Evidence map›Paper›PMID 41958931›Full record

ArticleFrontiers in pharmacology2026

Preclinical evaluation of CPL423: a novel potent small-molecule inhibitor of TAM family and FLT3 kinase for cancer therapy.

Agata Mikołajczyk, Delfina Popiel, Kinga Jastrzębska, Bartosz Wiernicki, Filip Mituła, Artur Janusz, Jakub Dominowski, Michał Górka, Tomasz Kornatowski, Joanna Hucz-Kalitowska and 9 more

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Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

19 authors.

Agata Mikołajczyk *Celon Pharma S.A., Preclinical Development Department, Lomianki, Poland.
Delfina Popiel *Celon Pharma S.A., Preclinical Development Department, Lomianki, Poland.
Kinga JastrzębskaCelon Pharma S.A., Preclinical Development Department, Lomianki, Poland.
Bartosz WiernickiCelon Pharma S.A., Preclinical Development Department, Lomianki, Poland.
Filip MitułaCelon Pharma S.A., Preclinical Development Department, Lomianki, Poland.
Artur JanuszCelon Pharma S.A., Preclinical Development Department, Lomianki, Poland.
Jakub DominowskiCelon Pharma S.A., Preclinical Development Department, Lomianki, Poland.
Michał GórkaCelon Pharma S.A., Preclinical Development Department, Lomianki, Poland.
Tomasz KornatowskiCelon Pharma S.A., Preclinical Development Department, Lomianki, Poland.
Joanna Hucz-KalitowskaCelon Pharma S.A., Preclinical Development Department, Lomianki, Poland.
Małgorzata Teska-KamińskaCelon Pharma S.A., Preclinical Development Department, Lomianki, Poland.
Damian SmugaCelon Pharma S.A., Medicinal Chemistry Department, Lomianki, Poland.
Monika DelisCelon Pharma S.A., Medicinal Chemistry Department, Lomianki, Poland.
Krystian KameckiCelon Pharma S.A., Preclinical Development Department, Lomianki, Poland.
Paweł MaliszewskiCelon Pharma S.A., Medicinal Chemistry Department, Lomianki, Poland.
Abdellah YamaniCelon Pharma S.A., Medicinal Chemistry Department, Lomianki, Poland.
Krzysztof DubielCelon Pharma S.A., Medicinal Chemistry Department, Lomianki, Poland.
Jerzy PieczykolanCelon Pharma S.A., Preclinical Development Department, Lomianki, Poland.
Maciej WieczorekCelon Pharma S.A., Preclinical Development Department, Lomianki, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The TAM family of receptor tyrosine kinases (TYRO3, AXL, MERTK) promotes tumor survival, metastasis, and immune evasion. Its dysregulation across solid and hematologic cancers is associated with therapy resistance and poor outcomes. FLT3 is a key oncogenic driver in acute myeloid leukemia (AML). We report the preclinical characterization of CPL423, a low-molecular-weight inhibitor of all TAMs and FLT3. Method: Result: CPL423 inhibited TAMs and FLT3 with sub-nanomolar IC50s (MERTK 0.47 nM; FLT3 0.94 nM) and high selectivity. It suppressed proliferation in MOLM-13 and MV4-11 (IC50 5.7 and 7.92 nM). In AML xenografts, it achieved up to 98% tumor growth inhibition without observable toxicity; in A375, TGI was 39.4% at 50 mg/kg on day 14 Ex vivo experiments showed that the compound altered the clearance of dying cells by dendritic cells (BMDCs), consistent with TAM-pathway modulation. CPL423 showed high permeability, metabolic stability, and low cardiovascular liability. Discussion: CPL423 provides direct antitumor activity via dual TAM/FLT3 inhibition and immune-mediated effects on antigen-presenting cells, addressing resistance mechanisms in AML and TAM/AXL-driven solid tumors and supporting further development, including combination regimens.

Indexed as

acute myeloid leukemia (AML)cancer therapyCPL423FLT3 Inhibitor, small-molecule inhibitorkinase inhibitionTAM kinasestumor phagocytic capacity

Identifiers

PMID41958931
PMCPMC13058478

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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.