Evidence map›Paper›PMID 40180622›Full record

ArticlemAbs2025

Maximizing activity and selectivity of antibody-mediated effector functions using antibody mixtures.

Tiexin Wang, Alec A Desai, Greg M Thurber, Peter M Tessier

Abstract read
In one paragraph

Article in mAbs, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

4 authors.

Tiexin WangDepartment of Chemical Engineering, University of Michigan, Ann Arbor, MI, USA.
Alec A DesaiDepartment of Chemical Engineering, University of Michigan, Ann Arbor, MI, USA.ORCID 0000-0002-8322-7096
Greg M ThurberDepartment of Chemical Engineering, University of Michigan, Ann Arbor, MI, USA.ORCID 0000-0001-7570-2080
Peter M TessierDepartment of Chemical Engineering, University of Michigan, Ann Arbor, MI, USA.ORCID 0000-0002-3220-007X

Funding

Department of Defense W81XWH-21-1-0039
6 · The paper itself

Abstract

Fc-mediated effector functions are key for conferring potent antibody-mediated killing of cancer cells. However, it is difficult to achieve highly selective targeting of cancer cells while minimizing toxicity on healthy tissue because of the expression of most receptors, albeit at lower levels, on non-cancer cells. Previous attempts to increase the selectivity of antibody-mediated effector functions have sought to reduce binding affinity and/or increase avidity, which typically results in modest improvements in selectivity. To overcome this limitation, we report the use of mixtures of antibody variants that achieve high selectivity based on receptor level while maintaining high activity for cells with high receptor levels. We have studied mixtures of two variants of an anti-HER2 antibody (trastuzumab), one that is affinity-reduced and effector-competent and a second high-affinity variant that is effectorless. Notably, we observe that the high-affinity, effectorless antibody reduces effector function for cells with low receptor levels, including reduced antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis (ADCP), while the high-avidity, effector-competent antibody mediates significant effector function for cells with high receptor levels. Moreover, replacing the effector-competent Fc region of the affinity-reduced antibody with high-affinity Fc domains that enhance effector function drives high activity while maintaining high selectivity for the antibody mixtures. These findings outline a general strategy for maximizing the therapeutic window by selectively targeting cancer cells based on receptor levels that could be applied to a wide range of applications involving antibody-mediated synapse formation, including antibody-drug conjugates and bispecific antibodies, such as T cell engagers.

Indexed as

Antibody-Dependent Cell CytotoxicityAntineoplastic Agents, ImmunologicalTrastuzumabAnimalsAntibody AffinityCell Line, TumorErb-b2 Receptor Tyrosine KinasesHumansPhagocytosisAntineoplastic Agents, ImmunologicalERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesTrastuzumabADCCADCPAviditycancerHER2mAbtherapeutic windowtoxicitytrastuzumab

Identifiers

PMID40180622
PMCPMC11980503

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LicenceCC BY-NC
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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.