ArticleJournal of pharmacokinetics and pharmacodynamics2025
A translational physiologically-based pharmacokinetic model for MMAE-based antibody-drug conjugates.
Article in Journal of pharmacokinetics and pharmacodynamics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Antibody-drug conjugate engineering: from design to efficacy and safety.Signal transduction and targeted therapy · 2026Review
- Pharmacokinetic/Pharmacodynamic Translation and Model-Informed Drug Development for Oligonucleotide Therapeutics.Journal of clinical pharmacology · 2026Review
- Subcutaneous administration of antibody-drug conjugates: current challenges, emerging opportunities, and future perspectives.Antibody therapeutics · 2026Review
- Comparative Molecular Insights and Computational Modeling of Multiple Myeloma and Osteosarcoma.International journal of molecular sciences · 2026Review
- Applications of Pharmacometrics in Antibody-Drug Conjugate Development.Pharmaceutics · 2026Review
- Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The objective of this work was to develop a translational physiologically-based pharmacokinetic (PBPK) model for antibody-drug conjugates (ADCs), using monomethyl auristatin E (MMAE)-based ADCs. A previously established dual-structured whole-body PBPK model for MMAE-based ADCs in mice was scaled to higher species (i.e., rats and monkeys) and humans. Species-specific physiological and drug-related parameters for the payload and antibody backbone of ADCs were obtained from literature. Parameters associated with payload release, including the deconjugation rate, were optimized using an allometric scaling approach, and antibody degradation rate was adjusted to account for the enhanced clearance of ADCs due to conjugation across different species. The translational PBPK model predicted the PK profiles for various ADC analytes in rats, monkeys, and humans reasonably well. The optimized PBPK model suggested decreased rate of deconjugation for ADCs in higher species, whereas the effects of payload conjugation on ADC clearance were more pronounced in higher species and humans. The translational PBPK model presented here may enable prediction of different ADC analyte PK at the site-of-action, offering valuable insights for the development of exposure-response relationships for ADCs. The modeling framework presented here can also serve as a platform for the development of PBPK model for other ADCs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.