Evidence map›Paper›PMID 38204232›Full record

ReviewCurrent medicinal chemistry2024

Developments of Fms-like Tyrosine Kinase 3 Inhibitors as Anticancer Agents for AML Treatment.

Chenchen Ma, Siyuan Cui, Ruirong Xu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current medicinal chemistry, 2024. 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. 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

3 authors.

Chenchen MaCollege of Integrated Traditional Chinese and Western Medicine, Shandong University of Traditional Chinese Medicine, Jinan 250014, China.ORCID 0000-0001-7631-4880
Siyuan CuiDepartment of Hematology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, 250014, China.ORCID 0000-0003-0560-2388
Ruirong XuDepartment of Hematology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, 250014, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFMS-like tyrosine kinase 3 (FLT3) is a commonly mutated gene in acute myeloid leukemia. As a receptor tyrosine kinase (RTK), FLT3 plays a role in the proliferation and differentiation of hematopoietic stem cells. As the most frequent molecular alteration in AML, FLT3 has drawn the attention of many researchers, and a lot of small molecule inhibitors targeting FLT3 have been intensively investigated as potential drugs for AML therapy.

methodsIn this paper, PubMed and SciFinder

resultsIn this study, the structural characterization and biological activities of representative FLT3 inhibitors were summarized. The major challenges and future directions for further research are discussed.

conclusionRecently, numerous FLT3 inhibitors have been discovered and employed in FLT3-mutated AML treatment. In order to overcome the drug resistance caused by FLT3 mutations, screening multitargets FLT3 inhibitors has become the main research direction. In addition, the emergence of irreversible FLT3 inhibitors also provides new ideas for discovering new FLT3 inhibitors.

Indexed as

Antineoplastic Agentsfms-Like Tyrosine Kinase 3Leukemia, Myeloid, AcuteProtein Kinase InhibitorsDrug DevelopmentHumansAntineoplastic AgentsFLT3 protein, humanfms-Like Tyrosine Kinase 3Protein Kinase InhibitorsAMLanticancer activityFLT3FLT3 inhibitorsSARs.structure modification

Identifiers

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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.