Studies have shown a reduction in oxidative metabolites likely by shunting metabolism away from CYP2E1 and a resultant decrease in liver injury in animals, independent of CYP2E1 interactions. Fomepizole's action is mediated by inhibition of CYP2E1 to prevent oxidant stress generation, and inhibition of c-Jun N-terminal kinase (JNK) to decrease amplification of oxidant stress signaling to mitochondria.

Eleven preclinical studies (in vitro and animal), fourteen case reports/series, and one human volunteer study were included. Reports on fomepizole as a therapeutic adjunct for APAP toxicity span heterogeneous types of evidence. The objective is to comprehensively review the literature on fomepizole as a potential adjunct antidote for acetaminophen toxicity.Ī scoping review was performed using standardized search terms from inception through July 2021. While N-acetylcysteine (NAC) is an effective antidote, it has therapeutic limitations in massive overdose or delayed presentation. Acetaminophen (paracetamol, APAP) poisoning is a prominent global cause of drug-induced liver injury.

Antidote for paracetamol poisoning