ArticleScientific reports2024
SMS121, a new inhibitor of CD36, impairs fatty acid uptake and viability of acute myeloid leukemia.
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.
What it found
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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.
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Who cites it
21 citing papers in PubMed, 22 citations in OpenAlex.
- Integrative Single-Cell Transcriptomics, Multi-Omics Analyses, and Computational Pharmacology Reveal Macrophage Heterogeneity and the Putative THBS1-CD36 Axis in Coronary Atherosclerosis.Chemical biology & drug design · 2026Article
- Integrin-linked kinase promotes hepatic fat accumulation via F-actin stabilization-dependent CD36 plasma membrane localization.iScience · 2026Article
- Methods to Study the Molecular Mechanism and Drive the Design of Protein Degraders.Chemical reviews · 2026Review
- Lipid metabolism as a central driver of immune remodeling and therapeutic vulnerability in metastatic colorectal cancer.Lipids in health and disease · 2026Review
- Aerobic glycolysis drives differentiation of unilocular adipocytes.Journal of lipid research · 2026Article
- Solute Carrier transporters in tumor metabolism and immune modulation: implications for therapy.Journal of translational medicine · 2026Review
- Metabolic crosstalk among cancer-associated fibroblasts, adipocytes and immune cells as an immunosuppressive tumor microenvironment driver.Experimental & molecular medicine · 2026Review
- Regulation of osteoclastogenesis and bone resorption by fatty acid metabolism: mechanisms and therapeutic opportunities.Frontiers in endocrinology · 2026Review
- The metabolic environment within solid tumors drives a complex crosstalk between macrophages and NK cells.Frontiers in immunology · 2026Review
- Structural Insights into Recognition and Translocation of Oxidized Phospholipid by CD36 Using Mass Spectrometry, Molecular Docking, Dynamics, and Metadynamics Simulations.Journal of the American Chemical Society · 2025Article
- Identification of New CD36 Antagonists by Structure-Based Virtual Screening.Chemical biology & drug design · 2025Article
- Linking mitochondria, fatty acids, and hematopoietic stem cell expansion during infection: implications for aging and metabolic diseases.Stem cells (Dayton, Ohio) · 2025Review
- Identification of new selective CD36 inhibitors to potentiate HER2-targeted therapy in HER2-positive breast cancer.Scientific reports · 2025Article
- Targeting lipid metabolism in acute myeloid leukemia: biological insights and therapeutic opportunities.Leukemia · 2025Review
- Pharmacological inhibition of Peroxisome Proliferation-Activated Receptor Delta (PPARδ) imparts selective leukemia cell death.Cancer & metabolism · 2025Article
- Identification of a Non-Retinoid Opsin Ligand Through Pharmacophore-Guided Virtual Screening-A Novel Potential Rhodopsin-Stabilizing Compound.Molecules (Basel, Switzerland) · 2025Article
- Unraveling lipid metabolism for acute myeloid leukemia therapy.Current opinion in hematology · 2025Review
- High-density lipoprotein cholesterol: how studying the 'good cholesterol' could improve cardiovascular health.Open biology · 2025Review
- Flow cytometric detection of leukemic stem cells in Acute Myeloid Leukemia: current status and future directions.Frontiers in pharmacology · 2025Review
- Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
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.
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Registered trials
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.