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The dose–response relationship, or exposure–response relationship, describes the magnitude of the response of an organism, as a function of exposure (or doses) to a stimulus or stressor (usually a chemical) after a certain exposure time. [1] Dose–response relationships can be described by dose–response curves. This is explained further ...
A quantal dose response curve shows the percentage of subjects where a response is noted in an all-or-none manner (y axis) over the dose of the drug (x axis). For competition binding assays and functional antagonist assays IC 50 is the most common summary measure of the dose-response curve.
Threshold dose is a dose of drug barely adequate to produce a biological effect in an animal. In dose-response assessment, the term ‘threshold dose’ is refined into several terminologies, such as NOEL, NOAEL, and LOAEL. They define the limits of doses resulting in biological responses or toxic effects. [3]
The IC 50 of a drug can be determined by constructing a dose-response curve and examining the effect of different concentrations of antagonist on reversing agonist activity. IC 50 values can be calculated for a given antagonist by determining the concentration needed to inhibit half of the maximum biological response of the agonist. [4]
The threshold dose-response model is widely viewed as the most dominant model in toxicology. [6] An alternative type of model in toxicology is the linear no-threshold model (LNT), while hormesis correspond to the existence of opposite effects at low vs. high dose, which usually gives a U- or inverted U-shaped dose response curve.
Toxciant concentration is on the X-axis and biological response is on the Y-axis. Point estimation is a technique to predict population parameters based on available sample data and can be used to relate the mass based concentration to a toxicity based metric. Point estimates in toxicology are frequently response endpoints on a dose response curve.
In toxicology it is specifically the highest tested dose or concentration of a substance (i.e. a drug or chemical) or agent (e.g. radiation), at which no such adverse effect is found in exposed test organisms where higher doses or concentrations resulted in an adverse effect. [3] [4] [5]
Central to PK/PD models is the concentration-effect or exposure-response relationship. [4] A variety of PK/PD modeling approaches exist to describe exposure-response relationships . PK/PD relationships can be described by simple equations such as linear model, Emax model or sigmoid Emax model . [ 5 ]