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midostaurin  (Novartis)

 
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    Novartis midostaurin
    Midostaurin, supplied by Novartis, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/midostaurin/midostaurin/us12551564-1110-146-148
    Average 86 stars, based on 1 article reviews
    midostaurin - by Bioz Stars, 2026-11
    86/100 stars

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    Related Articles

    other:

    Article Title: Avapritinib versus midostaurin or cladribine in advanced systemic mastocytosis: A retrospective real-world external control study.
    Article Snippet: A. Reiter was a member of the Study Steering Committee for the global trial of midostaurin (Novartis), the Response Assessment Committee (RAC) for studies of avapritinib in AdvSM (Blueprint Medicines Corporation), and the Study Steering Committee for the phase II trial of ripretinib in AdvSM (Deciphera Pharmaceuticals); has received research funding for the conduct of these trials; and has received honoraria and reimbursement of travel expenses from Novartis and Deciphera Pharmaceuticals.

    Article Title: SMARCA degraders and uses thereof
    Article Snippet: Approved VEGF inhibitors and kinase inhibitors useful in the present invention include: bevacizumab (Avastin, Genentech/Roche) an anti-VEGF monoclonal antibody; ramucirumab (Cyramza, Eli Lilly), an anti-VEGFR-2 antibody and ziv-aflibercept, also known as VEGF Trap (Zaltrap; Regeneron/Sanofi).

    Article Title: Crenolanib for treating FLT3 mutated proliferative disorders relapsed/refractory to prior treatment
    Article Snippet: FLT3 kinase inhibitors known in the art include lestaurtinib (also known as CEP-701, Kyowa Hakko, licensed to Cephalon); CHIR-258 (Chiron Corp.); EB10 and IMC-EB10 (ImcLone Systems Inc.); Midostaurin (also known as PKC412, Novartis AG); Tandutinib (also known as MLN-518, COR Therapeutics Inc., licensed to Millennium Pharmaceuticals Inc.); Sunitinib (also known as SU11248, Pfizer USA); Quizartinib (also known as AC220, Daiichi Sankyo); XL-999 (Exelixis USA); GTP 14564 (Merck Biosciences UK); AG1295 and AG1296; CEP-5214 and CEP-7055 (Cephalon); Gilteritinib (also known as ASP2215, Astellas Pharma Inc.); FF-10101-01 (Fujifilm Pharmaceutcials); HM43239 (Hanni Pharmaceuticals); Pacritinib (also known as SB1518, CTI Biopharma); MAX-40279 (Maxinovel Pty.

    Mutagenesis:

    Article Title: Physiologically based pharmacokinetic modeling of midostaurin and metabolites at steady-state to bridge drug interaction scenarios in lieu of clinical trials.
    Article Snippet: Midostaurin and its active metabolites are substrates, mixed inhibitors/inducers of cytochrome P450 (CYP)3A4.. The main objective of this study was to develop/refine a physiologically based pharmacokinetic (PBPK) model that incorporated recent clinical drug-drug interaction (DDI) data with midazolam after multiple dosing, to qualify the pharmacokinetic (PK) model simulations of midostaurin and its metabolites, and to apply it to predict untested clinical DDI scenarios with potential comedications.. In this study, Simcyp PBPK model of midostaurin and its 2 metabolites was refined from a previously published model associated with endogenous biomarker 4b-hydroxycholesterol data through further optimization of CYP3A4 inhibition/induction potency and was qualified to simulate midostaurin steadystate PK.



