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dabrafenib  (MedChemExpress)


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    MedChemExpress dabrafenib
    (A) Diagram of the experimental approach. Cultured BT-40 cells are treated with either of the drugs at day 0 for 24h, followed by a wash-out period of 6 days in the absence of drug, and analysed at day 7 both molecularly (RNA-seq) and by immunocytochemistry. (B) SA-β-Gal staining indicating the increase of blue-stained cells after drug treatment compared with vehicle-treated control. Kruskal-Wallis test, Dunn’s post-test; *: p<0.05, **: p<0.01. (C) p21 Cip1 immunostaining showing the accumulation of nuclear fluorescence signal in the drug-treated cells compare with vehicle controls. (D) Volcano plot of differentially expressed genes comparing proliferative and drug-treated BT-40 cells. Thresholds used: p-values < 0.05 and log2 FoldChange > 1. (E) Normalized enrichment scores (NES) from GSEA showing decreased proliferation-associated genesets and increased senescence and SASP-related genesets for each of the treatment <t>(Dabrafenib,</t> Trametinib and Vinblastine) compared with vehicle control cells. The crossed dots represent the NES integrating the three treated conditions versus the vehicle control. (F) Immunofluorescence staining of IL1B and CCL2 (red) at day 7 in vehicle-treated and drug-treated BT-40 cultured cells. DAPI in blue. Scale bars: 100 μm. (G) Heat maps showing the relative expression of selected SASP factors in vehicle-treated and drug-treated BT-40 cells. Note that there are specific differences between treatments. IL: Interleukin, GF: Growth factors, Pt ases : matrix proteases. n=6 biological replicates for vehicle-treated BT-40, n=3 biological replicates for dabrafenib, trametinib and vinblastine-treated BT-40.
    Dabrafenib, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 42 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/dabrafenib/product/MedChemExpress
    Average 94 stars, based on 42 article reviews
    dabrafenib - by Bioz Stars, 2026-02
    94/100 stars

    Images

    1) Product Images from "Standard treatment against paediatric BRAF-V600E glioma promotes senescence and sensitizes tumours to BCL-xL inhibition"

    Article Title: Standard treatment against paediatric BRAF-V600E glioma promotes senescence and sensitizes tumours to BCL-xL inhibition

    Journal: bioRxiv

    doi: 10.64898/2026.01.13.698644

    (A) Diagram of the experimental approach. Cultured BT-40 cells are treated with either of the drugs at day 0 for 24h, followed by a wash-out period of 6 days in the absence of drug, and analysed at day 7 both molecularly (RNA-seq) and by immunocytochemistry. (B) SA-β-Gal staining indicating the increase of blue-stained cells after drug treatment compared with vehicle-treated control. Kruskal-Wallis test, Dunn’s post-test; *: p<0.05, **: p<0.01. (C) p21 Cip1 immunostaining showing the accumulation of nuclear fluorescence signal in the drug-treated cells compare with vehicle controls. (D) Volcano plot of differentially expressed genes comparing proliferative and drug-treated BT-40 cells. Thresholds used: p-values < 0.05 and log2 FoldChange > 1. (E) Normalized enrichment scores (NES) from GSEA showing decreased proliferation-associated genesets and increased senescence and SASP-related genesets for each of the treatment (Dabrafenib, Trametinib and Vinblastine) compared with vehicle control cells. The crossed dots represent the NES integrating the three treated conditions versus the vehicle control. (F) Immunofluorescence staining of IL1B and CCL2 (red) at day 7 in vehicle-treated and drug-treated BT-40 cultured cells. DAPI in blue. Scale bars: 100 μm. (G) Heat maps showing the relative expression of selected SASP factors in vehicle-treated and drug-treated BT-40 cells. Note that there are specific differences between treatments. IL: Interleukin, GF: Growth factors, Pt ases : matrix proteases. n=6 biological replicates for vehicle-treated BT-40, n=3 biological replicates for dabrafenib, trametinib and vinblastine-treated BT-40.
    Figure Legend Snippet: (A) Diagram of the experimental approach. Cultured BT-40 cells are treated with either of the drugs at day 0 for 24h, followed by a wash-out period of 6 days in the absence of drug, and analysed at day 7 both molecularly (RNA-seq) and by immunocytochemistry. (B) SA-β-Gal staining indicating the increase of blue-stained cells after drug treatment compared with vehicle-treated control. Kruskal-Wallis test, Dunn’s post-test; *: p<0.05, **: p<0.01. (C) p21 Cip1 immunostaining showing the accumulation of nuclear fluorescence signal in the drug-treated cells compare with vehicle controls. (D) Volcano plot of differentially expressed genes comparing proliferative and drug-treated BT-40 cells. Thresholds used: p-values < 0.05 and log2 FoldChange > 1. (E) Normalized enrichment scores (NES) from GSEA showing decreased proliferation-associated genesets and increased senescence and SASP-related genesets for each of the treatment (Dabrafenib, Trametinib and Vinblastine) compared with vehicle control cells. The crossed dots represent the NES integrating the three treated conditions versus the vehicle control. (F) Immunofluorescence staining of IL1B and CCL2 (red) at day 7 in vehicle-treated and drug-treated BT-40 cultured cells. DAPI in blue. Scale bars: 100 μm. (G) Heat maps showing the relative expression of selected SASP factors in vehicle-treated and drug-treated BT-40 cells. Note that there are specific differences between treatments. IL: Interleukin, GF: Growth factors, Pt ases : matrix proteases. n=6 biological replicates for vehicle-treated BT-40, n=3 biological replicates for dabrafenib, trametinib and vinblastine-treated BT-40.

