ArticleNPJ systems biology and applications2025
Leveraging quantitative systems pharmacology modeling for elranatamab regimen optimization in relapsed or refractory multiple myeloma.
Article in NPJ systems biology and applications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
- From Prediction to Decision Making: PBPK and QSP as Regulatory-Grade NAMs.Clinical pharmacology and therapeutics · 2026Review
- Quantitative Systems Pharmacology (QSP): Bridging Biology and Mechanism with Clinical Drug Development Decisions.Journal of clinical pharmacology · 2026Review
- Utilizing Virtual Clinical Trials to Inform Target Coverage That Drives RSV Antiviral Efficacy.CPT: pharmacometrics & systems pharmacology · 2026Article
- Elranatamab: Mechanism of Action, Clinical, and Translational Science.Clinical and translational science · 2026Review
- Comparative Molecular Insights and Computational Modeling of Multiple Myeloma and Osteosarcoma.International journal of molecular sciences · 2026Review
- Pioneering pharmacometrics practice in Korea: an eight-year retrospective analysis of 192 projects from the first dedicated service organization (2016-2024).Translational and clinical pharmacology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elranatamab, an approved bispecific antibody (BsAb) for relapsed/refractory multiple myeloma, forms an immune synapse between the T-cell CD3 marker and B-cell maturation antigen (BCMA) on myeloma cells. Circulating soluble BCMA (sBCMA) is associated with disease burden and may reduce drug exposure, impacting efficacy. A quantitative systems pharmacology model that captures elranatamab's mechanism of action and disease dynamics was developed and calibrated to clinical datasets. Simulations explored model uncertainty and inter-patient variability with respect to biological, pharmacologic, and tumor-related components to inform clinical dose-response relationships and evaluate the effect of baseline sBCMA levels on dose and regimen. Model simulations supported 76 mg weekly as the optimal regimen, including in patients with high sBCMA. A left shift in the dose-response curve among virtual responders supported maintenance of efficacy with less frequent dosing. This work exemplifies how mechanistic models may support BsAb dose and regimen justification within the framework of model-informed drug development.
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Registered trials
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