N-Acetyl lysyltyrosylcysteine amide is a non-toxic, potent, reversible, and specific myeloperoxidase (MPO) tripeptide inhibitor that effectively inhibits MPO production in vivo, attenuates neuronal damage, preserves brain tissue and neurological function post-stroke, and inhibits MPO-dependent hypochlorite (HOCl) production, protein nitration, and LDL oxidation. It is also used in the study of bronchial dysplasia.

N-Acetyl lysyltyrosylcysteine amide (KYC) (10 mg/kg; i.p.; daily for 3-7 days; C57BL/6J mice) significantly reduces neurological severity scores and infarct size in MCAO mice.[1]
N-Acetyl lysyltyrosylcysteine amide (10 mg/kg; i.p.; daily for 7 days) significantly protects BBB function and decreased neutrophil infiltration.[1]
N-Acetyl lysyltyrosylcysteine amide (10 mg/kg; i.p.; daily for 7 days; C57BL/6J mice) significantly reduces microglia/macrophage activation and neuron loss in MCAO mice.[1]
N-Acetyl lysyltyrosylcysteine amide (10 mg/kg; i.p.; daily for 3-7 days; C57BL/6J mice) decreases apoptosis and cell injury in the brains of MCAO mice.[1]
N-Acetyl lysyltyrosylcysteine amide reduced MPO in the brains of MCAO mice. N-Acetyl lysyltyrosylcysteine amide reduces NO2Tyr and 4-HNE in MCAO mice. N-Acetyl lysyltyrosylcysteine amide 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]