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glesatinib  (MedChemExpress)


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    MedChemExpress glesatinib
    High-throughput screening of a small molecule library revealed inhibitors of S. rosetta cell proliferation. (A) Treatment of S. rosetta cultures with 1255 different small molecules (see Table S1, ESI ) resulted in a distribution of cell counts, assessed by flow cytometry, at the 24-hour endpoint. S. rosetta cell counts were normalized to the average of DMSO controls within the same plate (dark grey). Compounds determined to significantly inhibit S. rosetta cell proliferation by flow cytometry (based on two-tailed p -value <0.05 calculated from z -score), fall below the dotted line and are indicated in red. Compounds that were not detected as significant inhibitors by flow cytometry but were identified by imaging (based on two-tailed p -value <0.05 calculated from z -score) are in blue. Compounds that were not significant inhibitors for either screen are indicated in light grey. Sorafenib (SO), a focus of this study, is labeled. (B) The range of normalized cell counts measured by flow cytometry for compounds that significantly inhibited S. rosetta cell proliferation. Compounds that were the focus of further study – genistein (GE), <t>glesatinib</t> (GL), PP121, masitinib (MA), sotrastaurin (SOT) – are labeled. (C) Comparison of normalized values of compounds that inhibited S. rosetta cell proliferation, assessed by flow cytometry and the corresponding normalized values determined by imaging. Compounds determined to significantly inhibit S. rosetta cell proliferation (based on two-tailed p -value <0.05 calculated from z -score) by flow cytometry fall below the dotted line on the y -axis and by imaging, to the left of the dotted line on the x -axis.
    Glesatinib, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 3 article reviews
    glesatinib - by Bioz Stars, 2026-09
    93/100 stars

    Images

    1) Product Images from "A stress-responsive p38 signaling axis in choanoflagellates † "

    Article Title: A stress-responsive p38 signaling axis in choanoflagellates †

    Journal: RSC Chemical Biology

    doi: 10.1039/d4cb00122b

    High-throughput screening of a small molecule library revealed inhibitors of S. rosetta cell proliferation. (A) Treatment of S. rosetta cultures with 1255 different small molecules (see Table S1, ESI ) resulted in a distribution of cell counts, assessed by flow cytometry, at the 24-hour endpoint. S. rosetta cell counts were normalized to the average of DMSO controls within the same plate (dark grey). Compounds determined to significantly inhibit S. rosetta cell proliferation by flow cytometry (based on two-tailed p -value <0.05 calculated from z -score), fall below the dotted line and are indicated in red. Compounds that were not detected as significant inhibitors by flow cytometry but were identified by imaging (based on two-tailed p -value <0.05 calculated from z -score) are in blue. Compounds that were not significant inhibitors for either screen are indicated in light grey. Sorafenib (SO), a focus of this study, is labeled. (B) The range of normalized cell counts measured by flow cytometry for compounds that significantly inhibited S. rosetta cell proliferation. Compounds that were the focus of further study – genistein (GE), glesatinib (GL), PP121, masitinib (MA), sotrastaurin (SOT) – are labeled. (C) Comparison of normalized values of compounds that inhibited S. rosetta cell proliferation, assessed by flow cytometry and the corresponding normalized values determined by imaging. Compounds determined to significantly inhibit S. rosetta cell proliferation (based on two-tailed p -value <0.05 calculated from z -score) by flow cytometry fall below the dotted line on the y -axis and by imaging, to the left of the dotted line on the x -axis.
    Figure Legend Snippet: High-throughput screening of a small molecule library revealed inhibitors of S. rosetta cell proliferation. (A) Treatment of S. rosetta cultures with 1255 different small molecules (see Table S1, ESI ) resulted in a distribution of cell counts, assessed by flow cytometry, at the 24-hour endpoint. S. rosetta cell counts were normalized to the average of DMSO controls within the same plate (dark grey). Compounds determined to significantly inhibit S. rosetta cell proliferation by flow cytometry (based on two-tailed p -value <0.05 calculated from z -score), fall below the dotted line and are indicated in red. Compounds that were not detected as significant inhibitors by flow cytometry but were identified by imaging (based on two-tailed p -value <0.05 calculated from z -score) are in blue. Compounds that were not significant inhibitors for either screen are indicated in light grey. Sorafenib (SO), a focus of this study, is labeled. (B) The range of normalized cell counts measured by flow cytometry for compounds that significantly inhibited S. rosetta cell proliferation. Compounds that were the focus of further study – genistein (GE), glesatinib (GL), PP121, masitinib (MA), sotrastaurin (SOT) – are labeled. (C) Comparison of normalized values of compounds that inhibited S. rosetta cell proliferation, assessed by flow cytometry and the corresponding normalized values determined by imaging. Compounds determined to significantly inhibit S. rosetta cell proliferation (based on two-tailed p -value <0.05 calculated from z -score) by flow cytometry fall below the dotted line on the y -axis and by imaging, to the left of the dotted line on the x -axis.