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    midostaurin  (Selleck Chemicals)
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    Selleck Chemicals midostaurin
    (A) Schematic overview of the organelle proteomics pipeline. FLT3 ITD-JMD (TKI-sensitive) and FLT3 ITD-TKD (TKI-resistant) Ba/F3 cells were left untreated or treated with 100 nM <t>midostaurin</t> for 24 h. Sequential extraction with six buffers generated six subcellular fractions, which were analyzed by MS-based proteomics in biological quadruplicates. Peptides were subjected to global proteomic profiling and phosphopeptide enrichment. (B) Intensity profiles of organelle-specific marker proteins across the six fractions. (C) Hierarchical clustering of protein profiles (scaled intensities) across fractions for untreated and midostaurin-treated FLT3-ITD cells. Statistically significant enriched gene ontology terms in each cluster are indicated.
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    (A) Schematic overview of the organelle proteomics pipeline. FLT3 ITD-JMD (TKI-sensitive) and FLT3 ITD-TKD (TKI-resistant) Ba/F3 cells were left untreated or treated with 100 nM midostaurin for 24 h. Sequential extraction with six buffers generated six subcellular fractions, which were analyzed by MS-based proteomics in biological quadruplicates. Peptides were subjected to global proteomic profiling and phosphopeptide enrichment. (B) Intensity profiles of organelle-specific marker proteins across the six fractions. (C) Hierarchical clustering of protein profiles (scaled intensities) across fractions for untreated and midostaurin-treated FLT3-ITD cells. Statistically significant enriched gene ontology terms in each cluster are indicated.

    Journal: bioRxiv

    Article Title: Organelle proteomics reveals novel metabolic vulnerabilities in FLT3-ITD cells

    doi: 10.64898/2026.01.19.700272

    Figure Lengend Snippet: (A) Schematic overview of the organelle proteomics pipeline. FLT3 ITD-JMD (TKI-sensitive) and FLT3 ITD-TKD (TKI-resistant) Ba/F3 cells were left untreated or treated with 100 nM midostaurin for 24 h. Sequential extraction with six buffers generated six subcellular fractions, which were analyzed by MS-based proteomics in biological quadruplicates. Peptides were subjected to global proteomic profiling and phosphopeptide enrichment. (B) Intensity profiles of organelle-specific marker proteins across the six fractions. (C) Hierarchical clustering of protein profiles (scaled intensities) across fractions for untreated and midostaurin-treated FLT3-ITD cells. Statistically significant enriched gene ontology terms in each cluster are indicated.

    Article Snippet: Midostaurin (Selleck chemical, S8064) was used at 100 nM for 24 hours.

    Techniques: Extraction, Generated, Phospho-proteomics, Marker

    (A) Schematic representation of the bioinformatic strategy used to assign a cell compartment to proteins by using the SVM-algorithm. (B) Number of proteins assigned to cytosolic, nuclear, or organellar compartments in untreated and midostaurin treated FLT3-ITD cells. (C) Quantification of proteins changing their subcellular localization upon midostaurin treatment. (D) Sankey plot of protein translocation in midostaurin-treated FLT3 ITD-JMD . (E) Functional protein complexes redistributed between cytosol and nucleus in midostaurin-treated FLT3 ITD-JMD . (F) Sankey plot of protein translocation in midostaurin-treated FLT3 ITD-TKD cells. (G) Functional protein complexes redistributed between cytosol and nucleus in midostaurin-treated FLT3 ITD-TKD cells.

    Journal: bioRxiv

    Article Title: Organelle proteomics reveals novel metabolic vulnerabilities in FLT3-ITD cells

    doi: 10.64898/2026.01.19.700272

    Figure Lengend Snippet: (A) Schematic representation of the bioinformatic strategy used to assign a cell compartment to proteins by using the SVM-algorithm. (B) Number of proteins assigned to cytosolic, nuclear, or organellar compartments in untreated and midostaurin treated FLT3-ITD cells. (C) Quantification of proteins changing their subcellular localization upon midostaurin treatment. (D) Sankey plot of protein translocation in midostaurin-treated FLT3 ITD-JMD . (E) Functional protein complexes redistributed between cytosol and nucleus in midostaurin-treated FLT3 ITD-JMD . (F) Sankey plot of protein translocation in midostaurin-treated FLT3 ITD-TKD cells. (G) Functional protein complexes redistributed between cytosol and nucleus in midostaurin-treated FLT3 ITD-TKD cells.

    Article Snippet: Midostaurin (Selleck chemical, S8064) was used at 100 nM for 24 hours.

