Evidence map›Paper›PMID 42364971›Full record

ArticleClinical pharmacology and therapeutics2026

Patient-Specific Determinants of Response to BCMA- and GPRC5D-Targeted CAR T-Cell Therapy in Multiple Myeloma: A QSP Analysis of Clinical Trial and Real-World Data.

Vasiliki Kostiou, Vijayalakshmi Chelliah, Piet H van der Graaf, Andrzej M Kierzek, Tasmin Farzana, Sham Mailankody, Eric M Jurgens

Abstract read
In one paragraph

Article in Clinical pharmacology and therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Vasiliki KostiouCertara, Applied Biosimulation, Sheffield, UK.
Vijayalakshmi ChelliahCertara, Applied Biosimulation, Sheffield, UK.
Piet H van der GraafCertara, Applied Biosimulation, Sheffield, UK.
Andrzej M KierzekCertara, Applied Biosimulation, Sheffield, UK.
Tasmin FarzanaCellular Therapy Service, Division of Hematologic Malignancies, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Sham MailankodyMyeloma and Cellular Therapy Service, Division of Hematologic Malignancies, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA.ORCID 0000-0002-2815-9561
Eric M JurgensCellular Therapy Service, Division of Hematologic Malignancies, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA.

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Despite promising outcomes in CAR T-cell therapy for relapsed/refractory multiple myeloma (RRMM), nearly all patients eventually relapse. Resistance and relapse may be driven by CAR T-cell and tumor-intrinsic factors. Here, we developed a mechanistic quantitative systems pharmacology (QSP) model of multiple myeloma growth and CAR T-cell therapy using measurable biomarkers to predict and identify factors associated with response and relapse. The model incorporates key components to explore disease dynamics and CAR T-cell expansion. Our model reproduced published pharmacokinetics and biomarker response data from anti-BCMA and anti-GPRC5D CAR T-cell therapies. We then validated the model using clinical biomarker data from a total of 29 real-world RRMM patients treated with commercial anti-BCMA CAR T. Virtual trial simulations, exploring the impact of variable baseline disease and CAR T characteristics on response, predicted that factors associated with worse outcomes are intrinsic to tumor cells (disease burden, low-antigen expression) and CAR T cells (low CAR T-induced killing rate). Interestingly, simulations suggested that a lower baseline percentage of normal plasma cells is associated with higher overall response. The developed model was also used to predict the outcome of BCMA-targeted and GPRC5D-targeted combination CAR T-cell treatment. Sequential combination therapy simulations predicted a better response in scenarios starting with anti-GPRC5D CAR T infusion, followed by anti-BCMA CAR T infusion. Our model can serve as a framework to investigate response mechanisms as well as multi-antigen targeting, and to optimize clinical trial design and dosing regimens.

Indexed as

B-Cell Maturation AntigenImmunotherapy, AdoptiveMultiple MyelomaReceptors, Chimeric AntigenReceptors, G-Protein-CoupledBiomarkers, TumorHumansTreatment OutcomeB-Cell Maturation AntigenBiomarkers, TumorReceptors, Chimeric AntigenReceptors, G-Protein-CoupledTNFRSF17 protein, human

Identifiers

PMID42364971
PMCPMC13339306

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Registered trials

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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 OpenQuestion graph.