Evidence map›Paper›PMID 41907415›Full record

ArticleiScience2026

New selective and allosteric FLT3 inhibitors show efficacy against resistant acute myeloid leukemia cells.

Shuai-Shuai Ge, Qiao-Cheng Qiu, Jingsheng Hua, Jun Wang, Minfeng Yang, Jiahui Du, Yuan-Hong Huang, Chao-Ling Wan, Ling-Ling Liu, Hai-Ping Dai and 5 more

Abstract read
In one paragraph

Article in iScience, 2026. 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

15 authors.

Shuai-Shuai GeNational Clinical Research Center for Hematologic Diseases, Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Qiao-Cheng QiuNational Clinical Research Center for Hematologic Diseases, Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Jingsheng HuaDepartment of Hematology, Taizhou Municipal Hospital Affiliated to Taizhou University, Taizhou, China.
Jun WangNational Clinical Research Center for Hematologic Diseases, Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Minfeng YangSchool of Public Health, Nantong University, No. 9, Seyuan Road, Nantong, Jiangsu 226019, P.R. China.
Jiahui DuJiangsu Province Engineering Research Center of Molecular Target Therapy and Companion Diagnostics in Oncology, Suzhou Vocational Health College, Kehua Road 28, Suzhou, China.
Yuan-Hong HuangNational Clinical Research Center for Hematologic Diseases, Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Chao-Ling WanNational Clinical Research Center for Hematologic Diseases, Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Ling-Ling LiuNational Clinical Research Center for Hematologic Diseases, Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Hai-Ping DaiNational Clinical Research Center for Hematologic Diseases, Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Maofeng ZhangJiangsu Province Engineering Research Center of Molecular Target Therapy and Companion Diagnostics in Oncology, Suzhou Vocational Health College, Kehua Road 28, Suzhou, China.
Binghui ShenDepartment of Cancer Genetics and Epigenetics, Beckman Research Institute, City of Hope, 1500 East Duarte Road, Duarte, CA, USA.
Sheng-Li XueNational Clinical Research Center for Hematologic Diseases, Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Fang ChenHematology Laboratory, Shengjing Hospital of China Medical University, Shenyang 110022, P.R. China.
Song-Bai LiuJiangsu Province Engineering Research Center of Molecular Target Therapy and Companion Diagnostics in Oncology, Suzhou Vocational Health College, Kehua Road 28, Suzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activating FLT3 mutations confer a poor prognosis in acute myeloid leukemia (AML). FLT3 inhibitors significantly improved the clinical outcomes of FLT3-mutated AML. However, all clinically approved inhibitors target the ATP-binding pocket of FLT3. The acquired FLT3 mutations in the ATP-binding pocket, including mutations at D835 and F691, are common mechanisms of leukemia relapse. Using druggable site prediction (DSP) and high-throughput virtual screening, we revealed that the predicted site 1 region was promising for allosteric inhibitor development, and F-17 was identified as the first potential allosteric FLT3 inhibitor. F-17 exhibited high affinity for site 1 in an ATP non-competitive manner. KINOMEscan analysis showed that F-17 was significantly selective toward FLT3 over other homologous kinases of the RTK family. Moreover, F-17 showed potent selectivity and inhibition activity for FLT3-mutated cells both

Indexed as

CancerPharmacologyStructural biology

Identifiers

PMID41907415
PMCPMC13018901

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.