The pharmacology dictionary, in two languages.

The strength of binding between a drug and its receptor or target, determined by the rates of association and dissociation and usually expressed as the equilibrium dissociation constant (Kd) or its negative logarithm (pKd).

A drug or endogenous substance that binds to a receptor and activates it, producing a biological response; it possesses both affinity and efficacy (intrinsic activity).

A ligand that binds to a site on a receptor distinct from the orthosteric (endogenous agonist) site and changes the receptor's affinity for, or response to, the orthosteric agonist.

A drug that binds to a receptor or other target without activating it (affinity but no efficacy) and thereby prevents or reduces the response to an agonist.

Reversible antagonism in which the antagonist binds to the same site as the agonist, so the block can be overcome by raising the agonist concentration; the agonist curve shifts to the right in parallel without a fall in maximal response.

The equilibrium constant for dissociation of a drug–receptor complex, equal to the free drug concentration at which half of the receptors are occupied at equilibrium; a lower Kd means higher affinity.

A graph relating the dose or concentration of a drug to the magnitude of its effect (graded curve) or to the proportion of a population showing a specified all-or-none response (quantal curve).

The capacity of a drug to produce a response once bound to its receptor; in clinical terms, the maximal effect (Emax) a drug can produce, however much the dose is increased.

A member of the largest family of cell-surface receptors, a single polypeptide with seven transmembrane α-helices that transduces ligand binding into intracellular signals by activating heterotrimeric G proteins.

The concentration of a drug that produces 50% of its own maximal effect (Emax); the standard measure of agonist potency in concentration–response studies.

The concentration of an inhibitor that reduces a specified biological or biochemical activity (e.g. enzyme activity, ligand binding or cell growth) by 50% under the given assay conditions.

The equilibrium dissociation constant of an inhibitor from its enzyme, receptor or transporter; an assay-independent measure of inhibitor affinity, with lower Ki values indicating more potent inhibition.

The ability of a drug, once bound, to activate its receptor and produce a response, expressed relative to a full agonist on a scale from 0 (antagonist) to 1 (full agonist); inverse agonists have negative values.

A ligand that binds to a receptor with constitutive (ligand-independent) activity and reduces that basal activity, producing an effect opposite in direction to that of an agonist.

Any molecule, such as a drug, hormone or neurotransmitter, that binds to a specific site on a receptor or other macromolecule; binding alone does not imply activation or blockade.

A transmembrane ion channel that opens (or, less often, closes) directly when a specific ligand, usually a neurotransmitter, binds to it, producing rapid changes in membrane potential within milliseconds.

The dose of a drug that produces a specified effect in 50% of a population (quantal definition) or, in graded dose–response studies, the dose producing 50% of the maximal effect.

Antagonism that cannot be overcome by increasing the agonist concentration, because the antagonist binds irreversibly or acts at a site or step distinct from agonist binding; the maximal agonist response is reduced.

An agonist that, even when occupying all available receptors, produces a maximal response smaller than that of a full agonist; its intrinsic activity lies between 0 and 1.

The branch of pharmacology that studies what a drug does to the body: the biochemical and physiological effects of drugs, their mechanisms of action and the relationship between drug concentration and response.

The amount or concentration of a drug needed to produce an effect of a given intensity, usually expressed as the EC50 or ED50; the lower the value, the more potent the drug.

A macromolecule, usually a protein, to which a drug or endogenous ligand binds specifically and thereby initiates a change in cell function that produces a biological response.

A decrease in the number of receptors available at the cell surface or in the cell, typically in response to prolonged or excessive agonist stimulation, which reduces tissue responsiveness.

An increase in the number or sensitivity of receptors, typically after prolonged receptor blockade or reduced exposure to the endogenous agonist (e.g. denervation), leading to tissue supersensitivity.

A small intracellular signalling molecule or ion, such as cAMP, cGMP, IP3, diacylglycerol or Ca²⁺, whose concentration changes in response to receptor activation and which relays and amplifies the signal inside the cell.

The degree to which a drug acts on a particular target (receptor subtype, enzyme or tissue) rather than on others, usually expressed as the ratio of its affinities or potencies at different targets.

Receptors in excess of those needed to produce a maximal response, so that a full agonist can elicit its maximal effect while occupying only a fraction of the available receptors.

A rapidly developing decrease in response to a drug after repeated doses over a short period (minutes to hours), which often cannot be overcome by increasing the dose.

A measure of a drug's relative safety, classically the ratio of the dose producing toxicity (TD50) or death (LD50) in 50% of subjects to the dose producing the desired effect in 50% (ED50).

The range of doses or, more usually, plasma concentrations between the minimum effective concentration and the concentration at which unacceptable toxicity appears, within which most patients benefit safely.

A gradual reduction in response to a drug with repeated or continuous exposure, so that a higher dose is needed to reproduce the original effect; it develops over days to weeks.