Evidence map›Paper›PMID 38643249›Full record

ArticleScientific reports2024

SMS121, a new inhibitor of CD36, impairs fatty acid uptake and viability of acute myeloid leukemia.

Hannah Åbacka, Samuele Masoni, Giulio Poli, Peng Huang, Francesco Gusso, Carlotta Granchi, Filippo Minutolo, Tiziano Tuccinardi, Anna K Hagström-Andersson, Karin Lindkvist-Petersson

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
6.3field-weighted citation impact, top 3% of its field
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

21 citing papers in PubMed, 22 citations in OpenAlex.

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  20. Frontiers in cardiovascular medicine · 2025
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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 at 3 institutions in 3 countries.

Hannah ÅbackaDepartment of Experimental Medical Science, Lund University, BMC C13, 221 84, Lund, Sweden.
Samuele MasoniDepartment of Pharmacy, University of Pisa, Pisa, Italy.
Giulio PoliDepartment of Pharmacy, University of Pisa, Pisa, Italy. giulio.poli@unipi.it.
Peng HuangDepartment of Experimental Medical Science, Lund University, BMC C13, 221 84, Lund, Sweden.
Francesco GussoDepartment of Pharmacy, University of Pisa, Pisa, Italy.
Carlotta GranchiDepartment of Pharmacy, University of Pisa, Pisa, Italy.
Filippo MinutoloDepartment of Pharmacy, University of Pisa, Pisa, Italy.
Tiziano TuccinardiDepartment of Pharmacy, University of Pisa, Pisa, Italy.
Anna K Hagström-AnderssonDepartment of Laboratory Medicine, Division of Clinical Genetics, Lund University, Lund, Sweden.
Karin Lindkvist-PeterssonDepartment of Experimental Medical Science, Lund University, BMC C13, 221 84, Lund, Sweden. karin.lindkvist@med.lu.se.
University of Pisa · ITLund University · SEEngineering Link (Canada) · CA

Funding

Cancerfonden 20 0747 PjF
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults and the second most common among children. AML is characterized by aberrant proliferation of myeloid blasts in the bone marrow and impaired normal hematopoiesis. Despite the introduction of new drugs and allogeneic bone marrow transplantation, patients have poor overall survival rate with relapse as the major challenge, driving the demand for new therapeutic strategies. AML patients with high expression of the very long/long chain fatty acid transporter CD36 have poorer survival and very long chain fatty acid metabolism is critical for AML cell survival. Here we show that fatty acids are transferred from human primary adipocytes to AML cells upon co-culturing. A drug-like small molecule (SMS121) was identified by receptor-based virtual screening and experimentally demonstrated to target the lipid uptake protein CD36. SMS121 reduced the uptake of fatty acid into AML cells that could be reversed by addition of free fatty acids and caused decreased cell viability. The data presented here serves as a framework for the development of CD36 inhibitors to be used as future therapeutics against AML.

Indexed as

Fatty AcidsLeukemia, Myeloid, AcuteAcute DiseaseAdultBone MarrowChildCoculture TechniquesHumansFatty AcidsAcute myeloid leukemiaAdipocyteAMLCD36Fatty acid

Identifiers

PMID38643249
PMCPMC11032350
OpenAlexW4394988804

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.