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selinexor kpt- 330, atg- 010  (Selleck Chemicals)


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    Selleck Chemicals selinexor kpt- 330, atg- 010
    Selinexor Kpt 330, Atg 010, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/selinexor kpt- 330, atg- 010/product/Selleck Chemicals
    Average 90 stars, based on 1 article reviews
    selinexor kpt- 330, atg- 010 - by Bioz Stars, 2026-02
    90/100 stars

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    Selleck Chemicals selinexor kpt-330 atg-010
    Effects of <t>selinexor</t> on the MM cell lines. (A) MM cell lines (U266 and RPMI8226) were cultured in RPMI 1640 medium with the indicated concentration of selinexor for 72 h. Cell viability was evaluated using a cell counting kit‐8. (B) MM cell lines (U266 and RPMI8226) were treated with the indicated concentration of selinexor for 48 h. Caspase 3/7 activity was evaluated. **** p < 0.0001 vs. the control. (C) MM cell lines (U266 and RPMI8226) were treated with the specified concentrations of selinexor for 48 h. The cytotoxicity was subsequently assessed utilizing a Cytotoxicity LDH Assay kit. **** p < 0.0001, compared to control.
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    Selleck Chemicals kpt 330
    Effects of <t>selinexor</t> on the MM cell lines. (A) MM cell lines (U266 and RPMI8226) were cultured in RPMI 1640 medium with the indicated concentration of selinexor for 72 h. Cell viability was evaluated using a cell counting kit‐8. (B) MM cell lines (U266 and RPMI8226) were treated with the indicated concentration of selinexor for 48 h. Caspase 3/7 activity was evaluated. **** p < 0.0001 vs. the control. (C) MM cell lines (U266 and RPMI8226) were treated with the specified concentrations of selinexor for 48 h. The cytotoxicity was subsequently assessed utilizing a Cytotoxicity LDH Assay kit. **** p < 0.0001, compared to control.
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    Effects of <t>selinexor</t> on the MM cell lines. (A) MM cell lines (U266 and RPMI8226) were cultured in RPMI 1640 medium with the indicated concentration of selinexor for 72 h. Cell viability was evaluated using a cell counting kit‐8. (B) MM cell lines (U266 and RPMI8226) were treated with the indicated concentration of selinexor for 48 h. Caspase 3/7 activity was evaluated. **** p < 0.0001 vs. the control. (C) MM cell lines (U266 and RPMI8226) were treated with the specified concentrations of selinexor for 48 h. The cytotoxicity was subsequently assessed utilizing a Cytotoxicity LDH Assay kit. **** p < 0.0001, compared to control.
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    Selleck Chemicals xpo1 inhibitor selinexor kpt 330
    The CDK9 inhibitor AZD4573 and <t>XPO1</t> inhibitor Selinexor are effective as single agents and in combination vs. DLBCL cell lines. ( a ) AZD4375 (red) and Selinexor (white) reduce DLBCL cell line viability. A total of 9 treatments ranging from 20,000 to 78 nM are displayed across 6 cell lines. Results were measured after 96 h using Alamar Blue cell viability reagent. Standard deviation values for each treatment are displayed as error bars for each replicate population. ( b ) AZD4573 and Selinexor ED50 values range between 1nM to 7µM. ( c ) Key gene expression values in available cell lines. Data from Hardee et al. 2013 are displayed. The study performed RNA seq with 8 DLBCL cell lines across 22,156 genes. Z-scores were calculated for relevant genes across all cell lines. Four cell lines from this study matched Z-scores were calculated for relevant genes across all 8 cell lines in the study. ( d ) Combined treatment with AZD4375 and Selinexor results in synergistic losses of cell viability within 6 DLBCL cell lines. Bliss synergy scores were calculated using the Synergy Finder tool. ( e ) Combined treatment of the DHL6 cell line displays synergistic rates of cellular disruption
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    Effects of selinexor on the MM cell lines. (A) MM cell lines (U266 and RPMI8226) were cultured in RPMI 1640 medium with the indicated concentration of selinexor for 72 h. Cell viability was evaluated using a cell counting kit‐8. (B) MM cell lines (U266 and RPMI8226) were treated with the indicated concentration of selinexor for 48 h. Caspase 3/7 activity was evaluated. **** p < 0.0001 vs. the control. (C) MM cell lines (U266 and RPMI8226) were treated with the specified concentrations of selinexor for 48 h. The cytotoxicity was subsequently assessed utilizing a Cytotoxicity LDH Assay kit. **** p < 0.0001, compared to control.

