ArticleThe AAPS journal2010
Comparison of two pharmacodynamic transduction models for the analysis of tumor therapeutic responses in model systems.
Article in The AAPS journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- Practical Pharmacokinetic-Pharmacodynamic Models in Oncology.Pharmaceutics · 2025Review
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- Model-Based Evaluation of HangAmDan-B1 and Afatinib Combination Therapy in HCC827 Xenograft Mice with Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Towards a comprehensive assessment of QSP models: what would it take?Journal of pharmacokinetics and pharmacodynamics · 2024Review
- Model-based evaluation of image-guided fractionated whole-brain radiation therapy in pediatric diffuse intrinsic pontine glioma xenografts.CPT: pharmacometrics & systems pharmacology · 2021Article
- Exact solutions and equi-dosing regimen regions for multi-dose pharmacokinetics models with transit compartments.Journal of pharmacokinetics and pharmacodynamics · 2021Article
- Pharmacokinetic-Pharmacodynamic Modeling of Tumor Targeted Drug Delivery Using Nano-Engineered Mesenchymal Stem Cells.Pharmaceutics · 2021Article
- Evolution of the Systems Pharmacokinetics-Pharmacodynamics Model for Antibody-Drug Conjugates to Characterize Tumor Heterogeneity andThe Journal of pharmacology and experimental therapeutics · 2020Article
- Antibody Coadministration as a Strategy to Overcome Binding-Site Barrier for ADCs: a Quantitative Investigation.The AAPS journal · 2020Article
- A "Dual" Cell-Level Systems PK-PD Model to Characterize the Bystander Effect of ADC.Journal of pharmaceutical sciences · 2019Article
- A Cell-Level Systems PK-PD Model to Characterize In Vivo Efficacy of ADCs.Pharmaceutics · 2019Article
- Establishing in vitro-in vivo correlation for antibody drug conjugate efficacy: a PK/PD modeling approach.Journal of pharmacokinetics and pharmacodynamics · 2018Article
- Quantitative modeling of the dynamics and intracellular trafficking of far-red light-activatable prodrugs: implications in stimuli-responsive drug delivery system.Journal of pharmacokinetics and pharmacodynamics · 2017Article
- Quantitative characterization of in vitro bystander effect of antibody-drug conjugates.Journal of pharmacokinetics and pharmacodynamics · 2016Article
- Array of translational systems pharmacodynamic models of anti-cancer drugs.Journal of pharmacokinetics and pharmacodynamics · 2016Review
- Pharmacokinetic-pharmacodynamic modeling of the antitumor effect of TM208 and EGFR-TKI resistance in human breast cancer xenograft mice.Acta pharmacologica Sinica · 2016Article
- Biomarker- versus drug-driven tumor growth inhibition models: an equivalence analysis.Journal of pharmacokinetics and pharmacodynamics · 2015Article
- Model-based assessment of erlotinib effect in vitro measured by real-time cell analysis.Journal of pharmacokinetics and pharmacodynamics · 2015Article
- Developing Exposure/Response Models for Anticancer Drug Treatment: Special Considerations.CPT: pharmacometrics & systems pharmacology · 2015Article
- Lifespan based pharmacokinetic-pharmacodynamic model of tumor growth inhibition by anticancer therapeutics.PloS one · 2014Article
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3 authors.
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Abstract
Semi-mechanistic pharmacodynamic (PD) models that capture tumor responses to anticancer agents with fidelity can provide valuable insights that could aid in the optimization of dosing regimens and the development of drug delivery strategies. This study evaluated the utility and potential interchangeability of two transduction-type PD models: a cell distribution model (CDM) and a signal distribution model (SDM). The evaluation was performed by simulating dense and sparse tumor response data with one model and analyzing it using the other. Performance was scored by visual inspection and precision of parameter estimation. Capture of tumor response data was also evaluated for a liposomal formulation of paclitaxel in the paclitaxel-resistant murine Colon-26 model. A suitable PK model was developed by simultaneous fitting of literature data for paclitaxel formulations in mice. Analysis of the simulated tumor response data revealed that the SDM was more flexible in describing delayed drug effects upon tumor volume progression. Dense and sparse data simulated using the CDM were fit very well by the SDM, but under some conditions, data simulated using the SDM were fitted poorly by the CDM. Although both models described the dose-dependent therapeutic responses of Colon-26 tumors, the fit by the SDM contained less bias. The CDM and SDM are both useful transduction models that recapitulate, with fidelity, delayed drug effects upon tumor growth. However, they are mechanistically distinct and not interchangeable. Both fit some types of tumor growth data well, but the SDM appeared more robust, particularly where experimental data are sparse.
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