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.

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]