مقایسهٔ روش‌ها

	مدل محفظه‌ای فارماکوکینتیک	تحلیل هم‌ارزی زیستی (آزمون‌های دو سویه یک‌طرفه)	مدل Emax: تحلیل فارماکودینامیک پاسخ به دوز
حوزه	فارماکومتریک	فارماکومتریک	فارماکومتریک
خانواده	Regression model	Hypothesis test	Regression model
سال پیدایش	1982	1987	1981
پدیدآور	Gibaldi & Perrier	Donald J. Schuirmann	Holford & Sheiner
نوع	Deterministic ODE-based pharmacokinetic model	Parametric equivalence test	Nonlinear dose-response regression model
منبع بنیادین	Gibaldi, M., & Perrier, D. (1982). Pharmacokinetics (2nd ed.). Marcel Dekker. ISBN: 978-0-8247-1042-2	Schuirmann, D. J. (1987). A comparison of the two one-sided tests procedure and the power approach for assessing the equivalence of average bioavailability. Journal of Pharmacokinetics and Biopharmaceutics, 15(6), 657–680.	Holford, N. H. G., & Sheiner, L. B. (1981). Understanding the dose-effect relationship: clinical application of pharmacokinetic-pharmacodynamic models. Clinical Pharmacokinetics, 6(6), 429–453.
نام‌های دیگر	Mammillary Compartment Model, Multi-Compartment PK Model, Compartmental Analysis, Farmakokinetik Kompartman Modeli	TOST Procedure, Average Bioequivalence, BE Analysis, Biyoeşdeğerlik Analizi	Maximum Effect Model, Hyperbolic Emax Model, Sigmoidal Emax Model, Emax Farmakodynamik Modeli
مرتبط	3	2	2
خلاصه	The pharmacokinetic compartment model represents the body as one or more hypothetical compartments interconnected by first-order rate processes, describing how a drug is absorbed, distributed, and eliminated over time. Systematized by Gibaldi and Perrier in 1982, these models use ordinary differential equations to characterize plasma concentration-time profiles. They are the cornerstone of drug development, dosage regimen design, and regulatory submission pharmacokinetic analyses.	Bioequivalence Analysis is a regulatory-grade statistical framework used to determine whether a test drug formulation (generic or reformulated) delivers the active ingredient to the systemic circulation at a rate and extent comparable to a reference product. Introduced by Donald J. Schuirmann in 1987, the method operationalizes equivalence through the Two One-Sided Tests (TOST) procedure, replacing the ambiguous absence-of-difference paradigm with an explicit equivalence margin evaluated on log-transformed pharmacokinetic endpoints such as AUC and C_max.	The Emax model is a nonlinear pharmacodynamic model that describes the relationship between drug concentration and biological effect. Introduced by Holford and Sheiner in 1981, it characterizes dose-response curves using three fundamental parameters: the maximum achievable effect (Emax), the concentration producing half-maximal effect (EC50), and an optional baseline effect (E0). It remains the standard framework in clinical pharmacology and drug development for quantifying pharmacodynamic dose-response relationships.