bcl2 inhibitor venetoclax  (MedChemExpress)

Journal: Scientific Reports

Article Title: Effects of venetoclax, a BCL2 inhibitor, in systemic chronic active Epstein-Barr virus disease

doi: 10.1038/s41598-025-03719-9

Figure Lengend Snippet: The expression of BCL2 and the effect of venetoclax on EBV-positive T- or NK-cell lines. ( A ) The expression of BCL2 protein was detected in EBV-positive T- or NK-cell lines (SNT8, SNT15, SNT16, SNK1, SNK6 and SNK10). Karpas231 and SU-DHL10 were positive and negative control of BCL2, respectively. ( B – I ) EBV-infected T- or NK-cell lines and the control cell lines were treated with 0, 0.2, 1, 2 and 4 µM venetoclax as indicated, for 24 and 48 h, and the number of viable cells was estimated by an MTT assay and expressed in arbitrary units. The data are shown as mean ± standard deviations (SD) of three independent experiments. At each time point, 24 and 48 h after drug stimulation, the results for the control and each drug concentration were compared using ANOVA (Dunnett’s multiple comparisons test). * for p < 0.05, ** for p < 0.01, *** for p < 0.001 and **** for p < 0.0001.

Article Snippet: Venetoclax, a BCL2 inhibitor, was purchased from Selleck Chemicals (Houston, USA).

Techniques: Expressing, Negative Control, Infection, Control, MTT Assay, Concentration Assay

Journal: Scientific Reports

Article Title: Effects of venetoclax, a BCL2 inhibitor, in systemic chronic active Epstein-Barr virus disease

doi: 10.1038/s41598-025-03719-9

Figure Lengend Snippet: The expression of BCL2 in sCAEBV patients’ EBV-infected cells. ( A ) The expression of BCL2, BAK, and BAX was detected by western blotting analysis in five sCAEBV patients’ PBMCs. SNT16 and SNK10 were positive controls and SU-DHL10 was a negative control. ( B , C ) The densitometry ratio of BCL2/BAX ( B ) or BCL2/BAK ( C ) relative to β-actin for Fig. 3A was quantified by ImageJ. ( D – F ) The expression and the localization of BCL2, LMP1 in patients’ PBMCs was confirmed by immunofluorescence staining. Scale bar showed 20 μm.

Article Snippet: Venetoclax, a BCL2 inhibitor, was purchased from Selleck Chemicals (Houston, USA).

Techniques: Expressing, Infection, Western Blot, Negative Control, Immunofluorescence, Staining

Journal: bioRxiv

Article Title: Design of combination therapeutics from protein response to drugs in ovarian cancer cells

doi: 10.1101/2025.04.28.651139

Figure Lengend Snippet: (a) Dose-response curves of the single small-molecule inhibitors, used for the primary perturbation followed by MS protein response profiling in OVSAHO cells, including AKT inhibitor MK-2206 (AKTi), BCL2 inhibitor Venetoclax (BCL2i), GSK3β inhibitor CHIR-99021 (GSK3βi), MEK inhibitor PD-0325901 (MEKi), PKC inhibitor Bisindolylmaleimide VIII (BIM VIII, PKCi), and SRC inhibitor Bosutinib (SRCi). Data is aggregated from three biological replicates each with three technical replicates and error bars represent standard deviations of the data. (b) Label-free mass spectrometry (MS)-based proteomics workflow used to measure protein changes in response to drug treatment at IC50. Data-driven network analysis was later applied to the acquired MS data to identify potential resistance mechanisms for the nomination of drug combination candidates. (c) Number of proteins quantified upon each drug treatment of OVSAHO cells after 72h at inhibitor IC50 concentration. Error bars: standard deviation of three biological replicates for each condition. (d) Multidimensional scaling (MDS, Euclidean distance) 2D projection of protein levels measured after treatment. Colors indicate different drug perturbation conditions with weak dotted lines around each group of biological replicates to indicate the closeness of the replicates.

Article Snippet: The following drugs used in the experiments were all commercially available: AKT inhibitor MK-2206 2HCl (Selleckchem, #S1078), BCL2 inhibitor Venetoclax (ABT-199, Selleckchem, #S8048), GSK3β inhibitor CHIR-99021 (Selleckchem, #S1263), MEK inhibitor PD-0325901 (Selleckchem, #S1036), PKC inhibitor Bisindolylmaleimide VIII (Caymanchem, #13333), and SRC inhibitor Bosutinib (SKI-606, Selleckchem, #S1014).

Techniques: Mass Spectrometry, Concentration Assay, Standard Deviation

Journal: bioRxiv

Article Title: Design of combination therapeutics from protein response to drugs in ovarian cancer cells

doi: 10.1101/2025.04.28.651139

Figure Lengend Snippet: The combinations were chosen based on pathway analysis of protein response . TVB-2640 (‘TVB’, FASNi), rucaparib (‘Ruc’, PARPi), bortezomib (‘Bort’, proteasome inhibitor), Apcin (APCi), GC7 (DNA synthase inhibitor), novobiocin (‘Novo’, DNA polymerase inhibitor), infigratinib (‘Inf’, FGFR3i), venetoclax (‘Ven’, BCL2i), everolimus (‘Eve’, MTORi), Palbociclib (‘Pal’, CDK4/6i), PD-0325901 (‘PD’, MEKi), idelalisib (‘Ide’, PI3Ki), bosutinib (‘Bos’, SRCi), auranofin (‘Aur’, PRDXi), simvastatin (‘Sim’, statin), GPX4-IN-3 (‘GPX’, GPX4i), RSL3 (GPX4i), DM4 (tubulin inhibitor). Each drug was applied to OVCAR-4 cells with a serial dilution factor of 3 or 4 to establish a dose-response curve for the single drug. Each drug combination was applied at the same concentrations as the single drugs. The combination index for each drug pair is calculated using the Chou-Talalay method.

Article Snippet: The following drugs used in the experiments were all commercially available: AKT inhibitor MK-2206 2HCl (Selleckchem, #S1078), BCL2 inhibitor Venetoclax (ABT-199, Selleckchem, #S8048), GSK3β inhibitor CHIR-99021 (Selleckchem, #S1263), MEK inhibitor PD-0325901 (Selleckchem, #S1036), PKC inhibitor Bisindolylmaleimide VIII (Caymanchem, #13333), and SRC inhibitor Bosutinib (SKI-606, Selleckchem, #S1014).

Techniques: Serial Dilution