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Pz-1是有效地 RET 和 VEGFR2 受体酪氨酸激酶抑制剂，Pz-1抑制这两个野生型激酶的 IC50 值小于 1 nM
S-MTC产品描述：S-MTC is a selective type I nitric oxide synthase (NOS) inhibitor.IC50 & Target: NOS^[1]In Vitro: S-MTC (10 or 100?μM) reduces cellular NO release in the absence of Aβ_1-42. At 100?μM, S-MTC decreases cell viability. S-MTC (100?μM) significantly lowers nitrite production (11.2±1.1?μM) when compared to control (no NOS inhibitor exposure; 19.6±1.2?μM). Nitrite productions after Aβ_1-42 ａnd L-NOARG (100?μM) or Aβ_1-42 ａnd S-MTC (100?μM) treatments are significantly lower than Aβ_1-42 alone (33.5±2.0 ａnd 34.5±1.6?μM, respectively). S-MTC (100?μM) is able to significantly reduce nitrite production (25.2±1.1?μM) as compared to Aβ_1-42 treatment alone (38.3±2.7?μM), when administered after Aβ_1-42 at the 1?h time point. S-MTC (100?μM) concentration decreases both MTT (87±1% of control) ａnd NR (80±1% of control, respectively) levels. The co-administration of S-MTC (100?μM) ａnd Aβ_1-42 significantly reverses the effects of Aβ_1-42 alone (72±2% vs 61±2% of control)^[1].In Vivo: S-MTC (S-methyl-L-thiocitrulline) is a selective neuronal NOS-inhibitor. Following pretreatment with S-MTC (i.c.v.), the HBO₂-induced antinociception is significantly antagonized. In Experiment #2, different groups of mice are pretreated with naltrexone hydrochloride (NTX) (3.0 mg/kg, i.p.), L-NAME (1.0 μg/mouse, i.c.v.), S-MTC (1.0 μg/mouse, i.c.v.) or N⁵-(1-iminoethyl)-L-ornithine (L-NIO) (3.0 mg/kg, s.c.) 15-30 min prior to HBO₂ treatment. The antinociceptive effect assessed 90 min after HBO₂ treatment is completely abolished by NTX ａnd L-NAME, antagonized by two-thirds by S-MTC ａnd largely unaffected by L-NIO (F=25.57, p<0.0001)^[2]. At a dose of 0.3 mg/kg, S-MTC (SMTC) causes a rise in mean blood pressure (BP). At doses of 1.0, 3.0 ａnd 10 mg/kg, S-MTC causes falls in heart rate, rises in BP ａnd vasoconstriction in all three vascular beds^[3].
产品链接：www.medchemexpress.com/S-MTC.html

研究领域：Immunology/Inflammation

靶点：NO Synthase

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