Evidence map›Paper›PMID 40076604›Full record

ArticleInternational journal of molecular sciences2025

Interaction of Avapritinib with Congo Red in Pancreatic Cancer Cells: Molecular Modeling and Biophysical Studies.

Małgorzata Lasota, Daniel Jankowski, Anna Wiśniewska, Łukasz Szeleszczuk, Anna Misterka-Kozaka, Marta Kaczor-Kamińska, Marta Zarzycka, Maksym Patena, Tomasz Brzozowski

Abstract read
In one paragraph

Article in International journal of molecular sciences, 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. 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

9 authors.

Małgorzata LasotaCenter for Biomedicine and Interdisciplinary Sciences, Faculty of Medicine, Jagiellonian University Medical College, 16 Grzegórzecka Street, 31-531 Krakow, Poland.ORCID 0000-0002-3293-8568
Daniel JankowskiSSG of Targeted Therapy and Supramolecular Systems, Jagiellonian University Medical College, 16 Grzegórzecka Street, 31-531 Krakow, Poland.ORCID 0000-0002-7150-0649
Anna WiśniewskaChair of Pharmacology, Faculty of Medicine, Jagiellonian University Medical College, 16 Grzegórzecka Street, 31-531 Krakow, Poland.ORCID 0000-0001-7370-9879
Łukasz SzeleszczukDepartment of Organic and Physical Chemistry, Faculty of Pharmacy, Medical University of Warsaw, 1 Banacha Street, 02-097 Warsaw, Poland.ORCID 0000-0002-5302-3797
Anna Misterka-KozakaCenter for Biomedicine and Interdisciplinary Sciences, Faculty of Medicine, Jagiellonian University Medical College, 16 Grzegórzecka Street, 31-531 Krakow, Poland.
Marta Kaczor-KamińskaChair of Medical Biochemistry, Jagiellonian University Medical College, 7 Kopernika Street, 31-034 Krakow, Poland.ORCID 0000-0002-2592-7676
Marta ZarzyckaChair of Medical Biochemistry, Jagiellonian University Medical College, 7 Kopernika Street, 31-034 Krakow, Poland.ORCID 0000-0003-1129-5185
Maksym PatenaSSG of Targeted Therapy and Supramolecular Systems, Jagiellonian University Medical College, 16 Grzegórzecka Street, 31-531 Krakow, Poland.
Tomasz BrzozowskiCenter for Biomedicine and Interdisciplinary Sciences, Faculty of Medicine, Jagiellonian University Medical College, 16 Grzegórzecka Street, 31-531 Krakow, Poland.ORCID 0000-0002-5805-0065

Funding

Priority Research Area- qLife under the program Excellence Initiative - Research University at the Jagiellonian University in Krakow, Poland U1C/P04/NO/04.05
6 · The paper itself

Abstract

Pancreatic cancer is a malignant tumor with one of the worst prognoses among solid tumors, characterized by resistance to treatment. Therefore, there is an urgent need for new methods of targeted therapy. Previous studies have shown that the overexpression of receptor tyrosine kinases such as c-KIT or PDGFR can increase proliferation, migration, and invasion of cancer cells. The aim of our study was to analyze aggregates between a supramolecular carrier (Congo red, CR) and a tyrosine kinase inhibitor (BLU-258) as well as to investigate the effect of the free inhibitor and its aggregate with Congo red (CR-BLU-258) on selected properties of pancreatic cells, including these cells' viability and three-dimensional cell spheroid cultures. To better understand the interactions between Congo red and BLU-258, we used molecular modeling in addition to biophysical methods. These attempts allowed us to determine the optimal molar ratio, which we used for in vitro studies on pancreatic cancer cell lines. A significantly greater decrease in the viability of the tested 3D cultures was observed after 48 h of incubation with CR-BLU-258, which resulted in a lower IC

Indexed as

Antineoplastic AgentsCongo RedPancreatic NeoplasmsProtein Kinase InhibitorsCell Line, TumorCell ProliferationCell SurvivalHumansModels, MolecularSpheroids, CellularAntineoplastic AgentsCongo RedProtein Kinase Inhibitorsapoptosisavapritinib (BLU-258)cell viabilityCongo redmigrationpancreatic cancertargeted therapytumor growth

Identifiers

PMID40076604
PMCPMC11901030

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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.