    Techniques: Translocation Assay, Functional Assay

    Bar plots reporting the -log2 (p-value) of the GO-Term enrichment analysis of translocating proteins upon midostaurin treatment in sensitive and resistant FLT3-ITD cells. (C) Schematic representation of the spatial remodelling of key autophagic proteins upon midostaurin treatment in sensitive and resistant FLT3-ITD cells. (D) Heatmap reporting the intensity of the phosphorylation level of translocating autophagic proteins after midostaurin treatment in FLT3 ITD-JMD and FLT3 ITD-TKD . (E) Western blotting of LC3-II and p62 protein levels in FLT3 ITD-JMD and FLT3 ITD-TKD . Cells were treated with midostaurin with or without bafilomycin A1 for 24 hours. (F) Bar plot reporting the percentage of viable cells measured by MTT assay. FLT3 ITD-JMD and FLT3 ITD-TKD were treated with 100nm of midostaurin treatment for 24h either alone or combined with 3 hours of starvation.

    Journal: bioRxiv

    Article Title: Organelle proteomics reveals novel metabolic vulnerabilities in FLT3-ITD cells

    doi: 10.64898/2026.01.19.700272

    Figure Lengend Snippet: Bar plots reporting the -log2 (p-value) of the GO-Term enrichment analysis of translocating proteins upon midostaurin treatment in sensitive and resistant FLT3-ITD cells. (C) Schematic representation of the spatial remodelling of key autophagic proteins upon midostaurin treatment in sensitive and resistant FLT3-ITD cells. (D) Heatmap reporting the intensity of the phosphorylation level of translocating autophagic proteins after midostaurin treatment in FLT3 ITD-JMD and FLT3 ITD-TKD . (E) Western blotting of LC3-II and p62 protein levels in FLT3 ITD-JMD and FLT3 ITD-TKD . Cells were treated with midostaurin with or without bafilomycin A1 for 24 hours. (F) Bar plot reporting the percentage of viable cells measured by MTT assay. FLT3 ITD-JMD and FLT3 ITD-TKD were treated with 100nm of midostaurin treatment for 24h either alone or combined with 3 hours of starvation.

    Article Snippet: Midostaurin (Selleck chemical, S8064) was used at 100 nM for 24 hours.

    Techniques: Phospho-proteomics, Western Blot, MTT Assay

    (A) Bar plot reporting the ECAR based measurements of glycolysis and glycolytic capacity in FLT3 ITD-JMD and FLT3 ITD-TKD . Cells were treated with 100nm midostaurin for 24 hours and subjected to a glycolysis stress test. ( B ) OCR-derived assessments of basal respiration and ATP production in FLT3 ITD-JMD and FLT3 ITD-TKD . Cells were treated with 100nm midostaurin for 24 hours and subjected to a mitochondrial stress test. (C) Representative electron microscopy images of steady-state FLT3 ITD-JMD and FLT3 ITD-TKD cells (m=mitochondria). (D) Bar plots reporting the number of cristae, the total cristae area and total mitochondria area in steady-state FLT3 ITD-JMD and FLT3 ITD-TKD cells. (E) Intensity profiles of the 168 proteins annotated in the MitoCarta database as mitochondrial proteins across the six fractions in each experimental condition. Colored boxes indicate the enriched GO-Term biological processes and cell compartments. (F) Heatmaps reporting the protein levels (scaled intensities) of the OXPHOS related proteins across the 6 fractions in each experimental condition.

