Toxicology Assessment via Adverse Outcome Pathways & Signal Detection

Systematic toxicology analysis that links molecular initiating events (MIEs) through adverse outcome pathways (AOPs) to apical adverse outcomes, then triangulates with real-world FAERS signals, FDA label data, and toxicogenomic associations.

Domain Reasoning

Toxicity has many mechanisms, and the first interpretive question is temporal: is this acute toxicity (immediate effect from a high dose) or chronic toxicity (cumulative damage from long-term low-dose exposure)? Acute and chronic toxicity operate through different mechanisms — acute hepatotoxicity may reflect direct mitochondrial damage, while chronic hepatotoxicity may involve fibrosis from repeated low-level inflammation. They also have different regulatory frameworks: acute toxicity is captured by LD50 and emergency protocols, while chronic toxicity requires long-term carcinogenicity and repeat-dose studies.

LOOK UP DON'T GUESS

• Adverse outcome pathways for a chemical: query AOPWiki_list_aops and AOPWiki_get_aop; do not describe mechanisms from memory.
• FAERS adverse event signals: retrieve from FAERS_count_reactions_by_drug_event and FAERS_calculate_disproportionality; never estimate PRR values.
• FDA label warnings: call DailyMed_parse_adverse_reactions and related tools; do not state boxed warnings from memory.
• CTD chemical-gene and chemical-disease associations: query CTD_get_chemical_gene_interactions and CTD_get_chemical_diseases; do not infer gene targets without database evidence.