Evidence map›Paper›PMID 41328326›Full record

ArticleMedComm2025

KSQ-4279, an Inhibitor of Ubiquitin Specific Peptidase 1, Enhanced the Chemotherapeutic Efficacy in ABCB1/ABCG2/ABCC1-Mediated Multidrug Resistant Cancers.

Qihong Yang, Kewang Luo, Kenneth Kin Wah To, Can Pan, Kai Fu, Shuangli Zhu, Sijia Li, Fang Wang, Chuanan Wu, Liwu Fu

Abstract read
In one paragraph

Article in MedComm, 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. 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.

Qihong YangState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center For Cancer Sun Yat-sen University Cancer Center Guangzhou P. R. China.
Kewang LuoPeople's Hospital of Longhua Shenzhen P. R. China.
Kenneth Kin Wah ToSchool of Pharmacy The Chinese University of Hong Kong Hong Kong P. R. China.ORCID https://orcid.org/0000-0003-2755-0283
Can PanState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center For Cancer Sun Yat-sen University Cancer Center Guangzhou P. R. China.
Kai FuState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center For Cancer Sun Yat-sen University Cancer Center Guangzhou P. R. China.
Shuangli ZhuState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center For Cancer Sun Yat-sen University Cancer Center Guangzhou P. R. China.
Sijia LiState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center For Cancer Sun Yat-sen University Cancer Center Guangzhou P. R. China.
Fang WangState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center For Cancer Sun Yat-sen University Cancer Center Guangzhou P. R. China.
Chuanan WuPeople's Hospital of Longhua Shenzhen P. R. China.
Liwu FuState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center For Cancer Sun Yat-sen University Cancer Center Guangzhou P. R. China.ORCID https://orcid.org/0000-0001-6795-2506

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multidrug resistance (MDR) remarkably hinders the success of clinical chemotherapy in carcinomas. The ATP-binding cassette (ABC) transporter as ABCB1, ABCG2, and ABCC1 are most crucial to drive MDR. Regrettably, no MDR modulators have been accepted in clinic. Herein, KSQ-4279, a first-in-class ubiquitin-specific peptidase 1 (USP1) inhibitor in clinical development, was found as a pan-MDR modulator. Our study showed that KSQ-4279 strikingly intensified the cytotoxicity of multiple classical chemotherapeutic drugs in ABCB1/ABCG2/ABCC1-induced MDR cancers independent of its own cytotoxicity in vitro, and remarkably improved chemotherapeutic efficacy not only in ABCB1/ABCG2/ABCC1-overexpressing tumor xenografts in vivo, but also in ABCB1-overexpressing clinical lung cancers ex vivo. Mechanistically, KSQ-4279 weakened ABCB1/ABCG2/ABCC1 efflux function, thus increasing drugs' reservation in cells; more specifically, it was achieved by KSQ-4279 activating the ATPase activity and competing for the substrate-binding pockets of ABCB1/ABCG2/ABCC1. Besides, at the effective reversal concentrations, KSQ-4279 neither altered expression and localization of ABCB1/ABCG2/ABCC1, nor affected USP1's potential downstream AKT or ERK1/2 signaling. This is the first study to investigate the combination of USP1 inhibitor (KSQ-4279) with traditional chemotherapeutic drugs in reversing MDR, which surprisingly hinted ABCB1, ABCG2, and ABCC1 as the new targets of KSQ-4279, and advocated this promising combination therapy in clinical refractory MDR cancers.

Indexed as

ATP‐binding cassette transporterscombination chemotherapyKSQ‐4279multidrug resistanceubiquitin specific peptidase 1

Identifiers

PMID41328326
PMCPMC12664909

What Socratic holds

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LicenceCC BY
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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 Socratic graph.