Methamphetamine (MA) use during pregnancy is rising in Australia, with hundreds of children exposed in-utero each year. However, long-term impacts are poorly defined, and there are no FDA-approved treatments. To provide better insight into these impacts, and explore the potential of N-Acetyl Cysteine (NAC) as a prenatal intervention, we used an animal model of prenatal MA exposure with concurrent NAC treatment. Pregnant Long-Evans rats received MA (5 mg/kg/day) or saline via subcutaneous injections from gestational day 10 through to postnatal day 21, alongside bottles of NAC (1% w/v) or regular drinking water. Infant rats prenatally exposed to either MA or NAC demonstrated reduced early weight gain, indicating that each compound independently affects early growth. Adult rats prenatally exposed to MA demonstrated reduced lever-pressing in a sign-tracking task, consistent with impaired reward processing, while NAC had no effect. MA-exposed adults also showed deficits in associative interference during latent inhibition, suggesting persistent deficits in cognitive control. Critically, adult rats exposed to both MA and NAC exhibited intact performance in this task, indicating that NAC can prevent long-lasting cognitive impairments, which are likely driven by oxidative stress. These findings highlight the translational potential of NAC as a prenatal intervention to protect against persistent cognitive deficits from prenatal MA exposure. These results also suggest a promising strategy to mitigate developmental harm in children prenatally exposed to MA, with implications for public health policy and preventative treatment approaches.