    Techniques Used: High Throughput Screening Assay, Flow Cytometry, Two Tailed Test, Imaging, Labeling, Comparison

    Glesatinib and sorafenib, two multi-target tyrosine kinase inhibitors, disrupt S. rosetta cell proliferation and tyrosine phosphosignaling. (A) Treatment of S. rosetta cultures with 1 μM sorafenib and glesatinib led to a complete block of cell proliferation, while treatment with 1 μM masitinib or PP121 led to a partial reduction in cell proliferation relative to DMSO-treated cultures. Two biological replicates were conducted per treatment, and each point represents the mean of three measurements from each biological replicate. For timepoints at 40, 60, and 85 hours, cell densities of inhibitor-treated cultures were significantly different from vehicle (DMSO) ( p -value <0.01). Significance was determined by a two-way ANOVA multiple comparisons test. (B) S. rosetta cultures treated with 1 μM or 10 μM sorafenib, glesatinib, or PP121 for 24 hours had reduced normalized cell density, whereas masitinib only had reduced normalized cell density at 10 μM. Normalized cell densities were determined to be reduced if differences between treatments and vehicle (DMSO) were significant ( p -value <0.01) Significance was determined by determined by a two-way ANOVA multiple comparisons test. Movies show S. rosetta cells treated with 10 μM glesatinib that undergo cell lysis (Movie S1, ESI ) and sorafenib, that have cell body deformation (Movies S2 and S3, ESI ), in comparison to DMSO control (Movie S4, ESI ). (C) Western blot analysis of S. rosetta cultures treated with 1 μM sorafenib and glesatinib for 1 hour showed a decrease in tyrosine phosphorylation of proteins at ∼60 kDa, ∼45 kDa, and ∼35 kDa (indicated by arrows and detected with pY1000 anti-phosphotyrosine antibody) compared to vehicle (DMSO) control. Masitinib and PP121 did not reduce the phosphotyrosine signal.
    Figure Legend Snippet: Glesatinib and sorafenib, two multi-target tyrosine kinase inhibitors, disrupt S. rosetta cell proliferation and tyrosine phosphosignaling. (A) Treatment of S. rosetta cultures with 1 μM sorafenib and glesatinib led to a complete block of cell proliferation, while treatment with 1 μM masitinib or PP121 led to a partial reduction in cell proliferation relative to DMSO-treated cultures. Two biological replicates were conducted per treatment, and each point represents the mean of three measurements from each biological replicate. For timepoints at 40, 60, and 85 hours, cell densities of inhibitor-treated cultures were significantly different from vehicle (DMSO) ( p -value <0.01). Significance was determined by a two-way ANOVA multiple comparisons test. (B) S. rosetta cultures treated with 1 μM or 10 μM sorafenib, glesatinib, or PP121 for 24 hours had reduced normalized cell density, whereas masitinib only had reduced normalized cell density at 10 μM. Normalized cell densities were determined to be reduced if differences between treatments and vehicle (DMSO) were significant ( p -value <0.01) Significance was determined by determined by a two-way ANOVA multiple comparisons test. Movies show S. rosetta cells treated with 10 μM glesatinib that undergo cell lysis (Movie S1, ESI ) and sorafenib, that have cell body deformation (Movies S2 and S3, ESI ), in comparison to DMSO control (Movie S4, ESI ). (C) Western blot analysis of S. rosetta cultures treated with 1 μM sorafenib and glesatinib for 1 hour showed a decrease in tyrosine phosphorylation of proteins at ∼60 kDa, ∼45 kDa, and ∼35 kDa (indicated by arrows and detected with pY1000 anti-phosphotyrosine antibody) compared to vehicle (DMSO) control. Masitinib and PP121 did not reduce the phosphotyrosine signal.

    Techniques Used: Blocking Assay, Lysis, Comparison, Control, Western Blot, Phospho-proteomics

    Related Articles

    High Throughput Screening Assay:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Flow Cytometry:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Two Tailed Test:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Imaging:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Labeling:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Comparison:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Blocking Assay:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Lysis:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Control:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Western Blot:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Phospho-proteomics:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Microarray:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Recombinant:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Purification:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Membrane:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    SYBR Green Assay:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Viability Assay:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Kinase Assay:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Reverse Transcription:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Transcription Factor Assay:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Enzyme-linked Immunosorbent Assay:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Multiplex Assay:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Extraction:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Isolation:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    shRNA:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Sequencing:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Plasmid Preparation:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.

    Software:

    Article Title: EGFR-phosphorylated GDH1 harmonizes with RSK2 to drive CREB activation and tumor metastasis in EGFR-activated lung cancer
    Article Snippet: Glesatinib , MedChemExpress , Cat#HY-19642; CAS: 936694-12-1.