    Journal: Cancer Reports

    Article Title: Therapeutic Potential of Venetoclax and Selinexor in Targeting Hypoxia‐Induced Vulnerabilities in Multiple Myeloma

    doi: 10.1002/cnr2.70249

    Figure Lengend Snippet: Effects of selinexor on the MM cell lines. (A) MM cell lines (U266 and RPMI8226) were cultured in RPMI 1640 medium with the indicated concentration of selinexor for 72 h. Cell viability was evaluated using a cell counting kit‐8. (B) MM cell lines (U266 and RPMI8226) were treated with the indicated concentration of selinexor for 48 h. Caspase 3/7 activity was evaluated. **** p < 0.0001 vs. the control. (C) MM cell lines (U266 and RPMI8226) were treated with the specified concentrations of selinexor for 48 h. The cytotoxicity was subsequently assessed utilizing a Cytotoxicity LDH Assay kit. **** p < 0.0001, compared to control.

    Article Snippet: Selinexor (KPT‐330, ATG‐010), an XPO1 inhibitor, and venetoclax (ABT‐199, GDC‐0199), a BCL2 inhibitor, were obtained from Selleck Chemicals (Houston, TX, USA).

    Techniques: Cell Culture, Concentration Assay, Cell Counting, Activity Assay, Control, Lactate Dehydrogenase Assay

    The activity of selinexor and venetoclax on the MM cell lines. (A‐D) U266 and RPMI 8226 cells were cultured with selinexor and/or venetoclax for 48 or 72 h. (A) Cell viability, (B) caspase 3/7 activity, (C) cytotoxicity, and (D) apoptosis were evaluated. Significance was expressed as * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns: Not significant vs. the control. (E) U266 and RPMI 8226 cells were treated with selinexor and/or venetoclax for 48 h. The MMP was analyzed using a JC‐1 MitoMP Detection Kit. Significance is expressed as * p < 0.05, ** p < 0.01, and ns: Not significant vs. the control.

    Journal: Cancer Reports

    Article Title: Therapeutic Potential of Venetoclax and Selinexor in Targeting Hypoxia‐Induced Vulnerabilities in Multiple Myeloma

    doi: 10.1002/cnr2.70249

    Figure Lengend Snippet: The activity of selinexor and venetoclax on the MM cell lines. (A‐D) U266 and RPMI 8226 cells were cultured with selinexor and/or venetoclax for 48 or 72 h. (A) Cell viability, (B) caspase 3/7 activity, (C) cytotoxicity, and (D) apoptosis were evaluated. Significance was expressed as * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns: Not significant vs. the control. (E) U266 and RPMI 8226 cells were treated with selinexor and/or venetoclax for 48 h. The MMP was analyzed using a JC‐1 MitoMP Detection Kit. Significance is expressed as * p < 0.05, ** p < 0.01, and ns: Not significant vs. the control.

    Article Snippet: Selinexor (KPT‐330, ATG‐010), an XPO1 inhibitor, and venetoclax (ABT‐199, GDC‐0199), a BCL2 inhibitor, were obtained from Selleck Chemicals (Houston, TX, USA).

    Techniques: Activity Assay, Cell Culture, Control

    Efficacy of selinexor and venetoclax on the bortezomib‐resistant MM cell line and primary PCL sample. (A‐C) KMS‐11/BTZ cells were cultured with selinexor and/or venetoclax for 48 or 72 h. (A) Cell viability, (B) caspase 3/7 activity, (C) cytotoxicity, and (D) apoptosis were evaluated. ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns: Not significant vs. the control. (D) KMS‐11/BTZ cells were treated with selinexor and/or venetoclax for 48 h. The MMP was analyzed using a JC‐1 MitoMP Detection Kit. Significance is expressed as *** p < 0.001, and ns: Not significant vs. the control. (E–G) Primary PCL cells were cultured with selinexor and/or venetoclax for 48 or 72 h. (E) Cell viability, (F) caspase 3/7 activity, and (G) cytotoxicity were evaluated. ** p < 0.01, **** p < 0.0001, and ns: Not significant vs. the control.

