N-Acetyl lysyltyrosylcysteine amide is a potent, reversible, specific, and non-toxic tripeptide inhibitor of myeloperoxidase (MPO). N-Acetyl lysyltyrosylcysteine amide effectively inhibits MPO generation of toxic oxidants in vivo. N-Acetyl lysyltyrosylcysteine amide reduces neuronal damage and preserves brain tissue and neurological function in the stroked brain. N-Acetyl lysyltyrosylcysteine amide inhibits MPO-dependent hypochlorous acid (HOCl) generation, protein nitration, and LDL oxidation[1][2].
N-Acetyl lysyltyrosylcysteine amide (KYC) significantly decreases infarct size, blood-brain barrier leakage, infiltration of myeloid cells, loss of neurons, and apoptosis in the brains of middle cerebral artery occlusion (MCAO) mice[1].N-Acetyl lysyltyrosylcysteine amide (10 mg/kg; i.p.; daily for 3-7 days) significantly reduces neurological severity scores and infarct size in MCAO mice[1].N-Acetyl lysyltyrosylcysteine amide (10 mg/kg; i.p.; daily 7 days) significantly protects BBB function and decreased neutrophil infiltration. N-Acetyl lysyltyrosylcysteine amide (10 mg/kg; i.p.; daily 7 days) significantly reduces microglia/macrophage activation and neuron loss in MCAO mice. N-Acetyl lysyltyrosylcysteine amide (10 mg/kg; i.p.; daily for 3-7 days) decreases apoptosis and cell injury in the brains of MCAO mice. N-Acetyl lysyltyrosylcysteine amide reduced MPO in the brains of MCAO mice. N-Acetyl lysyltyrosylcysteine amide reduces NO2Tyr and 4-HNE in MCAO mice[1]. Animal Model: 8-10 weeks old C57BL/6J mice (middle cerebral artery occlusion (MCAO) mode)[1]
[1]. Yu G, et al. Inhibition of myeloperoxidase oxidant production by N-acetyl lysyltyrosylcysteine amide reduces brain damage in a murine model of stroke [published correction appears in J Neuroinflammation. 2016;13(1):166]. J Neuroinflammation. 2016;13(1):119. Published 2016 May 24. [2]. Zhang H, et al. N-acetyl lysyltyrosylcysteine amide inhibits myeloperoxidase, a novel tripeptide inhibitor. J Lipid Res. 2013;54(11):3016-3029.