals (IC 50 =63.07±1.44 μM), nitric oxide (IC 50 =155.8±4.88 μM), and hydroxyl radicals (IC 50 =58.45±1.74 μM)[3]. Nelonemdaz potassium (0.78-12.5 μM) decreases the amount of antimycin A-induced ROS/RNS formation in a dose-dependent manner, with an IC 50 of 2.21±0.11 μM[3]. Nelonemdaz potassium (0.19-12.5 μM) inhibits malondialdehyde (MDA) formation with an IC 50 of 2.72±0.26 μM[3]. Nelonemdaz potassium (0-125 μM) effectively reduces iron-ascorbate-induced lipid peroxidation (IC 50 =24.56±0.07 μM)[3].

Nelonemdaz potassium (0.5-20 mg/kg; i.v.) reduces cerebral infarct evolving 24 h after 60-mins occlusion of the middle cerebral artery occlusion (MCAO) substantially and dose dependently[1]. Nelonemdaz potassium (5 mg/kg; i.v.) protects white matter such as axons and myelin as well as gray matter from ischemic brain injury[1]. Animal Model: Male Sprague-Dawley rats (260 to 300 g) (clip occlusion model)[1]Dosage: 0.5-20 mg/kg Administration: I.v. administration 5 mins after reperfusion Result: Produced a large neuroprotective effect, with a maximal reduction in infarct volume of 66% at doses of 2.5 to 5 mg/kg. Not observed neuronal damage in the most vulnerable cortical area after administration of 5 mg/kg. Animal Model: Male Sprague-Dawley rats (260 to 300 g) (intraluminal thread occlusion model)[1]Dosage: 5 mg/kg Administration: I.v. administration 30 mins after reperfusion Result: Did not change physiologic variables such as arterial pH, PCO 2 , PO 2 , and hematocrit. Reduced infarct volume evolving in the cortex and the striatum substantially. Reduced white matter damage in the striatum and external capsule markedly.