    Techniques Used: Cell Culture, RNA Sequencing, Immunocytochemistry, Staining, Control, Immunostaining, Fluorescence, Immunofluorescence, Expressing

    (A) Schematic of the experimental design. Drug treatment is carried out for one day, followed by a wash-out period of 6 days in the absence of drug. At day 7, control proliferative and treatment-induced BT-40 cells are cultured in the presence of senolytics for 3 days. (B) Heatmap showing the drug sensitivity score (DSS) of several inhibitors of the Bcl-2 family of anti-apoptotic proteins and known senolytics used on cells pre-treated with vehicle, Dabrafenib, Trametinib or Vinblastine. Note that the highest DDSs are observed with Navitoclax, A-1155463, A-1331852 and Obatoclax, which all inhibit Bcl-xL, while the weak Bcl-xL inhibitor, but strong Bcl-2 inhibitor Venetoclax or the senolytics (Piperlongumine and Digoxin) show lower DSSs. (C) Dose response curves of Navitoclax on BT-40 cells pre-treated with either Dabrafenib, Trametinib, Vinblastine or vehicle control. Note that the IC50 values are lower in treatment-induced senescent cells than in proliferative BT-40 cells. (D) Navitoclax sensitivity (top: Selt_BT308.UP) and resistance (Marczyk_Navitoclax resistance) scores inferred from ssGSEA analysis of RNA sequencing data of drug-treated and vehicle controls. (E) Graph showing Caspase 3/7 enzymatic activity of treatment-induced senescent or proliferative, vehicle control BT-40 cells and cultured in the presence of 0.1uM or 1mM Navitoclax as shown in (A). Note the significant increase in senescent cells relative to proliferative control cells. AU Normalized activity by cell numbers. Kruskal-Wallis test, Dunn’s post-test; ***: p<0.001.
    Figure Legend Snippet: (A) Schematic of the experimental design. Drug treatment is carried out for one day, followed by a wash-out period of 6 days in the absence of drug. At day 7, control proliferative and treatment-induced BT-40 cells are cultured in the presence of senolytics for 3 days. (B) Heatmap showing the drug sensitivity score (DSS) of several inhibitors of the Bcl-2 family of anti-apoptotic proteins and known senolytics used on cells pre-treated with vehicle, Dabrafenib, Trametinib or Vinblastine. Note that the highest DDSs are observed with Navitoclax, A-1155463, A-1331852 and Obatoclax, which all inhibit Bcl-xL, while the weak Bcl-xL inhibitor, but strong Bcl-2 inhibitor Venetoclax or the senolytics (Piperlongumine and Digoxin) show lower DSSs. (C) Dose response curves of Navitoclax on BT-40 cells pre-treated with either Dabrafenib, Trametinib, Vinblastine or vehicle control. Note that the IC50 values are lower in treatment-induced senescent cells than in proliferative BT-40 cells. (D) Navitoclax sensitivity (top: Selt_BT308.UP) and resistance (Marczyk_Navitoclax resistance) scores inferred from ssGSEA analysis of RNA sequencing data of drug-treated and vehicle controls. (E) Graph showing Caspase 3/7 enzymatic activity of treatment-induced senescent or proliferative, vehicle control BT-40 cells and cultured in the presence of 0.1uM or 1mM Navitoclax as shown in (A). Note the significant increase in senescent cells relative to proliferative control cells. AU Normalized activity by cell numbers. Kruskal-Wallis test, Dunn’s post-test; ***: p<0.001.

