NATs are critical in the metabolism of a wide range of drugs, including isoniazid, sulfonamides, and procainamide. The acetylation process can either activate or deactivate these drugs. For example, isoniazid, used in the treatment of tuberculosis, is acetylated by NAT2. Slow acetylators may experience higher plasma levels of isoniazid, leading to an increased risk of adverse effects such as hepatotoxicity and peripheral neuropathy.
