Iran Pharmacy Ph.D. Entrance Exam key terms

The fraction of an administered dose of unchanged drug that reaches systemic circulation, expressed as a percentage relative to intravenous dosing; determined by extent of absorption and first-pass metabolism, and central to biopharmaceutic evaluation of oral products.

The absence of a significant difference in the rate and extent of absorption between two pharmaceutically equivalent products, judged by comparing AUC and Cmax confidence intervals against regulatory acceptance limits.

Presystemic elimination of an orally absorbed drug during passage through intestinal wall and liver before reaching systemic circulation, reducing oral bioavailability and often requiring dose adjustment or alternative routes.

Peak plasma concentration and the time at which it occurs after a dose; together with AUC they describe absorption rate and extent in pharmacokinetic and bioequivalence studies.

The integral of plasma concentration over time after dosing, proportional to total systemic drug exposure; calculated by trapezoidal methods and used to estimate extent of absorption and clearance.

Volume of plasma cleared of drug by the liver per unit time, depending on hepatic blood flow, intrinsic enzyme activity, and plasma protein binding; determines steady-state concentration and susceptibility to drug interactions.

In zero-order elimination a constant amount is removed per unit time regardless of concentration, while in first-order elimination a constant fraction is removed, giving exponential decay and a fixed half-life.

Time required for plasma concentration to fall by half during first-order elimination; determines time to steady state (about four to five half-lives) and guides dosing interval selection.

Apparent volume relating the amount of drug in the body to its plasma concentration; a large value indicates extensive tissue distribution, while a small value suggests confinement to plasma water.

Reversible association of drug with albumin, alpha-1-acid glycoprotein, and other plasma proteins; only unbound drug exerts effect and is available for metabolism and renal filtration.

Saturable, capacity-limited elimination described by a maximum rate and a Michaelis constant; at high concentrations clearance falls and half-life lengthens, as seen with phenytoin and ethanol.

Biopharmaceutics Classification System grouping drugs by aqueous solubility and intestinal permeability into four classes, guiding waiver of in vivo bioequivalence studies and formulation strategy.

In vitro measurement of drug released from a dosage form into a stirred medium under standardized conditions; used for quality control, formulation development, and as a surrogate for bioavailability in biowaivers.

Sustained-release systems slow drug liberation over time, whereas controlled-release systems aim to deliver drug at a predetermined rate largely independent of physiological conditions, giving more constant plasma levels.

An agonist binds a receptor and produces a conformational change triggering a biological response; an antagonist occupies the receptor without intrinsic activity, blocking agonist effects competitively or noncompetitively.

EC50 is the agonist concentration producing half of the maximal response; a lower EC50 denotes higher potency, reflecting greater receptor affinity and efficiency of signal transduction.

A ligand that binds the receptor and produces a submaximal response even at full occupancy, acting as a weak agonist and able to reduce the effect of a full agonist.

Ratio of the dose producing toxicity to the dose producing therapeutic effect, commonly TD50 divided by ED50; a narrow index demands therapeutic drug monitoring and careful titration.

Clinical measurement of plasma drug concentrations for drugs with narrow therapeutic indices or unpredictable kinetics, used to individualize dosing and avoid toxicity or treatment failure.

Inducers increase CYP enzyme synthesis, lowering substrate concentrations and effect; inhibitors reduce enzyme activity, raising substrate levels; both mechanisms underlie major pharmacokinetic drug interactions.

Systematic correlation between chemical structure features and biological activity, established by modifying substituents and measuring potency, to guide rational design of more active and selective analogues.

Replacement of a functional group with another of similar size, shape, or electronic properties to retain activity while improving potency, selectivity, metabolic stability, or pharmacokinetics.

Heuristic predicting oral absorption from molecular weight, lipophilicity (logP), hydrogen-bond donors and acceptors; violations suggest poor permeability or solubility and increased attrition in development.

The spatial arrangement of chemical features, such as hydrogen-bond donors, acceptors, aromatic rings, and charged groups, responsible for a molecule's biological activity at a target.