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    92
    Selleck Chemicals glesatinib
    High-throughput screening of a small molecule library revealed inhibitors of S. rosetta cell proliferation. (A) Treatment of S. rosetta cultures with 1255 different small molecules (see Table S1, ESI ) resulted in a distribution of cell counts, assessed by flow cytometry, at the 24-hour endpoint. S. rosetta cell counts were normalized to the average of DMSO controls within the same plate (dark grey). Compounds determined to significantly inhibit S. rosetta cell proliferation by flow cytometry (based on two-tailed p -value <0.05 calculated from z -score), fall below the dotted line and are indicated in red. Compounds that were not detected as significant inhibitors by flow cytometry but were identified by imaging (based on two-tailed p -value <0.05 calculated from z -score) are in blue. Compounds that were not significant inhibitors for either screen are indicated in light grey. Sorafenib (SO), a focus of this study, is labeled. (B) The range of normalized cell counts measured by flow cytometry for compounds that significantly inhibited S. rosetta cell proliferation. Compounds that were the focus of further study – genistein (GE), <t>glesatinib</t> (GL), PP121, masitinib (MA), sotrastaurin (SOT) – are labeled. (C) Comparison of normalized values of compounds that inhibited S. rosetta cell proliferation, assessed by flow cytometry and the corresponding normalized values determined by imaging. Compounds determined to significantly inhibit S. rosetta cell proliferation (based on two-tailed p -value <0.05 calculated from z -score) by flow cytometry fall below the dotted line on the y -axis and by imaging, to the left of the dotted line on the x -axis.
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    High-throughput screening of a small molecule library revealed inhibitors of S. rosetta cell proliferation. (A) Treatment of S. rosetta cultures with 1255 different small molecules (see Table S1, ESI ) resulted in a distribution of cell counts, assessed by flow cytometry, at the 24-hour endpoint. S. rosetta cell counts were normalized to the average of DMSO controls within the same plate (dark grey). Compounds determined to significantly inhibit S. rosetta cell proliferation by flow cytometry (based on two-tailed p -value <0.05 calculated from z -score), fall below the dotted line and are indicated in red. Compounds that were not detected as significant inhibitors by flow cytometry but were identified by imaging (based on two-tailed p -value <0.05 calculated from z -score) are in blue. Compounds that were not significant inhibitors for either screen are indicated in light grey. Sorafenib (SO), a focus of this study, is labeled. (B) The range of normalized cell counts measured by flow cytometry for compounds that significantly inhibited S. rosetta cell proliferation. Compounds that were the focus of further study – genistein (GE), glesatinib (GL), PP121, masitinib (MA), sotrastaurin (SOT) – are labeled. (C) Comparison of normalized values of compounds that inhibited S. rosetta cell proliferation, assessed by flow cytometry and the corresponding normalized values determined by imaging. Compounds determined to significantly inhibit S. rosetta cell proliferation (based on two-tailed p -value <0.05 calculated from z -score) by flow cytometry fall below the dotted line on the y -axis and by imaging, to the left of the dotted line on the x -axis.

    Journal: RSC Chemical Biology

    Article Title: A stress-responsive p38 signaling axis in choanoflagellates †

    doi: 10.1039/d4cb00122b

    Figure Lengend Snippet: High-throughput screening of a small molecule library revealed inhibitors of S. rosetta cell proliferation. (A) Treatment of S. rosetta cultures with 1255 different small molecules (see Table S1, ESI ) resulted in a distribution of cell counts, assessed by flow cytometry, at the 24-hour endpoint. S. rosetta cell counts were normalized to the average of DMSO controls within the same plate (dark grey). Compounds determined to significantly inhibit S. rosetta cell proliferation by flow cytometry (based on two-tailed p -value <0.05 calculated from z -score), fall below the dotted line and are indicated in red. Compounds that were not detected as significant inhibitors by flow cytometry but were identified by imaging (based on two-tailed p -value <0.05 calculated from z -score) are in blue. Compounds that were not significant inhibitors for either screen are indicated in light grey. Sorafenib (SO), a focus of this study, is labeled. (B) The range of normalized cell counts measured by flow cytometry for compounds that significantly inhibited S. rosetta cell proliferation. Compounds that were the focus of further study – genistein (GE), glesatinib (GL), PP121, masitinib (MA), sotrastaurin (SOT) – are labeled. (C) Comparison of normalized values of compounds that inhibited S. rosetta cell proliferation, assessed by flow cytometry and the corresponding normalized values determined by imaging. Compounds determined to significantly inhibit S. rosetta cell proliferation (based on two-tailed p -value <0.05 calculated from z -score) by flow cytometry fall below the dotted line on the y -axis and by imaging, to the left of the dotted line on the x -axis.

