A liver enzyme breaks this drug down at a genotype-specific rate. Poor metabolizers carry a slow variant, normal metabolizers the typical variant, and ultra-rapid metabolizers a hyperactive variant — the same enzyme family (e.g. CYP2D6) that clears roughly a quarter of all prescribed drugs.
C(t) = Σ dose·ka /(Vd·(ka−ke)) · (e^(−ke·Δt) − e^(−ka·Δt))
ke: poor ≪ normal ≪ ultra-rapid
This 2D version puts the dose and dosing interval directly in your hands instead of a fixed preset: raise the dose or shrink the interval for a poor metabolizer and watch the trough climb into the toxic zone before dose six; do the same for an ultra-rapid metabolizer and the curve barely clears subtherapeutic. Auto-adjust solves for the dose that lands this genotype's regimen peak in the middle of the therapeutic window at the current interval — the pharmacogenomic-testing answer, computed live instead of looked up.
- Therapeutic window (green band) — the concentration range where the drug works without being dangerous.
- Toxic zone (above the band) — accumulation past this line risks adverse effects.
- Subtherapeutic (below the band) — too little drug in the blood to have the intended effect.
This is the clinical case for pre-emptive pharmacogenomic testing: knowing a patient's metabolizer status before the first prescription lets a clinician pick the right starting dose instead of discovering it by trial, toxicity, or treatment failure.