biophase

In order to derive equations to account for the very slow onset and offset kinetics of competitive antagonists as compared to the fast kinetics of agonists, I developed a biophase model in which the agents moved between an aqueous extracellular phase and a lipid membrane phase containing the receptors.

Robert F. Furchgott - Autobiography 1999

In this equation, the pharmacological effect may be expressed, when Pharmacokinetic-pharmacodynamic the drug concentration is zero, as: (PK/PD) modeling E0 ¼ m lnðC0 Þ Single-compartment, time-independent PK/PD models As mentioned earlier, for functional data based on biophase, plasma or tissue measurements, we often The simplest model is where

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Note testing. that the sigmoidicity parameter (n) does not neces - In dose-response time models, the underlying sarily have a direct biological interpretation and assumption is that pharmacodynamic data gives us should be viewed as an extension of the original information on the kinetics of drug in the biophase Emax model to account for curvature. (i.e. the tissue or compartment precisely where the The larger the value of the exponent, the more drug exhibits its effect).

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The reason for this is that it can response relationship for the wanted effects of the check that there has not been some supersensitivity investigational drug is well understood, of orthodox state induced in the biophase by the disease causing sigmoid form, when there is no active metabolite (s), the renal insuf fi ciency, and thus to exclude a false - and when the dose or concentration-response rela - negative conclusion when purely pharmacokinetic tionship for unwanted effects is also well understood data are analyzed. and a long way to the right of the curve for ef fi cacy.

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