CD36 inhib 
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  • ||||||||||  Journal, IO biomarker:  Bach2 repression of CD36 regulates lipid-metabolism-linked effector functions in follicular B cells. (Pubmed Central) -  Oct 16, 2024   
    Mechanistically, Bach2 acts as a repressor of Cd36, and inhibition of CD36 or fatty acid oxidation reduces the differentiation of naive B cells into IL-6- and antibody-secreting cells. These results indicate Bach2 as a key metabolic checkpoint regulator crucial for maintaining a functionally quiescent state of follicular B cells.
  • ||||||||||  Journal, PD(L)-1 Biomarker, IO biomarker:  Targeting CD36-Mediated Lipid Metabolism by Selective Inhibitor-Augmented Antitumor Immune Responses in Oral Cancer. (Pubmed Central) -  Sep 14, 2024   
    In vivo SSO administration significantly attenuated mouse tumor growth with an increased proportion of immune cells, including CD4+ T, CD8+ T, and dendritic cells; it also decreased the proportion of immune suppressive cells, such as myeloid-derived suppressor and regulatory T cells. These results suggest that the selective inhibition of CD36 can induce direct and indirect antitumor effects by facilitating host antitumor immune responses in OSCCs.
  • ||||||||||  Journal:  Integrated multi-omics profiling landscape of organising pneumonia. (Pubmed Central) -  Jul 31, 2024   
    activation, and provided a potential therapeutic target for the management of retinal degeneration. Our findings reveal a significant association between organising pneumonia and lipid metabolism reprogramming and will make a substantial contribution to the understanding of the mechanism of organising pneumonia in patients.
  • ||||||||||  etomoxir (MIQ-001) - Meta / IQ
    Journal:  Potential Application of the Myocardial Scintigraphy Agent [123I]BMIPP in Colon Cancer Cell Imaging. (Pubmed Central) -  Jul 31, 2024   
    The accumulation of [123I]BMIPP was evaluated in the presence of sulfosuccinimidyl oleate (SSO), a CD36 inhibitor, and lipofermata, a fatty acid transport protein (FATP) inhibitor, under low-temperature conditions and in the presence of etomoxir, a carnitine palmitoyl transferase I (CPT1) inhibitor...Therefore, [123I]BMIPP may be useful for imaging cancers with activated fatty acid metabolism, such as colon cancer. However, the development of novel imaging radiotracers based on the chemical structure analog of [123I]BMIPP is needed.
  • ||||||||||  Excessive free fatty acids sensing in pituitary lactotrophs elicits liver steatosis by decreasing prolactin levels (Vienna Hall) -  Jul 1, 2024 - Abstract #EASD2024EASD_586;    
    We reported previously unknown mechanisms of excessive free fatty acids sensing in pituitary lactotrophs elicits liver steatosis by decreasing prolactin levels. This study provided a new insight into the understanding of inter-organ mechanisms of hepatic lipid homeostasis, and targeted inhibition of FFA sensing in pituitary may be a potential therapeutic target for liver steatosis
  • ||||||||||  Peroxisome Proliferator-Activated Receptor Delta (PPAR?) (Poster Hall (West A4-B2); 475) -  May 20, 2024 - Abstract #ADA2024ADA_2772;    
    Targeting PPAR? in these cells effectively dampened the inflammatory response, offering a promising therapeutic avenue against TB, especially for those with diabetes.
  • ||||||||||  acetylcysteine solution / Generic mfg.
    Journal:  CD36-mediated podocyte lipotoxicity promotes foot process effacement. (Pubmed Central) -  Apr 8, 2024   
    The antioxidant N-acetylcysteine suppressed PA-induced podocyte FP effacement and ROS generation. CD36 participated in fatty acid-induced FP effacement in podocytes via oxidative stress, and CD36 inhibitors may be helpful for early treatment of kidney injury.
  • ||||||||||  pioglitazone / Generic mfg.
    CD36-mediated hepatocyte-macrophage coordination drives hepatic fibrosis in MASLD (Poster Area) -  Apr 2, 2024 - Abstract #EASLILC2024EASL_ILC_1088;    
    CD36 serves as a facilitator for the transfer of lipids from hepatic cells to LAMs, thereby initiating the activation of hepatic stellate cells and promoting the progression of liver fibrosis. The identification of CD36 as a potential therapeutic target offers promising prospects for the treatment of advanced liver fibrosis associated with MASLD.
  • ||||||||||  pitavastatin / Generic mfg.
    Journal:  CD36 inhibition reduces non-small-cell lung cancer development through AKT-mTOR pathway. (Pubmed Central) -  Feb 6, 2024   
    At the molecular level, we found that CD36 inhibition, either with pitavastatin or plasmid, reduced proliferation- and migration-related protein expression through the AKT/mTOR pathway. Taken together, we demonstrate that inhibition of CD36 expression by pitavastatin or other inhibitors may be a viable strategy for NSCLC treatment.
  • ||||||||||  SU6656 / Pfizer, Hokkaido University
    Journal, IO biomarker:  Amphipathic Helical Peptide L37-pA Protects Against Lung Vascular Endothelial Dysfunction Caused by Truncated Oxidized Phospholipids via Antagonism with CD36 Receptor. (Pubmed Central) -  Jan 2, 2024   
    The Src inhibitor SU6656 attenuated KOdia-PC-induced EC permeability and inflammation, but inhibition of the Toll-like receptors (TLRs) TLR1, TLR2, TLR4, and TLR6 had no such protective effects...CD36 knockout mice were more resistant to Tr-OxPLs-induced lung injury and L37pA was equally effective in ameliorating Tr-OxPL-induced vascular leak and lung inflammation in mice as determined by Evans blue extravasation assay and total cells and protein content in BAL. Altogether, these results demonstrate an essential role of CD36 in mediating Tr-OxPL-induced EC dysfunction and suggest a strong therapeutic potential of CD36 inhibitory peptides in mitigating lung injury and inflammation.
