NAT2 Acetylator Phenotype Simulator (2D)

NAT2 Genotype

Rapid acetylator — two functional NAT2*4-type alleles. Fast enzymatic N-acetylation clears isoniazid quickly; standard once-daily dosing rarely accumulates.

Dosing

Isoniazid dose 300 mg

Simulation speed 6 h/s

Live Readouts

Plasma conc.

0.0 mg/L

Elapsed time

0.0 h

Half-life t½

1.1 h

Doses given

Steady-state accumulation ratio (24 h dosing)

1.03×

How it works

NAT2 (N-acetyltransferase 2) acetylates isoniazid in the liver. Its gene carries common SNPs (NAT2*5, *6, *7 among others) that each cut enzyme activity; the phenotype depends on how many of your two alleles are "slow":

0 slow alleles → Rapid acetylator   → t½ ≈ 1.1 h
1 slow allele  → Intermediate       → t½ ≈ 1.9 h
2 slow alleles → Slow acetylator    → t½ ≈ 3.2 h

Isoniazid follows one-compartment first-order kinetics. Each dose adds Dose/V_d to the plasma concentration; between doses it decays exponentially:

C(t) = C₀ · e^(−k·t),   k = ln(2) / t½
Repeated dosing (interval τ) accumulates to steady state:
  Accumulation ratio R = 1 / (1 − e^(−k·τ))

The dots orbiting the bloodstream loop on the left represent circulating drug molecules; the liver grid on the right converts them (they fade and vanish) at a rate set by k. A slow acetylator's grid glows dimmer and clears molecules far more slowly, which is exactly why slow acetylators accumulate isoniazid over daily dosing and carry higher risk of peripheral neuropathy, while rapid acetylators clear it fast enough that standard doses can under-treat.

This 2D sibling reuses the exact same one-compartment exponential-decay pharmacokinetics as the 3D version — same half-lives, same C(t)=C₀·e^(−kt) decay and dosing schedule, verified by comparing the plasma-concentration trace side by side; only the rendering (a flat orbit loop instead of an orbit-controlled 3D scene) is different.

Active isoniazid Liver / NAT2 enzyme