Every dose is absorbed from the gut into plasma, metabolised by the liver, and — once there — competitively blocks HMG-CoA reductase, the enzyme hepatocytes use to build cholesterol. Less enzyme activity means less LDL synthesised, so circulating LDL-C drifts down over days toward a new, lower steady state. This 2D view drives the exact same equations as the 3D lab, drawn as a flat schematic instead of an orbitable scene.
PK (one-compartment, oral):
dA/dt = −ka·A (gut)
dC/dt = ka·A/Vd − ke·C (plasma)
PD (Hill equation, enzyme block):
Inhibition = Imax·Cⁿ / (IC50ⁿ + Cⁿ)
LDL kinetics:
dLDL/dt = ksyn·(1−Inhibition) − kclear·LDL
- Statin — sets absorption rate ka, elimination half-life and IC50 (binding potency); rosuvastatin is slow-cleared and potent, simvastatin is fast-cleared and weaker.
- Daily dose — amount reaching the gut compartment each 24h; higher doses push plasma concentration further past IC50 on the Hill curve, but returns diminish once inhibition nears its Imax ceiling.
- Simulated speed — LDL turnover takes days-to-weeks in real patients; this compresses that into seconds so you can watch the new steady state emerge.
- Hepatic metabolism — models CYP3A4 activity variability between patients: faster clearance (>1×) needs a higher dose for the same effect, slower clearance raises plasma levels and risk of side effects at a given dose.