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N-acetyl lysyltyrosylcysteine amide

  Cat. No.:  DC21358   Featured
Chemical Structure
1287585-40-3
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Field of application
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.
Cas No.: 1287585-40-3
Chemical Name: N-acetyl lysyltyrosylcysteine amide
Synonyms: Myeloperoxidase inhibitor KYC
SMILES: SC[C@@H](C(N)=O)NC([C@H](CC1=CC=C(O)C=C1)NC([C@H](CCCCN)NC(C)=O)=O)=O
Formula: C20H31N5O5S
M.Wt: 453.56
Purity: >98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Publication: [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.
Description: N-acetyl lysyltyrosylcysteine amide (KYC) is a potent, tripeptide inhibitor of myeloperoxidase (MPO), inhibits MPO-mediated hypochlorous acid (HOCl) formation (IC50=7 uM) and nitration/oxidation of LDL; completely inhibits HOCl production at 25 uM, decreases vascular oxidative stress and increases vasodilatation in sickle cell disease mice; reduces oxidative stress-mediated inflammation, neuronal damage, and neural stem cell injury in murine model of stroke.
In Vivo: 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. 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. 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.
References: [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):11 [2]. Zhang H, et al. N-acetyl lysyltyrosylcysteine amide inhibits myeloperoxidase, a novel tripeptide inhibitor. J Lipid Res. 2013;54(11):3016-3029.
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