    Techniques Used: Control, Cell Culture, RNA Sequencing, Activity Assay



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    (A) Diagram of the experimental approach. Cultured BT-40 cells are treated with either of the drugs at day 0 for 24h, followed by a wash-out period of 6 days in the absence of drug, and analysed at day 7 both molecularly (RNA-seq) and by immunocytochemistry. (B) SA-β-Gal staining indicating the increase of blue-stained cells after drug treatment compared with vehicle-treated control. Kruskal-Wallis test, Dunn’s post-test; *: p<0.05, **: p<0.01. (C) p21 Cip1 immunostaining showing the accumulation of nuclear fluorescence signal in the drug-treated cells compare with vehicle controls. (D) Volcano plot of differentially expressed genes comparing proliferative and drug-treated BT-40 cells. Thresholds used: p-values < 0.05 and log2 FoldChange > 1. (E) Normalized enrichment scores (NES) from GSEA showing decreased proliferation-associated genesets and increased senescence and SASP-related genesets for each of the treatment <t>(Dabrafenib,</t> Trametinib and Vinblastine) compared with vehicle control cells. The crossed dots represent the NES integrating the three treated conditions versus the vehicle control. (F) Immunofluorescence staining of IL1B and CCL2 (red) at day 7 in vehicle-treated and drug-treated BT-40 cultured cells. DAPI in blue. Scale bars: 100 μm. (G) Heat maps showing the relative expression of selected SASP factors in vehicle-treated and drug-treated BT-40 cells. Note that there are specific differences between treatments. IL: Interleukin, GF: Growth factors, Pt ases : matrix proteases. n=6 biological replicates for vehicle-treated BT-40, n=3 biological replicates for dabrafenib, trametinib and vinblastine-treated BT-40.
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    (A) Diagram of the experimental approach. Cultured BT-40 cells are treated with either of the drugs at day 0 for 24h, followed by a wash-out period of 6 days in the absence of drug, and analysed at day 7 both molecularly (RNA-seq) and by immunocytochemistry. (B) SA-β-Gal staining indicating the increase of blue-stained cells after drug treatment compared with vehicle-treated control. Kruskal-Wallis test, Dunn’s post-test; *: p<0.05, **: p<0.01. (C) p21 Cip1 immunostaining showing the accumulation of nuclear fluorescence signal in the drug-treated cells compare with vehicle controls. (D) Volcano plot of differentially expressed genes comparing proliferative and drug-treated BT-40 cells. Thresholds used: p-values < 0.05 and log2 FoldChange > 1. (E) Normalized enrichment scores (NES) from GSEA showing decreased proliferation-associated genesets and increased senescence and SASP-related genesets for each of the treatment <t>(Dabrafenib,</t> Trametinib and Vinblastine) compared with vehicle control cells. The crossed dots represent the NES integrating the three treated conditions versus the vehicle control. (F) Immunofluorescence staining of IL1B and CCL2 (red) at day 7 in vehicle-treated and drug-treated BT-40 cultured cells. DAPI in blue. Scale bars: 100 μm. (G) Heat maps showing the relative expression of selected SASP factors in vehicle-treated and drug-treated BT-40 cells. Note that there are specific differences between treatments. IL: Interleukin, GF: Growth factors, Pt ases : matrix proteases. n=6 biological replicates for vehicle-treated BT-40, n=3 biological replicates for dabrafenib, trametinib and vinblastine-treated BT-40.
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    Image Search Results


