Evidence map›Paper›PMID 40327396›Full record

ArticleJCI insight2025

Imlunestrant a next-generation oral SERD overcomes ESR1 mutant resistance in estrogen receptor-positive breast cancer.

Shira Sherman, Zachary M Sandusky, Douglas Russo, David Zak, Agostina Nardone, Delia Friel, Francisco Hermida-Prado, Capucine Heraud, Genevra Kuziel, Ana Verma and 6 more

Abstract read
In one paragraph

Article in JCI insight, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. 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

16 authors.

Shira ShermanDepartment of Medical Oncology and.
Zachary M SanduskyDepartment of Medical Oncology and.
Douglas RussoDepartment of Medical Oncology and.
David ZakDepartment of Cancer Biology, Loyola University Stritch School of Medicine, Maywood, Illinois, USA.
Agostina NardoneDepartment of Medical Oncology and.
Delia FrielDepartment of Medical Oncology and.
Francisco Hermida-PradoDepartment of Medical Oncology and.
Capucine HeraudDepartment of Medical Oncology and.
Genevra KuzielDepartment of Medical Oncology and.
Ana VermaHarvard Medical School, Boston, Massachusetts, USA.
Giorgio GagliaHarvard Medical School, Boston, Massachusetts, USA.
Sheheryar KabrajiDepartment of Medical Oncology and.
Quang-De NguyenLurie Family Imaging Center, Center for Biomedical Imaging in Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
Sandro SantagataHarvard Medical School, Boston, Massachusetts, USA.
Sean W FanningDepartment of Cancer Biology, Loyola University Stritch School of Medicine, Maywood, Illinois, USA.
Rinath JeselsohnDepartment of Medical Oncology and.

Funding

VectorP30CA006516 · NCI · DANA-FARBER CANCER INSTITUTE · PI Irene M. Ghobrial · 1985 to 2026
$330.6M
Cancer Chemical Biology and Metabolism Training ProgramT32CA236754 · NCI · DANA-FARBER CANCER INST · PI Nika N Danial, THOMAS M ROBERTS · 2019 to 2026
$2.6M
Optimizing CDK7 Inhibitor Therapeutic Strategies for ER+ Breast CancerR01CA237414 · NCI · DANA-FARBER CANCER INST · PI Rinath M. Jeselsohn · 2019 to 2026
$2.3M
Structural-Transcriptional Relationships that Improve Y537S Estrogen Receptor AntagonismR37CA279341 · NCI · LOYOLA UNIVERSITY CHICAGO · PI Sean William Fanning · 2023 to 2026
$1.4M
NCI NIH HHS P30 CA006516NCI NIH HHS R01 CA237414NCI NIH HHS R37 CA279341NCI NIH HHS T32 CA236754
6 · The paper itself

Abstract

Estrogen receptor α (ER) is a critical driver of tumorigenesis and tumor progression in most breast cancers. Endocrine therapies (ET) targeting ER are central to treating hormone receptor-positive breast cancer, but resistance poses a clinical challenge. Some resistance mechanisms, particularly those involving estrogen-independent activity such as the ESR1 mutations, rely on ER signaling, supporting the need for next-generation ET. We investigated the preclinical efficacy of imlunestrant, an oral selective ER degrader, in ER-positive breast cancer preclinical models, including models harboring the Y537S ESR1 mutation, an activating mutation. Imlunestrant demonstrated antagonistic activity and effective degradation of both WT and mutant ER, resulting in cell growth suppression. In vivo, imlunestrant outperformed fulvestrant, leading to tumor regression in a patient-derived xenograft harboring the Y537S ESR1 mutation. Cyclic mutiplexed immunofluorescence and transcriptomic analysis revealed enhanced cell cycle arrest and downregulation of estrogen-responsive genes with imlunestrant treatment. Additionally, a genome-wide CRISPR knock-out screen identified several vulnerabilities that were either persistent or acquired after imlunestrant treatment, providing a rationale for future studies of combination treatments with imlunestrant. Collectively, these results highlight the on-target and selective activity of imlunestrant, which can circumvent resistance engendered by the Y537S ESR1 mutation.

Indexed as

Breast NeoplasmsDrug Resistance, NeoplasmEstrogen Receptor alphaAnimalsCell Line, TumorFemaleFulvestrantHumansMiceMutationXenograft Model Antitumor AssaysESR1 protein, humanEstrogen Receptor alphaFulvestrantBreast cancerCell biologyOncology

Identifiers

PMID40327396
PMCPMC12226049

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.