selinexor  (TargetMol)

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

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

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

Journal: bioRxiv

Article Title: Nuclear Phase Separation Drives NPM1-mutant Acute Myeloid Leukemia

doi: 10.1101/2025.05.23.655671

Figure Lengend Snippet: (A) Stacked bar plots showing distributions of CUT&RUN data from DMSO-treated NPM1 WT/Degron OCI-AML3 cells, with genomic peaks annotated as TSSs, promoters, exons, introns, and intergenic regions. (B) Venn diagram of TSS-promoter peaks from DMSO-treated CUT&RUN sequencing depicting unique genes bound by at least 3 of 4 antibody targets (including XPO1, NUP98, KMT2A, and MENIN) ( n = 235) and NPM1c target genes identified by ChIP-seq ( n = 33, Uckelmann et al. 2023) and annotated table of genes found in both datasets. (C) RDF of NUP98 and HOXA9 in top (red) and bottom (purple) quartiles in comparison to the average ( n = 69). (D) Immunoblotting analysis of protein lysates from OCI-AML3 and IMS-m2 cells treated with DMSO or dTAG for 72h using anti-GFP, anti-NPM1wt and anti-Gapdh-Rhodamine antibodies. (E) Relative mRNA levels of HOXA/MEIS1 in OCI-AML3 cells treated with VTP50469 or Selinexor. (F) Mean CD11b level in OCI-AML3 cells treated with VTP50469, dTAG-13, Selinexor or DMSO for 4 weeks and (G) representative histograms of CD11b level. (H) Representative Integrated Genome Viewer (IGV) tracks (duplicates per sample) for IgG (black), H3K27me3 (Gray), XPO1 (Red), NUP98 (Blue), KMT2A (Green), and MENIN (Orange) treated with DMSO, dTAG-13 (500nM), Eltanexor (100nM), or VTP50469 (300nM) for 24 hours. Fisher’s Exact test was used for statistical testing.

Article Snippet: To inhibit XPO1-NPM1c interactions, cells were treated with 100nM Eltanexor (Selleckchem, S8397) or 100nM Selinexor (Selleckchem, S7252) for 24hrs as previously described .

Techniques: Sequencing, ChIP-sequencing, Comparison, Western Blot

Journal: bioRxiv

Article Title: Nuclear Phase Separation Drives NPM1-mutant Acute Myeloid Leukemia

doi: 10.1101/2025.05.23.655671

Figure Lengend Snippet: (A-D) Immunostaining of NPM1 WT/Degron OCI-AML3 cells with antibodies targeting XPO1, NUP98, KMT2A, and MENIN after DMSO, Selinexor, or MI-503 treatments. ( E) RDF of XPO1, NUP98, KMT2A, and MENIN with DMSO or MI-503 treatment ( n = 50). All cells were treated for 24hrs prior to immunostaining (Selinexor = 100nM, MI-503 = 2.5µM). All images are shown in Fire LUT except colocalization (cyan and magenta). White scale bars = 2µm. RDF data for DMSO samples is repeated from .

Article Snippet: To inhibit XPO1-NPM1c interactions, cells were treated with 100nM Eltanexor (Selleckchem, S8397) or 100nM Selinexor (Selleckchem, S7252) for 24hrs as previously described .

Techniques: Immunostaining