Evidence map›Paper›PMID 40958869›Full record

ArticleFrontiers in oncology2025

Evaluation of anti-liver cancer activity and anticancer mechanism of one novel small molecule compound (THY-10A62) targeting FAK pathway.

Wanqiu Huang, Rong Zou, Jie Xu, Yuliang Deng, Dongping Zhang, Yiguo Hu, Qian Zhang, Jian Huang, Zhaoqi Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Wanqiu HuangKey Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Centre for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Rong ZouKey Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Centre for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Jie XuKey Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Centre for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Yuliang DengKey Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Centre for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Dongping ZhangDepartment of Medicinal Chemistry, School of Pharmacy, Fudan University, Shanghai, China.
Yiguo HuDepartment of Thyroid Surgery and National Clinical Research Center for Geriatrics, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy, Chengdu, China.
Qian ZhangDepartment of Medicinal Chemistry, School of Pharmacy, Fudan University, Shanghai, China.
Jian HuangKey Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Centre for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Zhaoqi ZhangKey Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Centre for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Focal adhesion kinase (FAK) is a promising therapeutic target, and its aberrant overexpression has been implicated in the growth and metastasis of multiple cancers, including hepatocellular carcinoma (HCC). This study preliminarily evaluated the antitumor activity and mechanisms of THY-10A62, a novel FAK inhibitor, Methods: The maximum tolerated dose (MTD) and median lethal dose (LD Results: The MTD of THY-10A62 in mice was < 45 mg/kg, and the LD₅₀ in female mice was 49 mg/kg. At 15 mg/kg, THY-10A62 significantly inhibited liver tumor growth (TGI > 40%), with greater suppression than PF-562271 at the tested conditions. In PDX tumors, THY-10A62 markedly down-regulated FAK phosphorylation. Phospho-proteomic profiling indicated altered phosphorylation of downstream effectors, including BRAF and RASGRF1, consistent with inhibition of FAK-mediated signaling. Discussion: THY-10A62 demonstrates

Indexed as

FAK inhibitorliver cancermechanismsignal pathwaysmall molecule compoundTHY-10A62

Identifiers

PMID40958869
PMCPMC12433887

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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.