N-Acetylcysteine amide is a thiol antioxidant and a neuroprotective agent with cell permeability and blood-brain barrier permeability. N-Acetylcysteine amide reduces ROS production.

方法：人肝癌细胞 HepaRG 用 N-Acetylcysteine amide 或 N-acetylcysteine (0.1-10 mM) 处理 24 h，通过 Calcein AM assay 检测细胞活力。
结果：N-Acetylcysteine amide 在 1 mM 以下无毒；然而，N-acetylcysteine 在 0.75 mM 以上的 HepaRG 细胞中诱导了毒性。[1]
方法：心肌细胞 H9c2 用 N-Acetylcysteine amide (750 µM) 和 DOX (5 µM) 处理 24 h，通过 DCF 荧光强度检测细胞内 ROS 测量。
结果：DOX 治疗组的 ROS 增加了 56%，在 N-Acetylcysteine amide 存在的情况下，增加量降至对照组水平。[2]

方法：为研究对甲基苯丙胺 (METH) 毒性的影响，将 N-Acetylcysteine amide (250 mg/kg) 腹腔注射给 CD-1 小鼠。随后，在 8 h 内每 2 h 注射一次 METH 或生理盐水。
结果：暴露于 METH 的 NACA 治疗动物的肾脏、肝脏和大脑中的氧化应激明显低于未治疗组。这表明 METH 会在各种器官中引起氧化应激，NACA 作为神经或组织保护剂的组合，可能会有效治疗 METH 滥用者。[3]

To determine effectiveness of NACA and NAC in protection of H9c2 cells from DOX-induced toxicity, cells were treated with NACA or NAC at 0.75 mM for 2 h followed by exposure to freshly prepared cell culture medium with DOX in presence or absence of NACA or NAC at designated concentrations. The concentrations of DOX were 0.25 μM, 0.75 μM, 2 μM, 5 μM, 20 μM, and 100 μM. The exposure durations were 24 h, 48 h, or 48 h. Cells incubated with NACA or NAC alone were used as the control[1].

rats were randomly divided into three groups (n=6-8 animals/group): N-acetylcysteine amide?loaded pump (18.5?mg/kg/hr) and a single 150 mg/kg bolus intraperitoneal (IP) injection of NACA given (30 min post-injury) ?N-acetylcysteine amide?(18.5 mg/kg/hr) loaded pump and a single 150 mg/kg bolus injection of N-acetylcysteine amide?given IP (30 min post-injury) ?Vehicle loaded pump and?single vehicle bolus injection given IP (30 min post-injury).?Following random distribution of all animals into one of the three previous groups, experimenters were blinded to treatment group.?The osmotic mini pumps were assembled and implanted immediately after injury and remained in the animals for 7 days[2]