  • ||||||||||  Journal:  Immune Regulation of the Liver Through the PCSK9/CD36 Pathway During Heart Transplant Rejection. (Pubmed Central) -  Oct 23, 2023   
    Taken together, the results suggest that inhibition of CD36 and Nogo-B can reduce the proliferation and migration of TNBC, which provides new targets for the development of drugs against TNBC. This study reveals a novel mechanism for immune regulation by the liver through the PCSK9/CD36 pathway during HTR, which influences the phenotype and function of macrophages and suggests that the modulation of this pathway may be a potential therapeutic target to prevent HTR.
  • ||||||||||  Journal:  CD36 drives metastasis and relapse in acute myeloid leukemia. (Pubmed Central) -  Oct 22, 2023   
    In xenograft mouse models, CD36 inhibition reduced metastasis of blasts and prolonged survival of chemotherapy-treated mice. These results pave the way for the development of CD36 as an independent marker of poor prognosis in AML patients and a promising actionable target to improve the outcome of patients.
  • ||||||||||  Biomarker, Journal:  sTREM2 is a plasma biomarker for human NASH and promotes hepatocyte lipid accumulation. (Pubmed Central) -  Oct 11, 2023   
    Elevated levels of sTREM2 due to TREM2 shedding may directly contribute to the pathogenesis of NAFLD by promoting hepatocyte lipid accumulation, as well as serving as a biomarker for distinguishing patients with NASH versus NAFL. Further investigation of sTREM2 as a clinically useful diagnostic biomarker and of the therapeutic effects of targeting sTREM2 in NASH is warranted.
  • ||||||||||  Review, Journal:  Role of CD36 in central nervous system diseases. (Pubmed Central) -  Sep 18, 2023   
    Moreover, we predicted the structures of binding sites between CD36 and antagonists. These sites can provide targets for more efficient and safer CD36 antagonists for the treatment of central nervous system diseases.
  • ||||||||||  cisplatin / Generic mfg.
    Journal:  Visible light-activatable platinum(IV) prodrugs harnessing CD36 for ovarian cancer therapy. (Pubmed Central) -  Jul 25, 2023   
    Once the Pt(IV) metallodrugs enter the cancer cells, they can be activated to form Pt(II) with characteristics of cisplatin under visible light (490 nm) irradiation, promoting photoinduced electron transfer from the attached fluorophore to the metal center. This light-induced activation can increase the cytotoxicity of the Pt(IV) metallodrugs by up to 20 times toward ovarian cancer cells, inducing DNA damage and enabling efficient elimination of drug-resistant cancer cells.
  • ||||||||||  CD36 regulates FFA-Fetuin-A mediated inflammation and lipid accumulation in pancreatic beta cells (Short Oral Event B) -  Jul 2, 2023 - Abstract #EASD2023EASD_287;    
    in pancreatic beta cell during hyperlipidemic condition. Also, Palmitate along with Fetuin-A promotes intracellular lipid accumulation in beta cells involving both CD36 and TLR4 indicating a possible crosstalk between CD36 and TLR4 that results islet inflammation and lipid accumulation culminating in insulin secretory defects.
  • ||||||||||  Preclinical, Journal:  Bioinformatics analysis reveals lipid metabolism may play an important role in the SiO-stimulated rat model. (Pubmed Central) -  Jun 14, 2023   
    In addition, at the cellular level, SiO-stimulated lead to lipid metabolism disorder in NR8383, and silencing CD36 inhibited SiO-induced lipid metabolism disorder. These results indicate that lipid metabolism plays an important role in the progression of silicosis, and the genes and pathways reported in this study may provide new ideas for the pathogenesis of silicosis.
  • ||||||||||  Glutamine regulates BCR/Abl expression in hypoxic chronic myeloid leukemia cells via fatty acids metabolism (Poster and Exhibition Hall) -  Jun 13, 2023 - Abstract #EACR2023EACR_628;    
    In these conditions, CML cells rapidly lose BCR/Abl expression, a phenomenon which was validated by the treatment with exogenous BSA-Palmitate, capable to reduce BCR/Abl expression, while the use of the sulfosuccinimidyl oleate, a specific CD36 inhibitor, sustained the oncoprotein maintenance instead.ConclusionOur results suggest that FA may play a fundamental role in hypoxic-induced BCR/Abl suppression and that such FA degradation might be needed for the oncoprotein re-expression once in normoxic conditions. This phenomenon might be therefore exploited to sustain BCR/Abl expression in hypoxic cells to be more susceptible to TKi.
  • ||||||||||  Venclexta (venetoclax) / Roche, AbbVie, Walter and Eliza Hall Institute
    ACUTE MYELOID LEUKEMIA REPROGRAMS LIPID METABOLISM BY DOWNREGULATING CD36 EXPRESSION IN HEPATOCYTES. (Poster area) -  May 12, 2023 - Abstract #EHA2023EHA_1889;    
    Our in vivo and in vitro studies indicate that AML cells secrete cytokines which reduce CD36 and CPT1 expression in hepatocytes andthus the FA metabolism in the liver. Increasing our understanding of how AML is able to access large amounts of metabolites, allowing the disease to successfully infiltrate and expand throughout healthy BM, may aid in the development of novel therapeutic targets.