Evidence map›Paper›PMID 40946229›Full record

ArticleChemMedChem2025

Hybrid Molecules of p53 Activators and Protoflavones to Target Multiple Myeloma.

Francisca Lopes, Gábor Girst, Rafael Rincón, Ricardo J F Ferreira, Lídia M Gonçalves, Lucília Saraiva, Hui-Chun Wang, Muriel Cuendet, Attila Hunyadi, Maria M M Santos

Abstract read
In one paragraph

Article in ChemMedChem, 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. Article
  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

10 authors.

Francisca LopesResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Av. Prof. Gama Pinto, 1649-003, Lisboa, Portugal.
Gábor GirstInstitute of Pharmacognosy, University of Szeged, Eötvös str. 6, H-6720, Szeged, Hungary.
Rafael RincónSchool of Pharmaceutical Sciences, University of Geneva, Rue Michel-Servet 1, 1211, Genève 4, Switzerland.
Ricardo J F FerreiraResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Av. Prof. Gama Pinto, 1649-003, Lisboa, Portugal.
Lídia M GonçalvesResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Av. Prof. Gama Pinto, 1649-003, Lisboa, Portugal.
Lucília SaraivaLAQV/REQUIMTE, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira 228, 4050-313, Porto, Portugal.
Hui-Chun WangGraduate Institute of Natural Products, Kaohsiung Medical University, Shih-Chuan first Road. 100, Kaohsiung, 807, Taiwan.
Muriel CuendetSchool of Pharmaceutical Sciences, University of Geneva, Rue Michel-Servet 1, 1211, Genève 4, Switzerland.
Attila HunyadiInstitute of Pharmacognosy, University of Szeged, Eötvös str. 6, H-6720, Szeged, Hungary.ORCID https://orcid.org/0000-0003-0074-3472
Maria M M SantosResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Av. Prof. Gama Pinto, 1649-003, Lisboa, Portugal.ORCID https://orcid.org/0000-0002-2239-9353

Funding

bilateral action 2018-2.1.15-TÉT-PT-2018-00016bilateral action 5183/2019COSTEuropean Regional Development FundFundação para a Ciência e a Tecnologia UID/50006Fundação para a Ciência e a Tecnologia UID/50006;UID/04138;PTDC/QUI-QOR/1304/2020;2022.11539.BDHungarian Academy of Sciences NKM2024-16/2024National Science and Technology Council, Taiwan NSTC-HAS 111-2927-I-037-501NMR Network Nº 022161Swiss National Science Foundation #310030_184790
6 · The paper itself

Abstract

Multiple myeloma is a rare blood cancer that develops from abnormal plasma cells in the bone marrow. Treatment of multiple myeloma remains an enormous challenge. In this work, hybrid compounds are developed and studied for their potential use against multiple myeloma. The compounds are designed to act by a dual mechanism of action, activation of the p53 pathway, and inhibition of the ataxia telangiectasia and Rad3-related protein (ATR). To evaluate the selectivity for the p53 pathway, the compounds are first evaluated in an isogenic pair of HCT116 colon cancer cell lines, with and without p53, and in two breast cancer cell lines expressing different forms of p53. Then, the growth inhibitory effect of the hybrid compounds is tested against the multiple myeloma cell lines RPMI 8226 (mutant p53) and MM.1S (wild-type p53). At the same time, compound 15 is confirmed to inhibit doxorubicin- but not UV-induced DNA damage response via the ATR/Chk1 signaling pathway. The hybrids show lower IC

Indexed as

Antineoplastic AgentsMultiple MyelomaTumor Suppressor Protein p53Ataxia Telangiectasia Mutated ProteinsCell Line, TumorCell ProliferationDNA DamageDose-Response Relationship, DrugDrug Screening Assays, AntitumorHumansMolecular StructureStructure-Activity RelationshipAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsATR protein, humanTumor Suppressor Protein p53cancerhybridsp53protoflavonestryptophanol

Identifiers

PMID40946229
PMCPMC12597214

What OpenQuestion holds

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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.