    (A) Diagram of the experimental approach. Cultured BT-40 cells are treated with either of the drugs at day 0 for 24h, followed by a wash-out period of 6 days in the absence of drug, and analysed at day 7 both molecularly (RNA-seq) and by immunocytochemistry. (B) SA-β-Gal staining indicating the increase of blue-stained cells after drug treatment compared with vehicle-treated control. Kruskal-Wallis test, Dunn’s post-test; *: p<0.05, **: p<0.01. (C) p21 Cip1 immunostaining showing the accumulation of nuclear fluorescence signal in the drug-treated cells compare with vehicle controls. (D) Volcano plot of differentially expressed genes comparing proliferative and drug-treated BT-40 cells. Thresholds used: p-values < 0.05 and log2 FoldChange > 1. (E) Normalized enrichment scores (NES) from GSEA showing decreased proliferation-associated genesets and increased senescence and SASP-related genesets for each of the treatment (Dabrafenib, Trametinib and Vinblastine) compared with vehicle control cells. The crossed dots represent the NES integrating the three treated conditions versus the vehicle control. (F) Immunofluorescence staining of IL1B and CCL2 (red) at day 7 in vehicle-treated and drug-treated BT-40 cultured cells. DAPI in blue. Scale bars: 100 μm. (G) Heat maps showing the relative expression of selected SASP factors in vehicle-treated and drug-treated BT-40 cells. Note that there are specific differences between treatments. IL: Interleukin, GF: Growth factors, Pt ases : matrix proteases. n=6 biological replicates for vehicle-treated BT-40, n=3 biological replicates for dabrafenib, trametinib and vinblastine-treated BT-40.

    Journal: bioRxiv

    Article Title: Standard treatment against paediatric BRAF-V600E glioma promotes senescence and sensitizes tumours to BCL-xL inhibition

    doi: 10.64898/2026.01.13.698644

    Figure Lengend Snippet: (A) Diagram of the experimental approach. Cultured BT-40 cells are treated with either of the drugs at day 0 for 24h, followed by a wash-out period of 6 days in the absence of drug, and analysed at day 7 both molecularly (RNA-seq) and by immunocytochemistry. (B) SA-β-Gal staining indicating the increase of blue-stained cells after drug treatment compared with vehicle-treated control. Kruskal-Wallis test, Dunn’s post-test; *: p<0.05, **: p<0.01. (C) p21 Cip1 immunostaining showing the accumulation of nuclear fluorescence signal in the drug-treated cells compare with vehicle controls. (D) Volcano plot of differentially expressed genes comparing proliferative and drug-treated BT-40 cells. Thresholds used: p-values < 0.05 and log2 FoldChange > 1. (E) Normalized enrichment scores (NES) from GSEA showing decreased proliferation-associated genesets and increased senescence and SASP-related genesets for each of the treatment (Dabrafenib, Trametinib and Vinblastine) compared with vehicle control cells. The crossed dots represent the NES integrating the three treated conditions versus the vehicle control. (F) Immunofluorescence staining of IL1B and CCL2 (red) at day 7 in vehicle-treated and drug-treated BT-40 cultured cells. DAPI in blue. Scale bars: 100 μm. (G) Heat maps showing the relative expression of selected SASP factors in vehicle-treated and drug-treated BT-40 cells. Note that there are specific differences between treatments. IL: Interleukin, GF: Growth factors, Pt ases : matrix proteases. n=6 biological replicates for vehicle-treated BT-40, n=3 biological replicates for dabrafenib, trametinib and vinblastine-treated BT-40.

    Article Snippet: DMSO (Santa Cruz Biotechnology [SCB]) was used as vehicle control; Dabrafenib (MedChemExpress [MCE] - HY-14660), Trametinib (ApexBio - A3018), Vinblastine (SCB - sc-491749), Navitoclax (ABT-262; ApexBio - A3007), A-1155463 (MCE - HY-19725), A-1331852 (MCE - HY-19741), Obatoclax (MCE - HY-10969), Venetoclax (ABT-199; ApexBio - A8194), Piperlongumine (ApexBio - A4455), Digoxin (ApexBio - B7684).

