MIND4-17 是一种有效的NRF2激活剂,可共价修饰 Keap1 的 C151 残基。MIND4-17 破坏 Keap1-Nrf2 结合,导致 Nrf2 蛋白稳定和核易位。MIND4-17 具有强大的抗氧化活性。
生物活性 | MIND4-17 is a potentNRF2activator that covalently modifies a C151 residue of Keap1. MIND4-17 disruptsKeap1-Nrf2association, leading to Nrf2 protein stabilization and nuclear translocation. MIND4‐17 exerts potent antioxidant activity[1][2]. |
体外研究 (In Vitro) | MIND4-17(0.1-2 μM;24 小时)以浓度依赖性显着增加典型 ARE 基因 Nqo1、Hmox1、Srx1 的表达,并在较小程度上增加 Gclc[1]。 MIND4-17(0.1-2 μM;24 小时)在 WT 和 HD 突变体 ST14A 细胞中显示浓度依赖性诱导 NQO1 和 GCLM 蛋白[1]。 MIN4-17 (0.1-10 μM) 降低小胶质细胞中的 ROS 水平和氮中间产物的产生[1]。
RT-PCR[1] Cell Line: | Rat corticostriatal neuronal | Concentration: | 1 μM, 5 μM | Incubation Time: | 4 hours, 16 hours | Result: | Significantly and concentration-dependently increased the expression of the canonical ARE genes Nqo1, Hmox1, Srx1, and to a lesser degree Gclc. |
Western Blot Analysis[1] Cell Line: | Wild-type (WT) and Huntington's disease (HD) mutant ST14A cells | Concentration: | 0.1 μM, 0.2 μM, 0.5 μM, 0.7 μM, 1 μM, 1.5 μM, 2 μM | Incubation Time: | 24 hours | Result: | Showed a concentration-dependent induction of NQO1 and GCLM proteins. |
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体内研究 (In Vivo) | MIND4-17(2 mg/kg;玻璃体内注射;一次)激活 Nrf2 信号并减轻小鼠光损伤引起的视网膜功能障碍[2]。
Animal Model: | BALB/c mice bearing white fluorescent light exposure[2] | Dosage: | 2 mg/kg | Administration: | Intravitreal injection; once | Result: | Activated Nrf2 signaling and attenuated retinal dysfunction by light damage in mice. |
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运输条件 | Room temperature in continental US; may vary elsewhere. |
储存方式 | Please store the product under the recommended conditions in the Certificate of Analysis. |