Liver Toxin Metabolism & DILI Simulator DILIN +400% USA Trend

Cellular enzyme saturation kinetics, CYP2E1 bioactivation (NAPQI), and Glutathione (GSH) rescue window

Hepatocyte Micro-Reactor (p5.js Kinetics)

T+ 0.0 hrs
Glutathione (GSH) 100.0% Critical: <30%
NAPQI Electrophile 0.0 µM Adduct forming
Phase II Saturation 18.4% Vmax capacity
Hepatocyte Viability 100.0% Membrane intact
Acute Acetaminophen Dose 8,000 mg
CYP2E1 Activity Multiplier (Ethanol / Fasting) 1.4x
Dose Administration Pattern Single Bolus
Simulation Speed 1.0x Realtime

N-Acetylcysteine (NAC) Antidote Protocol

Glutathione substrate donor is currently inactive. Deliver to replenish GSH pool.

Real-time Kinetic Trajectories (0 - 24 Hours)

APAP Serum (mg/L)
GSH Reserve (%)
Toxic NAPQI (µM)
Necrotic Index (%)
Crit GSH 30% 100% 50% 0% 0h 6h 12h 18h 24h
Glutathione reserve depleting rapidly due to Phase II saturation. Acute bioactivation risk.

U.S. DILIN Epidemiological Longitudinal Data >400% Rise Since 2000

  • Acetaminophen (APAP): Now #1 leading cause of acute liver failure (ALF) in the US (~50% of all ALF cases), having surpassed alcohol and viral hepatitis.
  • Inadvertent Staggered Overdose: ~48% of APAP poisonings occur unintentionally through multi-product combination formulations (cough/cold syrups + pain relievers).
  • Mechanistic Pathway: Glucuronidation (UGT) and Sulfation (SULT) saturate at >4,000mg/24h. Excess flux redirects to CYP2E1, synthesizing electrophilic NAPQI which covalently binds mitochondrial proteins once GSH drops <30%.
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