    Techniques: Cell Culture, RNA Sequencing, Immunocytochemistry, Staining, Control, Immunostaining, Fluorescence, Immunofluorescence, Expressing

    (A) Schematic of the experimental design. Drug treatment is carried out for one day, followed by a wash-out period of 6 days in the absence of drug. At day 7, control proliferative and treatment-induced BT-40 cells are cultured in the presence of senolytics for 3 days. (B) Heatmap showing the drug sensitivity score (DSS) of several inhibitors of the Bcl-2 family of anti-apoptotic proteins and known senolytics used on cells pre-treated with vehicle, Dabrafenib, Trametinib or Vinblastine. Note that the highest DDSs are observed with Navitoclax, A-1155463, A-1331852 and Obatoclax, which all inhibit Bcl-xL, while the weak Bcl-xL inhibitor, but strong Bcl-2 inhibitor Venetoclax or the senolytics (Piperlongumine and Digoxin) show lower DSSs. (C) Dose response curves of Navitoclax on BT-40 cells pre-treated with either Dabrafenib, Trametinib, Vinblastine or vehicle control. Note that the IC50 values are lower in treatment-induced senescent cells than in proliferative BT-40 cells. (D) Navitoclax sensitivity (top: Selt_BT308.UP) and resistance (Marczyk_Navitoclax resistance) scores inferred from ssGSEA analysis of RNA sequencing data of drug-treated and vehicle controls. (E) Graph showing Caspase 3/7 enzymatic activity of treatment-induced senescent or proliferative, vehicle control BT-40 cells and cultured in the presence of 0.1uM or 1mM Navitoclax as shown in (A). Note the significant increase in senescent cells relative to proliferative control cells. AU Normalized activity by cell numbers. Kruskal-Wallis test, Dunn’s post-test; ***: p<0.001.

    Journal: bioRxiv

    Article Title: Standard treatment against paediatric BRAF-V600E glioma promotes senescence and sensitizes tumours to BCL-xL inhibition

    doi: 10.64898/2026.01.13.698644

    Figure Lengend Snippet: (A) Schematic of the experimental design. Drug treatment is carried out for one day, followed by a wash-out period of 6 days in the absence of drug. At day 7, control proliferative and treatment-induced BT-40 cells are cultured in the presence of senolytics for 3 days. (B) Heatmap showing the drug sensitivity score (DSS) of several inhibitors of the Bcl-2 family of anti-apoptotic proteins and known senolytics used on cells pre-treated with vehicle, Dabrafenib, Trametinib or Vinblastine. Note that the highest DDSs are observed with Navitoclax, A-1155463, A-1331852 and Obatoclax, which all inhibit Bcl-xL, while the weak Bcl-xL inhibitor, but strong Bcl-2 inhibitor Venetoclax or the senolytics (Piperlongumine and Digoxin) show lower DSSs. (C) Dose response curves of Navitoclax on BT-40 cells pre-treated with either Dabrafenib, Trametinib, Vinblastine or vehicle control. Note that the IC50 values are lower in treatment-induced senescent cells than in proliferative BT-40 cells. (D) Navitoclax sensitivity (top: Selt_BT308.UP) and resistance (Marczyk_Navitoclax resistance) scores inferred from ssGSEA analysis of RNA sequencing data of drug-treated and vehicle controls. (E) Graph showing Caspase 3/7 enzymatic activity of treatment-induced senescent or proliferative, vehicle control BT-40 cells and cultured in the presence of 0.1uM or 1mM Navitoclax as shown in (A). Note the significant increase in senescent cells relative to proliferative control cells. AU Normalized activity by cell numbers. Kruskal-Wallis test, Dunn’s post-test; ***: p<0.001.

    Article Snippet: DMSO (Santa Cruz Biotechnology [SCB]) was used as vehicle control; Dabrafenib (MedChemExpress [MCE] - HY-14660), Trametinib (ApexBio - A3018), Vinblastine (SCB - sc-491749), Navitoclax (ABT-262; ApexBio - A3007), A-1155463 (MCE - HY-19725), A-1331852 (MCE - HY-19741), Obatoclax (MCE - HY-10969), Venetoclax (ABT-199; ApexBio - A8194), Piperlongumine (ApexBio - A4455), Digoxin (ApexBio - B7684).

    Techniques: Control, Cell Culture, RNA Sequencing, Activity Assay