ADME
Definition
ADME refers to the four key pharmacokinetic processes that determine drug behavior in the body: Absorption (drug entry into bloodstream), Distribution (drug transport to tissues), Metabolism (biochemical modification, primarily hepatic), and Excretion (elimination from the body). These processes collectively determine drug bioavailability, therapeutic concentration, duration of action, and potential toxicity. ADME properties are critical in drug development, as poor pharmacokinetic profiles account for significant drug candidate failures. Understanding ADME involves studying transporter proteins (P-glycoprotein, OATs), metabolizing enzymes (cytochrome P450 family), binding proteins (albumin), and elimination pathways (renal, biliary). ADME characteristics influence dosing regimens, drug-drug interactions, and inter-individual variability in therapeutic response.
Visualize ADME in Nodes Bio
Researchers can map ADME networks showing relationships between drug candidates, metabolizing enzymes, transporter proteins, and metabolites. Visualize how genetic variants in CYP450 enzymes affect drug metabolism pathways, or explore connections between transporters and tissue distribution patterns. Network analysis reveals bottlenecks in elimination pathways and predicts potential drug-drug interactions through shared metabolic enzymes.
Visualization Ideas:
- Drug metabolism pathway networks showing parent compounds, metabolizing enzymes, and metabolite products
- Transporter-tissue distribution maps connecting ABC and SLC transporters to target organs
- Drug-drug interaction networks linking compounds through shared CYP450 enzymes and competitive inhibition
Example Use Case
A pharmaceutical team developing a kinase inhibitor discovers unexpected hepatotoxicity in Phase I trials. Using network analysis, they map the drug's metabolic pathway, identifying CYP3A4 as the primary metabolizing enzyme producing a reactive intermediate. The visualization reveals that co-administered medications in the trial also inhibit CYP3A4, causing accumulation of the parent compound. By examining transporter networks, they identify that the drug is a P-glycoprotein substrate with poor brain penetration, informing reformulation strategies for improved distribution profiles.