Evidence map›Paper›PMID 40671559›Full record

ArticleProtein science : a publication of the Protein Society2025

A computational dynamic model of combination treatment for type II inhibitors with asciminib.

J Roadnight Sheehan, Astrid S de Wijn, Ran Friedman

Abstract read
In one paragraph

Article in Protein science : a publication of the Protein Society, 2025. 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. A computational dynamic model of combination treatment for type II inhibitors with asciminib.Protein science : a publication of the Protein Society · 2025
    Article
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

3 authors.

J Roadnight SheehanDepartment of Mechanical and Industrial Engineering, Norwegian University of Science and Technology, Trondheim, Norway.
Astrid S de WijnDepartment of Mechanical and Industrial Engineering, Norwegian University of Science and Technology, Trondheim, Norway.
Ran FriedmanDepartment of Chemistry and Biomedical Sciences, Linnaeus University, Kalmar, Sweden.ORCID 0000-0001-8696-3104

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite continuous strides forward in drug development, resistance to treatment looms large in the battle against cancer as well as communicable diseases. Chronic myeloid leukemia (CML) is treated with targeted therapy and treatment is personalized when resistance arises. It has been extensively studied and is used as a model for targeted therapy. In this study, we examine combination treatments of type II Abl1 inhibitors and asciminib (an allosteric regulator) through a computational model at patient relevant concentrations. Due to the separate binding sites of type II inhibitors and asciminib, we propose their combination treatment as potentially robust to resistance. We find that the simultaneous cobinding of type II inhibitors and asciminib is high in synergetic combinations. As an aid to designing and comparing combination treatments, we put forward an equation that expands on the previously published effective ratio of IC

Indexed as

Fusion Proteins, bcr-ablLeukemia, Myelogenous, Chronic, BCR-ABL PositiveProtein Kinase InhibitorsPyrazolesHumansMolecular Dynamics SimulationNiacinamideasciminibFusion Proteins, bcr-ablNiacinamideProtein Kinase InhibitorsPyrazolesasciminibkinase inhibitorleukemiaresistance mutations

Identifiers

PMID40671559
PMCPMC12268125

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.