D-Ribose-L-cysteine

D-Ribose-L-cysteine is an orally effective glutathione (GSH) precursor that crosses the blood-brain barrier. D-Ribose-L-cysteine exhibits potent antioxidant, anti-inflammatory, and neuro- and organ-protective activities. D-Ribose-L-cysteine exerts dual antioxidant and anti-inflammatory effects by promoting endogenous GSH synthesis to scavenge reactive oxygen species (ROS) and inhibiting NF-κB and the expression of its downstream pro-inflammatory factors (TNF-α, IL-6), thereby inhibiting apoptosis. D-Ribose-L-cysteine also reverses Scopolamine (HY-N0296)-induced memory impairment by inhibiting acetylcholinesterase (AChE) activity. D-Ribose-L-cysteine can be used in research on Alzheimer's disease, cardiometabolic syndrome, atherosclerosis, and non-alcoholic fatty liver disease^{[1][2][3][4][5][6][7][8][9][10]}. In Vivo:D-Ribose-L-cysteine (25-100 mg/kg; p.o.; once daily; 7 days) attenuates memory deficits in the LPS (HY-D1056)-induced memory deficit model in Swiss mice by inhibiting oxidative stress, pro-inflammatory cytokine release, and NF-κB expression^[8].
D-Ribose-L-cysteine (25-100 mg/kg; p.o.; once daily; 7 days) enhances memory and attenuates oxidative stress and acetylcholinesterase (AChE) activity in the Scopolamine (HY-N0296)-induced amnesia model in male Swiss mice^[7].
D-Ribose-L-cysteine (200 mg/kg; p.o.; once daily; 2 weeks) attenuates manganese-induced neurotoxicity in rats by improving antioxidant status, reducing oxidative and inflammatory markers, protecting hippocampal dendritic morphology, and modulating Bax/Bcl-2, TNF-α, and ERK responses^[5].
D-Ribose-L-cysteine (200 mg/kg; p.o.; once daily; 14 days) improves glutathione levels, prevents neuronal and mitochondrial ultrastructural damage, and attenuates apoptosis and microglial and astrocyte activation in a manganese-induced neurotoxicity model in Wistar rats^[4].
D-ribose-L-cysteine (250 mg/kg; p.o.; daily; 8 weeks) prevents oxidative stress and cardiometabolic syndrome in HFHF diet-fed male Wistar rats^[2].
D-Ribose-L-cysteine (125-250 mg/kg; p.o.; once daily; 8 weeks) increases cardiac GSH and decreases the atherogenic index in normal Wistar rats^[3].


D-Ribose-L-cysteine (250 mg/kg/d; p.o.; once daily; 8 weeks) prevents hepatic and systemic oxidative stress and reduces TNF-α-related pro-inflammatory responses in male Wistar rats fed a high-fructose high-fat diet^[10].
D-Ribose-L-cysteine (10-50 mg/kg; p.o.; once daily; 28 days) attenuates CuSO₄ (HY-Y1878)-induced memory decline and liver injury in mice by restoring antioxidant defenses and reducing pro-inflammatory cytokines, brain AChE, and hepatic enzyme activities^[1].
D-Ribose-L-cysteine (250 mg/kg/d; p.o.; once daily; 8 weeks) decreases malondialdehyde, uric acid, and CRP and increases SOD in Wistar rats fed a normal diet^[10].
D-Ribose-L-Cysteine (200 mg/kg; p.o.; once daily; two weeks) attenuates manganese-induced weight loss, cognitive and motor deficits, oxidative damage, distortion of striatal and cortical cytoarchitecture, neuronal loss, and microglial activation in rats, with similar efficacy regardless of pre-administration, co-administration, or post-administration regimens^[6].
D-Ribose-L-cysteine (0.16 g/kg; p.o. in drinking water; continuous administration; 8 weeks) increases glutathione-based antioxidant status and decreases LDL and Lp (a) in a human Lp (a) transgenic mouse atherosclerosis model^[9].
D-Ribose-L-cysteine (25-100 mg/kg; p.o.; single dose) enhances spatial and non-spatial memory performance in Swiss mice^[7].