Evidence map›Paper›PMID 39480610›Full record

ArticleMolecular diversity2025

A potent dual inhibitor targeting COX-2 and HDAC of acute myeloid leukemia cells.

Xiang Qin, Xueting Wang, Chunmei Yang, Fan Wang, Tingting Fang, Didi Gu, Qulian Guo, Qiuyu Meng, Wenjun Liu, Lu Yang

Abstract read
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In one paragraph

Article in Molecular diversity, 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. 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

10 authors.

Xiang Qin *Department of Pediatrics (Hematological Oncology), Children Hematological Oncology and Birth Defects Laboratory, Sichuan Clinical Research Center for Birth Defects, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Xueting Wang *Department of Pediatrics (Hematological Oncology), Children Hematological Oncology and Birth Defects Laboratory, Sichuan Clinical Research Center for Birth Defects, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Chunmei Yang *Department of Radiology, Nuclear Medicine and Molecular Imaging Key Laboratory of Sichuan Province, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Fan WangDepartment of Newborn Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Tingting FangDepartment of Pediatrics (Hematological Oncology), Children Hematological Oncology and Birth Defects Laboratory, Sichuan Clinical Research Center for Birth Defects, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Didi GuDepartment of Radiology, Nuclear Medicine and Molecular Imaging Key Laboratory of Sichuan Province, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Qulian GuoDepartment of Pediatrics (Hematological Oncology), Children Hematological Oncology and Birth Defects Laboratory, Sichuan Clinical Research Center for Birth Defects, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Qiuyu MengKey Laboratory of Pollution Exposure and Health Intervention of Zhejiang Province, Interdisciplinary Research Academy (IRA), Zhejiang Shuren University, Hangzhou, 310015, China. qiuyumeng@zjsru.edu.cn.
Wenjun LiuDepartment of Pediatrics (Hematological Oncology), Children Hematological Oncology and Birth Defects Laboratory, Sichuan Clinical Research Center for Birth Defects, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China. wenjun_liu@swmu.edu.cn.
Lu YangDepartment of Radiology, Nuclear Medicine and Molecular Imaging Key Laboratory of Sichuan Province, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China. yanglu@swmu.edu.cn.

Funding

National Natural Science Foundation of China No. 81903460National Natural Science Foundation of China No. 82304311
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is an aggressive cancer with complex issues of drug resistance and a poor prognosis; thus, effective therapeutics is urgently needed for AML. In this study, we designed and synthesized dual cyclooxygenase-2 (COX-2) and histone deacetylase (HDAC) inhibitors, IMC-HA and IMC-OPD, and applied them for the treatment of AML. IMC-HA comprised a COX-2 inhibitor skeleton of indomethacin (IMC) and an HDAC inhibitor moiety of the hydroxamic group and was found to exhibit potent antiproliferative activity against AML cells (THP-1 and U937) and low cytotoxicity toward normal cells. Molecular docking simulations suggested that IMC-HA had a high binding affinity for HDAC and COX-2, with binding energies of -6.8 and -9.0 kcal/mol, respectively. Mechanistic studies revealed that IMC-HA induced apoptosis and G0/G1 phase arrest in AML cells, which were characterized by alterations in the expression of apoptotic and cell cycle-related proteins. Further study demonstrated that IMC-HA also inhibited the MEK/ERK signaling pathway in AML cells. Overall, we believe that IMC-HA could serve as a potent COX-2/HDAC dual inhibitor and improve the treatment of AML.

Indexed as

Antineoplastic AgentsCyclooxygenase 2Cyclooxygenase 2 InhibitorsHistone Deacetylase InhibitorsHistone DeacetylasesLeukemia, Myeloid, AcuteApoptosisCell Line, TumorCell ProliferationHumansMolecular Docking SimulationAntineoplastic AgentsCyclooxygenase 2Cyclooxygenase 2 InhibitorsHistone Deacetylase InhibitorsHistone DeacetylasesAcute myeloid leukemiaCyclooxygenase-2Dual-mode inhibitorHistone deacetylasesMEK/ERK signaling pathways

Identifiers

PMID39480610

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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.