Computational method predicting the preferred orientation and binding affinity of a ligand within a protein binding site, used to prioritize compounds in virtual screening and structure-based design.

A pharmacologically inactive derivative converted in the body to the active drug, used to improve solubility, permeability, stability, or targeting, for example ester prodrugs hydrolyzed by esterases.

A natural compound not essential for basic growth, such as alkaloids, terpenoids, and phenolics, produced by plants and microorganisms and often responsible for pharmacological activity.

A nitrogen-containing basic natural product, typically of plant origin, with marked pharmacological activity; examples include morphine, atropine, and quinine, usually extracted as salts.

Techniques for separating active constituents from plant material using solvents; maceration is cold soaking with occasional agitation, while percolation and Soxhlet extraction use continuous solvent flow.

Adjustment of a herbal preparation to a defined content of one or more marker or active constituents, ensuring batch-to-batch consistency of efficacy and safety through validated analytical methods.

Separation technique using a packed column under high pressure and a liquid mobile phase; the workhorse for assay, impurity profiling, dissolution testing, and herbal marker quantification.

Planar chromatographic method separating analytes on a coated plate with a moving solvent front; inexpensive and rapid, widely used for identity tests and impurity screening of natural products.

Plot of instrument response against known analyte concentrations; linearity over the working range, assessed by regression and correlation coefficient, is required for quantitative analytical validation.

The lowest analyte amount reliably distinguished from noise (detection limit) and the lowest amount measurable with acceptable precision and accuracy (quantification limit), derived from signal-to-noise or standard deviation.

Performance criteria demonstrating method suitability: accuracy, precision, specificity, linearity, range, detection and quantification limits, and robustness, as defined in international analytical guidelines.

A drug whose toxic and therapeutic doses are close, so small pharmacokinetic changes risk harm; examples include digoxin, warfarin, lithium, and phenytoin, requiring careful dosing and monitoring.

Coordinated program promoting appropriate antibiotic selection, dose, route, and duration to optimize outcomes, reduce resistance, and limit adverse effects and cost.

Techniques joining DNA fragments from different sources and expressing them in host cells, underpinning production of human insulin, growth hormone, and monoclonal antibodies.

Antibody derived from a single B-cell clone, binding one specific epitope; humanized and fully human forms are major biopharmaceuticals for cancer, autoimmune, and infectious disease.

In vitro enzymatic amplification of a specific DNA segment through repeated denaturation, primer annealing, and extension cycles; used in diagnosis, cloning, and pharmacogenomic genotyping.

Study of how inherited genetic variation affects drug response, including metabolizing enzyme polymorphisms, transporter variants, and target mutations, enabling genotype-guided prescribing.

Prospective study randomly allocating participants to intervention or control, minimizing selection bias and supporting causal inference about treatment effect; the reference design for clinical evidence.

Confounding occurs when a third variable distorts the exposure-outcome association; bias is systematic error from selection, measurement, or analysis that shifts results away from the truth.

Analysis including all randomized participants in their assigned groups regardless of adherence, preserving randomization and giving a conservative estimate of effectiveness.

The p-value is the probability of observed data or more extreme results under the null hypothesis; the confidence interval gives a range of plausible effect sizes with a stated coverage probability.

A type I error is rejecting a true null hypothesis (false positive, rate alpha); a type II error is failing to reject a false null (false negative, rate beta), with power equal to one minus beta.

Sensitivity is the proportion of truly diseased people correctly identified as positive; specificity is the proportion of truly healthy people correctly identified as negative by a diagnostic test.

Voluntary agreement by a competent person after receiving and understanding information about purpose, procedures, risks, benefits, and alternatives, documented before participation in research or treatment.

Independent committee reviewing research protocols for ethical acceptability, protecting participants' rights and welfare, and ensuring compliance with regulations before and during a study.

Use of an inactive or sham treatment as control; deception about its use requires justification, minimal risk, and debriefing, since it conflicts with fully informed consent.