Evidence map›Paper›PMID 39849917›Full record

ArticlemAbs2025

Engineered ipilimumab variants that bind human and mouse CTLA-4.

Brett Robison, S J Diong, Anusha Kumar, Thomas M Moon, Olin Chang, Bryant Chau, Christine Bee, Ishita Barman, Arvind Rajpal, Alan J Korman and 3 more

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. Review
  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

13 authors.

Brett RobisonDiscovery Biotherapeutics, Bristol Myers Squibb, Redwood City, CA, USA.ORCID 0000-0003-1159-9808
S J DiongDiscovery Biotherapeutics, Bristol Myers Squibb, Redwood City, CA, USA.ORCID 0000-0002-4516-8355
Anusha KumarDiscovery Biotherapeutics, Bristol Myers Squibb, Redwood City, CA, USA.
Thomas M MoonDiscovery Biotherapeutics, Bristol Myers Squibb, Redwood City, CA, USA.
Olin ChangDiscovery Biotherapeutics, Bristol Myers Squibb, Redwood City, CA, USA.
Bryant ChauLarge Molecule Drug Discovery, Genentech, Research and Early Development, South San Francisco, CA, USA.
Christine BeeBiochemistry and Biophysics, Merck, South San Francisco, CA, USA.
Ishita BarmanProtein and Antibody Portfolio, Genscript, South San Francisco, CA, USA.
Arvind RajpalResearch, Xaira Therapeutics, Brisbane, CA, USA.
Alan J KormanResearch, Vir Biotechnology, San Francisco, CA, USA.
Sean WestDiscovery Biotherapeutics, Bristol Myers Squibb, Redwood City, CA, USA.
Pavel StropResearch, Tallac Therapeutics, Burlingame, CA, USA.
Peter S LeeBiotherapeutics and Genetic Medicine, AbbVie, South San Francisco, CA, USA.ORCID 0000-0002-8745-4034

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Testing of candidate monoclonal antibody therapeutics in preclinical models is an essential step in drug development. Identification of antibody therapeutic candidates that bind their human targets and cross-react to mouse orthologs is often challenging, especially for targets with low sequence homology. In such cases, surrogate antibodies that bind mouse orthologs must be used. The antibody 9D9, which binds mouse CTLA-4, is a commonly used surrogate for CTLA-4 checkpoint blockade studies in mouse cancer models. In this work, we reveal that 9D9 has significant biophysical dissimilarities to therapeutic CTLA-4 antibodies. The 9D9-mCTLA4 complex crystal structure was determined and shows that the surrogate antibody binds an epitope distinct from ipilimumab and tremelimumab. In addition, while ipilimumab has pH-independent binding to hCTLA-4, 9D9 loses binding to mCTLA-4 at physiologically relevant acidic pH ranges. We used phage and yeast display to engineer ipilimumab to bind mouse CTLA-4 with single-digit nM affinity from an initial state with no apparent binding. The engineered variants showed pH-independent and cross-reactive binding to both mouse and human CTLA-4. Crystal structures of a variant in complex with both mouse and human CTLA-4 confirmed that it targets an equivalent epitope as ipilimumab. These cross-reactive ipilimumab variants may facilitate improved translatability and future mechanism-of-action studies for anti-CTLA-4 targeting in murine models.

Indexed as

Antibodies, MonoclonalCTLA-4 AntigenIpilimumabAnimalsCross ReactionsCrystallography, X-RayEpitopesHumansMiceProtein EngineeringAntibodies, MonoclonalCTLA-4 AntigenCTLA4 protein, humanCtla4 protein, mouseEpitopesIpilimumabAntibody engineeringCTLA-4immune checkpointphage displayspecies cross reactivityyeast display

Identifiers

PMID39849917
PMCPMC11776466

What Socratic holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.