Evidence map›Paper›PMID 40299789›Full record

ArticleMolecular cancer therapeutics2025

Zidesamtinib Selective Targeting of Diverse ROS1 Drug-Resistant Mutations.

Anupong Tangpeerachaikul, Scot Mente, Joe Magrino, Franklin Gu, Joshua C Horan, Henry E Pelish

Abstract read
In one paragraph

Article in Molecular cancer therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Zidesamtinib (Jideytro®): a new selective, brain-penetrant ROS1 inhibitor approved for the treatment of ROS1-positive non-small cell lung cancer.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
  3. Chemoresistance: The hidden barrier in cancer treatment.Cancer pathogenesis and therapy · 2026
    Review
  4. 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

6 authors.

Anupong TangpeerachaikulNuvalent, Inc., Cambridge, Massachusetts.ORCID 0000-0002-6965-2678
Scot MenteNuvalent, Inc., Cambridge, Massachusetts.ORCID 0000-0003-1355-4697
Joe MagrinoNuvalent, Inc., Cambridge, Massachusetts.ORCID 0000-0003-0740-7017
Franklin GuNuvalent, Inc., Cambridge, Massachusetts.ORCID 0009-0004-8303-3218
Joshua C HoranNuvalent, Inc., Cambridge, Massachusetts.ORCID 0000-0003-4700-5215
Henry E PelishNuvalent, Inc., Cambridge, Massachusetts.ORCID 0000-0003-2940-0326

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zidesamtinib (NVL-520) is a ROS1-selective macrocyclic tyrosine kinase inhibitor designed with the aim to address clinical challenges for patients with non-small cell lung or other cancers that are ROS1 fusion-positive. These challenges include emergent ROS1 resistance mutations and brain metastases that can lead to disease progression and central nervous system adverse events attributed to off-target tropomyosin-related kinase inhibition that can be treatment-limiting. We evaluated zidesamtinib in accelerated mutagenesis screens and a brain tumor model, comparing it with other approved or investigational ROS1 inhibitors. At clinically relevant concentrations, zidesamtinib robustly inhibited >1,500 pooled ROS1 mutants with virtually no resistance emerging (≤1%), outperforming comparators crizotinib, entrectinib, and repotrectinib. Zidesamtinib also induced more durable responses than repotrectinib and taletrectinib in an aggressive intracranial ROS1 G2032R xenograft model. A 2.2 Å cocrystal structure with ROS1 G2032R, the most frequently identified ROS1 resistance mutation, reveals that zidesamtinib uniquely accommodates the mutated residue while potentially clashing with tropomyosin-related kinases, consistent with its selective ROS1-targeting design and supported by computational modeling. Taken together, these data support zidesamtinib's potential as a novel best-in-class ROS1 inhibitor.

Indexed as

Drug Resistance, NeoplasmMutationProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene ProteinsAnimalsBrain NeoplasmsCell Line, TumorHumansMiceXenograft Model Antitumor AssaysProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene ProteinsROS1 protein, human

Identifiers

PMID40299789
PMCPMC12214885

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.