    Article Snippet: Glesatinib (#HY-19642A), masitinib (#HY-10209), lapatinib (#HY-50898), PP121 (#HY-10372), gliteritinib (#HY-12432), brigatinib (#HY-12857), RAF265 (#HY-10248), vemurafenib (#HY12057), skepinone-L (#HY-15300), BIRB 796 (#HY-10320), were purchased from MedChem Express.

    Techniques: High Throughput Screening Assay, Flow Cytometry, Two Tailed Test, Imaging, Labeling, Comparison

    Glesatinib and sorafenib, two multi-target tyrosine kinase inhibitors, disrupt S. rosetta cell proliferation and tyrosine phosphosignaling. (A) Treatment of S. rosetta cultures with 1 μM sorafenib and glesatinib led to a complete block of cell proliferation, while treatment with 1 μM masitinib or PP121 led to a partial reduction in cell proliferation relative to DMSO-treated cultures. Two biological replicates were conducted per treatment, and each point represents the mean of three measurements from each biological replicate. For timepoints at 40, 60, and 85 hours, cell densities of inhibitor-treated cultures were significantly different from vehicle (DMSO) ( p -value <0.01). Significance was determined by a two-way ANOVA multiple comparisons test. (B) S. rosetta cultures treated with 1 μM or 10 μM sorafenib, glesatinib, or PP121 for 24 hours had reduced normalized cell density, whereas masitinib only had reduced normalized cell density at 10 μM. Normalized cell densities were determined to be reduced if differences between treatments and vehicle (DMSO) were significant ( p -value <0.01) Significance was determined by determined by a two-way ANOVA multiple comparisons test. Movies show S. rosetta cells treated with 10 μM glesatinib that undergo cell lysis (Movie S1, ESI ) and sorafenib, that have cell body deformation (Movies S2 and S3, ESI ), in comparison to DMSO control (Movie S4, ESI ). (C) Western blot analysis of S. rosetta cultures treated with 1 μM sorafenib and glesatinib for 1 hour showed a decrease in tyrosine phosphorylation of proteins at ∼60 kDa, ∼45 kDa, and ∼35 kDa (indicated by arrows and detected with pY1000 anti-phosphotyrosine antibody) compared to vehicle (DMSO) control. Masitinib and PP121 did not reduce the phosphotyrosine signal.

    Journal: RSC Chemical Biology

    Article Title: A stress-responsive p38 signaling axis in choanoflagellates †

    doi: 10.1039/d4cb00122b

    Figure Lengend Snippet: Glesatinib and sorafenib, two multi-target tyrosine kinase inhibitors, disrupt S. rosetta cell proliferation and tyrosine phosphosignaling. (A) Treatment of S. rosetta cultures with 1 μM sorafenib and glesatinib led to a complete block of cell proliferation, while treatment with 1 μM masitinib or PP121 led to a partial reduction in cell proliferation relative to DMSO-treated cultures. Two biological replicates were conducted per treatment, and each point represents the mean of three measurements from each biological replicate. For timepoints at 40, 60, and 85 hours, cell densities of inhibitor-treated cultures were significantly different from vehicle (DMSO) ( p -value <0.01). Significance was determined by a two-way ANOVA multiple comparisons test. (B) S. rosetta cultures treated with 1 μM or 10 μM sorafenib, glesatinib, or PP121 for 24 hours had reduced normalized cell density, whereas masitinib only had reduced normalized cell density at 10 μM. Normalized cell densities were determined to be reduced if differences between treatments and vehicle (DMSO) were significant ( p -value <0.01) Significance was determined by determined by a two-way ANOVA multiple comparisons test. Movies show S. rosetta cells treated with 10 μM glesatinib that undergo cell lysis (Movie S1, ESI ) and sorafenib, that have cell body deformation (Movies S2 and S3, ESI ), in comparison to DMSO control (Movie S4, ESI ). (C) Western blot analysis of S. rosetta cultures treated with 1 μM sorafenib and glesatinib for 1 hour showed a decrease in tyrosine phosphorylation of proteins at ∼60 kDa, ∼45 kDa, and ∼35 kDa (indicated by arrows and detected with pY1000 anti-phosphotyrosine antibody) compared to vehicle (DMSO) control. Masitinib and PP121 did not reduce the phosphotyrosine signal.

    Article Snippet: Glesatinib (#HY-19642A), masitinib (#HY-10209), lapatinib (#HY-50898), PP121 (#HY-10372), gliteritinib (#HY-12432), brigatinib (#HY-12857), RAF265 (#HY-10248), vemurafenib (#HY12057), skepinone-L (#HY-15300), BIRB 796 (#HY-10320), were purchased from MedChem Express.

    Techniques: Blocking Assay, Lysis, Comparison, Control, Western Blot, Phospho-proteomics