Absorption |
1st order absorption kinetics within the therapeutic range. Absorption through passive transport resulting in plasma concentrations in the nano- to micromolar range. |
Nonlinear absorption kinetics due to a mixture of saturable active transport through SVCT1 and facilitated diffusion through GLUT transporters resulting in micromolar plasma concentrations and millimolar tissue concentrations. |
Distribution |
Primarily distributed through passive diffusion. Immediate distribution primarily determined by blood flow and tissue perfusion. Homeostasis largely based on physical-chemical properties of the drugs including lipofilicity, pKa and protein binding. |
Primarily distributed through active transport. Immediate distribution based on tissue priority governed by SVCT2 transporter expression and saturation kinetics. Homeostasis depends on adequacy of dose and vitamin C status of bodily compartments. |
Metabolism |
Catabolized unspecifically by phase I & II enzymes potentially generating a range of metabolites and/or conjugates with increased water solubility. |
Specifically and unspecifically oxidized through electron donor and antioxidant properties, respectively, but efficiently regenerated intracellularly to its reduced form by numerous cell types. |
Excretion |
Most often 1st order elimination kinetics though passive glomerular filtration and passive reabsorption depending on pKa. Overall relatively rapid excretion of parent compound and metabolites through urine and bile. |
Nonlinear concentration-dependent elimination kinetics resulting in anything from 0 to 100% active renal reabsorption depending on vitamin C availability and saturation of bodily compartments. |
Modelling |
Kinetics can usually be modelled well by simple compartment and non-compartment models. |
Does not comply with the basic assumption of terminal 1st order kinetics used in both compartmental and non-compartmental analysis. |