TY - CHAP
T1 - Breadth of Pharmacology Modeling
T2 - Fundamentals of Pharmacokinetics, Pharmacodynamics, and Mechanistic Modeling
AU - Mager, Donald E.
N1 - Publisher Copyright:
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025.
PY - 2025
Y1 - 2025
N2 - The basic principles of pharmacokinetics and pharmacodynamics represent the foundational knowledge base upon which complex quantitative systems pharmacology models of drug action are built. This chapter provides a high-level overview of fundamental factors that determine the disposition and physiological responses to drugs and the application of compartmental models to characterize the time-course of drug exposure and pharmacological effects. Many of these processes are subject to capacity-limitation, which is defined by a nonlinear function containing a driving substrate concentration and parameters representing the capacity of the process and a substrate affinity constant. Most contemporary mechanism-based pharmacodynamic models are developed by integrating an appropriate drug exposure forcing function, a mathematical model of the interaction between the drug and its target (i.e., binding and transduction), and the physiological turnover (or production and loss) of the biomarker of drug response. Numerous complexities can be introduced to basic models, such as homeostatic feedback, tolerance mechanisms, disease progression, drug interactions, circadian rhythms, and many others. These basic and advanced models can be viewed as the groundwork for the development of comprehensive quantitative systems pharmacology models that are applicable across biological spatiotemporal scales.
AB - The basic principles of pharmacokinetics and pharmacodynamics represent the foundational knowledge base upon which complex quantitative systems pharmacology models of drug action are built. This chapter provides a high-level overview of fundamental factors that determine the disposition and physiological responses to drugs and the application of compartmental models to characterize the time-course of drug exposure and pharmacological effects. Many of these processes are subject to capacity-limitation, which is defined by a nonlinear function containing a driving substrate concentration and parameters representing the capacity of the process and a substrate affinity constant. Most contemporary mechanism-based pharmacodynamic models are developed by integrating an appropriate drug exposure forcing function, a mathematical model of the interaction between the drug and its target (i.e., binding and transduction), and the physiological turnover (or production and loss) of the biomarker of drug response. Numerous complexities can be introduced to basic models, such as homeostatic feedback, tolerance mechanisms, disease progression, drug interactions, circadian rhythms, and many others. These basic and advanced models can be viewed as the groundwork for the development of comprehensive quantitative systems pharmacology models that are applicable across biological spatiotemporal scales.
KW - Mathematical modeling
KW - Pharmacodynamics
KW - Pharmacokinetics
KW - Systems pharmacology
KW - Target-binding
KW - Turnover
UR - https://www.scopus.com/pages/publications/105017314230
U2 - 10.1007/164_2025_746
DO - 10.1007/164_2025_746
M3 - Chapter
C2 - 40323416
AN - SCOPUS:105017314230
T3 - Handbook of Experimental Pharmacology
SP - 21
EP - 73
BT - Handbook of Experimental Pharmacology
PB - Springer Science and Business Media Deutschland GmbH
ER -