Nelonemdaz (Salfaprodil) potassium is an NR2B-selective and uncompetitive antagonist of N-methyl-D-aspartate (NMDA). Nelonemdaz potassium is also a free radical scavenger. Nelonemdaz potassium has excellent neuroprotection against NMDA- and free radical-induced cell death[2].IC50 & Target: NMDAIn Vitro: Nelonemdaz potassium (10-300 μM) shows apparent neuroprotection against 300 μM N-methyl-d-aspartate (NMDA) at doses as low as 30 μM.
Nelonemdaz potassium (10-500 μM) inhibits the electrophysiologic response of cultured cortical neurons to 300 μM NMDA in a concentration-dependent manner.
Nelonemdaz potassium (0.1-1 μM) produces a marked reduction of Fe2+-induced neurotoxicity, even at doses of 0.1 to 0.3 μM.
Nelonemdaz potassium (0.1-1 μM) blocks the degeneration of neurons and glia in cortical cell cultures.
Nelonemdaz potassium (0-350 μM) effectively scavenges superoxide radicals (IC50=63.07±1.44 μM), nitric oxide (IC50=155.8±4.88 μM), and hydroxyl radicals (IC50=58.45±1.74 μM).
Nelonemdaz potassium (0.78-12.5 μM) decreases the amount of antimycin A-induced ROS/RNS formation in a dose-dependent manner, with an IC50 of 2.21±0.11 μM.
Nelonemdaz potassium (0.19-12.5 μM) inhibits malondialdehyde (MDA) formation with an IC50 of 2.72±0.26 μM.
Nelonemdaz potassium (0-125 μM) effectively reduces iron-ascorbate-induced lipid peroxidation (IC50=24.56±0.07 μM).In Vivo: 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.
Nelonemdaz potassium (5 mg/kg; i.v.) protects white matter such as axons and myelin as well as gray matter from ischemic brain injury.