    Journal: Cancer Reports

    Article Title: Therapeutic Potential of Venetoclax and Selinexor in Targeting Hypoxia‐Induced Vulnerabilities in Multiple Myeloma

    doi: 10.1002/cnr2.70249

    Figure Lengend Snippet: Efficacy of selinexor and venetoclax on the bortezomib‐resistant MM cell line and primary PCL sample. (A‐C) KMS‐11/BTZ cells were cultured with selinexor and/or venetoclax for 48 or 72 h. (A) Cell viability, (B) caspase 3/7 activity, (C) cytotoxicity, and (D) apoptosis were evaluated. ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns: Not significant vs. the control. (D) KMS‐11/BTZ cells were treated with selinexor and/or venetoclax for 48 h. The MMP was analyzed using a JC‐1 MitoMP Detection Kit. Significance is expressed as *** p < 0.001, and ns: Not significant vs. the control. (E–G) Primary PCL cells were cultured with selinexor and/or venetoclax for 48 or 72 h. (E) Cell viability, (F) caspase 3/7 activity, and (G) cytotoxicity were evaluated. ** p < 0.01, **** p < 0.0001, and ns: Not significant vs. the control.

    Article Snippet: Selinexor (KPT‐330, ATG‐010), an XPO1 inhibitor, and venetoclax (ABT‐199, GDC‐0199), a BCL2 inhibitor, were obtained from Selleck Chemicals (Houston, TX, USA).

    Techniques: Cell Culture, Activity Assay, Control

    The CDK9 inhibitor AZD4573 and XPO1 inhibitor Selinexor are effective as single agents and in combination vs. DLBCL cell lines. ( a ) AZD4375 (red) and Selinexor (white) reduce DLBCL cell line viability. A total of 9 treatments ranging from 20,000 to 78 nM are displayed across 6 cell lines. Results were measured after 96 h using Alamar Blue cell viability reagent. Standard deviation values for each treatment are displayed as error bars for each replicate population. ( b ) AZD4573 and Selinexor ED50 values range between 1nM to 7µM. ( c ) Key gene expression values in available cell lines. Data from Hardee et al. 2013 are displayed. The study performed RNA seq with 8 DLBCL cell lines across 22,156 genes. Z-scores were calculated for relevant genes across all cell lines. Four cell lines from this study matched Z-scores were calculated for relevant genes across all 8 cell lines in the study. ( d ) Combined treatment with AZD4375 and Selinexor results in synergistic losses of cell viability within 6 DLBCL cell lines. Bliss synergy scores were calculated using the Synergy Finder tool. ( e ) Combined treatment of the DHL6 cell line displays synergistic rates of cellular disruption

    Journal: Annals of Hematology

    Article Title: MYC networks associate with decreased CD8 T-cell presence in diffuse large B-cell lymphoma and may be addressed by the synergistic combination of AZD4573 and Selinexor – a preliminary analysis

    doi: 10.1007/s00277-025-06298-x

    Figure Lengend Snippet: The CDK9 inhibitor AZD4573 and XPO1 inhibitor Selinexor are effective as single agents and in combination vs. DLBCL cell lines. ( a ) AZD4375 (red) and Selinexor (white) reduce DLBCL cell line viability. A total of 9 treatments ranging from 20,000 to 78 nM are displayed across 6 cell lines. Results were measured after 96 h using Alamar Blue cell viability reagent. Standard deviation values for each treatment are displayed as error bars for each replicate population. ( b ) AZD4573 and Selinexor ED50 values range between 1nM to 7µM. ( c ) Key gene expression values in available cell lines. Data from Hardee et al. 2013 are displayed. The study performed RNA seq with 8 DLBCL cell lines across 22,156 genes. Z-scores were calculated for relevant genes across all cell lines. Four cell lines from this study matched Z-scores were calculated for relevant genes across all 8 cell lines in the study. ( d ) Combined treatment with AZD4375 and Selinexor results in synergistic losses of cell viability within 6 DLBCL cell lines. Bliss synergy scores were calculated using the Synergy Finder tool. ( e ) Combined treatment of the DHL6 cell line displays synergistic rates of cellular disruption

    Article Snippet: The XPO1 inhibitor Selinexor (KPT-330) was obtained from SelleckChem.

    Techniques: Standard Deviation, Gene Expression, RNA Sequencing, Disruption