    Journal: bioRxiv

    Article Title: Organelle proteomics reveals novel metabolic vulnerabilities in FLT3-ITD cells

    doi: 10.64898/2026.01.19.700272

    Figure Lengend Snippet: (A) Bar plot reporting the ECAR based measurements of glycolysis and glycolytic capacity in FLT3 ITD-JMD and FLT3 ITD-TKD . Cells were treated with 100nm midostaurin for 24 hours and subjected to a glycolysis stress test. ( B ) OCR-derived assessments of basal respiration and ATP production in FLT3 ITD-JMD and FLT3 ITD-TKD . Cells were treated with 100nm midostaurin for 24 hours and subjected to a mitochondrial stress test. (C) Representative electron microscopy images of steady-state FLT3 ITD-JMD and FLT3 ITD-TKD cells (m=mitochondria). (D) Bar plots reporting the number of cristae, the total cristae area and total mitochondria area in steady-state FLT3 ITD-JMD and FLT3 ITD-TKD cells. (E) Intensity profiles of the 168 proteins annotated in the MitoCarta database as mitochondrial proteins across the six fractions in each experimental condition. Colored boxes indicate the enriched GO-Term biological processes and cell compartments. (F) Heatmaps reporting the protein levels (scaled intensities) of the OXPHOS related proteins across the 6 fractions in each experimental condition.

    Article Snippet: Midostaurin (Selleck chemical, S8064) was used at 100 nM for 24 hours.

    Techniques: Derivative Assay, Electron Microscopy

    (A) Heatmap reporting the number of translocating proteins involved in carbohydrate, amino acids, peroxisome and lipid metabolism in FLT3 ITD-JMD and FLT3 ITD-TKD . (B) Bar plot reporting the ΔOCR of basal respiration after the inhibition of glucose usage (UK5099), glutamine usage (BPTES) and lipid usage (ETOMOXIR) for OXPHOS in FLT3 ITD-JMD and FLT3 ITD-TKD in absence and presence of 100nM midostaurin treatment for 24h. (C) Bar plot reporting the percentage of viable cells measured by MTT assay. FLT3 ITD-JMD and FLT3 ITD-TKD were treated with 100nm of midostaurin treatment for 24h either alone or combined with glucose, amino acid and lipid deprivation. (D) Representative immunofluorescence images of FLT3 localization before and after lipid deprivation in both permeabilized and non-permealized FLT3 ITD-JMD and FLT3 ITD-TKD . (E) Barplots showing the percentage of treatment-induced apoptosis (100 * (dead cells after treatment – death cells in control) / viable cells in control) in patient-derived blasts carrying FLT3-ITD in i) the JM domain, ii) both the JM and TK domain and iii) the TK domain upon the indicated treatments. Percentage of apoptotic cells was assessed by Annexin-V labeling.

    Journal: bioRxiv

    Article Title: Organelle proteomics reveals novel metabolic vulnerabilities in FLT3-ITD cells

    doi: 10.64898/2026.01.19.700272

    Figure Lengend Snippet: (A) Heatmap reporting the number of translocating proteins involved in carbohydrate, amino acids, peroxisome and lipid metabolism in FLT3 ITD-JMD and FLT3 ITD-TKD . (B) Bar plot reporting the ΔOCR of basal respiration after the inhibition of glucose usage (UK5099), glutamine usage (BPTES) and lipid usage (ETOMOXIR) for OXPHOS in FLT3 ITD-JMD and FLT3 ITD-TKD in absence and presence of 100nM midostaurin treatment for 24h. (C) Bar plot reporting the percentage of viable cells measured by MTT assay. FLT3 ITD-JMD and FLT3 ITD-TKD were treated with 100nm of midostaurin treatment for 24h either alone or combined with glucose, amino acid and lipid deprivation. (D) Representative immunofluorescence images of FLT3 localization before and after lipid deprivation in both permeabilized and non-permealized FLT3 ITD-JMD and FLT3 ITD-TKD . (E) Barplots showing the percentage of treatment-induced apoptosis (100 * (dead cells after treatment – death cells in control) / viable cells in control) in patient-derived blasts carrying FLT3-ITD in i) the JM domain, ii) both the JM and TK domain and iii) the TK domain upon the indicated treatments. Percentage of apoptotic cells was assessed by Annexin-V labeling.

    Article Snippet: Midostaurin (Selleck chemical, S8064) was used at 100 nM for 24 hours.

    Techniques: Inhibition, MTT Assay, Immunofluorescence, Control, Derivative Assay, Labeling