GPAT key terms

The fraction of an administered dose of unchanged drug that reaches systemic circulation, expressed as rate and extent. Intravenous dosing is taken as 100%, while oral values are lower because of incomplete absorption and first-pass metabolism.

Presystemic elimination of a drug in gut wall or liver before it reaches systemic circulation after oral dosing. It reduces oral bioavailability and can be saturated or bypassed by routes such as sublingual, rectal, or parenteral administration.

The absence of a clinically significant difference in rate and extent of absorption between two pharmaceutically equivalent products. It is demonstrated by comparative pharmacokinetic studies, usually with 90% confidence intervals for AUC and Cmax falling within accepted limits.

The integral of plasma drug concentration over time after a dose, reflecting total systemic exposure. It is estimated by linear or trapezoidal methods and is central to calculating clearance, bioavailability, and bioequivalence.

Elimination in which a constant amount of drug is removed per unit time, independent of concentration, so plasma levels fall linearly. It occurs with saturation of metabolizing enzymes or transport, as with ethanol and phenytoin at high doses.

Elimination in which a constant fraction of the drug present is removed per unit time, so plasma concentration decays exponentially. Most drugs follow this pattern, giving a constant half-life independent of dose.

The time required for plasma drug concentration to fall by half during first-order elimination. It determines dosing interval and time to steady state, which is reached in roughly four to five half-lives.

An apparent volume relating the amount of drug in the body to its plasma concentration. A large value indicates extensive tissue distribution; a small value suggests confinement to plasma and extracellular fluid.

The volume of plasma from which a drug is completely removed per unit time. Total clearance is the sum of hepatic, renal, and other clearances and, with volume of distribution, determines elimination half-life.

The condition during repeated dosing when the amount of drug absorbed per interval equals the amount eliminated, so plasma concentrations fluctuate around a constant mean. It is reached after about four to five half-lives.

An initial larger dose given to reach therapeutic plasma concentrations rapidly rather than waiting several half-lives. It is calculated from the target concentration and volume of distribution, not from clearance.

Measurement of plasma drug concentrations to individualize dosing for drugs with narrow therapeutic indices, poor correlation of dose with response, or marked pharmacokinetic variability. Sampling time relative to the dose is critical for interpretation.

A property of drugs whose toxic and therapeutic plasma concentrations are close, so small dose or concentration changes risk toxicity or loss of efficacy. Such drugs typically require careful titration and therapeutic drug monitoring.

A ligand that binds a receptor and activates it to produce a biological response. Full agonists produce maximal response, while partial agonists produce submaximal responses even at full receptor occupancy.

A ligand that binds a receptor without activating it and blocks agonist action. Competitive antagonists shift agonist dose-response curves rightward and are surmountable; noncompetitive antagonists reduce maximal response.

A drug that binds and activates a receptor but produces less than the maximal response achievable, even at full occupancy. It can act as a functional antagonist when competing with a full agonist.

The concentration of an agonist that produces 50% of its maximal response, a measure of potency. A lower EC50 indicates higher potency, and the value is read from the concentration-response curve.

Reversible association of drug with plasma proteins such as albumin and alpha-1-acid glycoprotein. Only unbound drug exerts effect and undergoes elimination, and displacement can raise free fraction and toxicity.

A pharmacologically inactive derivative that is converted in the body to the active drug, often to improve absorption, stability, or targeting. Examples include ester prodrugs hydrolyzed to active carboxylic acids.

The relationship between a molecule's chemical structure and its biological activity. Systematic modification of functional groups identifies pharmacophores and guides optimization of potency, selectivity, and pharmacokinetic properties.

The spatial arrangement of chemical features in a molecule that is essential for a specific biological activity. It is used in ligand design and virtual screening to identify compounds likely to bind a target.

A chemical group that replaces another group in a molecule while retaining similar biological activity. Classical examples include replacing a hydrogen with fluorine or an oxygen with sulfur to modify metabolism or potency.

The property of a molecule that is not superimposable on its mirror image, usually due to a stereogenic carbon. Enantiomers can differ markedly in receptor affinity, metabolism, and toxicity.

A separation technique in which components distribute between a stationary phase and a mobile phase. Differences in affinity cause differential migration, enabling identification and quantification of analytes in mixtures.

The time between injection and the maximum of a chromatographic peak. It is used for qualitative identification when compared with a reference standard under identical conditions, and must be reproducible.

A plot of instrument response against known analyte concentrations, used to determine unknown concentrations. Linearity, slope, and intercept are assessed, and the method should be validated over the intended range.

A known amount of a compound added to all samples and standards to correct for variability in sample preparation and instrument response. It should be chemically similar but well resolved from the analyte.

Documented evidence that an analytical procedure is suitable for its intended purpose. Typical parameters include accuracy, precision, specificity, linearity, range, detection and quantitation limits, and robustness.

The lowest analyte concentration that can be measured with acceptable accuracy and precision. It is estimated from signal-to-noise ratio or standard deviation of response and slope of the calibration curve.

An in vitro test measuring the rate at which drug dissolves from a dosage form into a specified medium under controlled conditions. It is used for quality control and to predict in vivo release behavior.

A dosage form designed to release drug gradually over an extended period, reducing dosing frequency and plasma fluctuations. It may use matrix, reservoir, or osmotic systems and depends on controlled dissolution or diffusion.

An inactive ingredient included in a dosage form to aid manufacture, stability, or drug delivery, such as binders, fillers, disintegrants, and lubricants. Excipients must be compatible with the active ingredient and safe for the route.

A naturally occurring nitrogen-containing basic compound found mainly in plants, often with potent pharmacological activity. Examples include morphine, quinine, and atropine, usually extracted after basification with organic solvents.

A compound in which a sugar is linked to a non-sugar aglycone, often through an oxygen or nitrogen atom. Many plant glycosides, such as cardiac glycosides, are pharmacologically active and hydrolyze readily.

The study of drugs derived from natural sources, including plants, animals, and microorganisms, covering their identification, chemistry, cultivation, and biological activity. It underpins quality control of crude drugs and herbal products.

Establishing and applying measurable criteria to ensure consistent composition and quality of a natural product or preparation. It may be based on marker compounds, biological assays, or chromatographic fingerprints.

Reduction of enzyme catalytic activity by a molecule that binds the enzyme or enzyme-substrate complex. Inhibitors may be competitive, noncompetitive, or irreversible, and many drugs act through this mechanism.

A model describing enzyme-catalyzed reaction velocity as a function of substrate concentration, characterized by Vmax and Km. At low substrate, velocity rises steeply; at saturation, it approaches Vmax.

Reversible inhibition in which inhibitor and substrate compete for the same active site. It raises apparent Km without changing Vmax and can be overcome by increasing substrate concentration.

The substrate concentration at which an enzyme-catalyzed reaction proceeds at half its maximal velocity. It is an inverse measure of enzyme affinity for substrate under defined conditions.

A category under Indian drug law listing prescription-only medicines that may be sold only on the prescription of a registered medical practitioner and only by licensed pharmacies. The container must bear the prescribed warning label.

Formal authorization issued by a licensing authority permitting manufacture, sale, or distribution of drugs under specified conditions. It is granted after inspection and compliance with statutory requirements and is subject to renewal.

A set of quality-assurance requirements ensuring that products are consistently produced and controlled to appropriate quality standards. It covers premises, personnel, documentation, validation, and quality control testing.

A written or electronic order from a registered medical practitioner authorizing dispensing of a medicine for a named patient, including drug, dose, and directions. It is a legal document and must be retained as required.