molecule inhibitor ac2 26  (TargetMol)

Journal: Synthetic and Systems Biotechnology

Article Title: Leveraging ANXA1 to enhance recombinant protein yields in CHO cells: A UPR-Mediated bioprocessing approach

doi: 10.1016/j.synbio.2025.12.001

Figure Lengend Snippet: Schematic overview of the experimental workflow for generating ANXA1-knockdown CHO cell lines and AC2-26 inhibitor treatment. (A) Generation and validation of ANXA1-knockdown cell lines for rADM antibody production. (B) AC2-26 inhibitor treatment in low-producer CHO cells (ADM-14) and subsequent rADM expression analysis.

Article Snippet: On day 3 of suspension culture, the small molecule inhibitor AC2-26 (Topscience Co., Ltd., China) was added [ ], using DMSO (Solarbio Life Sciences, China) as the solvent control.

Techniques: Knockdown, Biomarker Discovery, Expressing

Journal: Synthetic and Systems Biotechnology

Article Title: Leveraging ANXA1 to enhance recombinant protein yields in CHO cells: A UPR-Mediated bioprocessing approach

doi: 10.1016/j.synbio.2025.12.001

Figure Lengend Snippet: AC2-26 effect on ADM-14 CHO cells. (A) Cell density/viability under AC2-26 treatment (n = 3). (B) rADM expression by Western blot with quantification (n = 3). (C) ANXA1 mRNA/protein comparison (n = 3). Quantification was performed using ImageJ (for Western blot densitometry) and GraphPad Prism 10 (for statistical analysis). (∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001). n: represents independent biological replicates.

Article Snippet: On day 3 of suspension culture, the small molecule inhibitor AC2-26 (Topscience Co., Ltd., China) was added [ ], using DMSO (Solarbio Life Sciences, China) as the solvent control.

Techniques: Expressing, Western Blot, Comparison

Journal: Molecular Therapy. Nucleic Acids

Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

doi: 10.1016/j.omtn.2025.102804

Figure Lengend Snippet: Design of anti-transcription γPNA and combination treatments to target the c-Myc oncogene (A) Schematic representation of gamma peptide nucleic (γPNA)-mediated inhibition of human c-Myc transcription and target site (NCBI database RefSeq: NG_007161.2 ). (B) Design of γPNA conjugated with nuclear localization signal (NLS) to target the indicated sites. ScR-γPNA2 is the scramble control. (C) Graphic representation of combination treatments with anti-transcription, γPNA1. The combination treatments include histone deacetylase inhibitors (HDACis), MYC/MAX inhibitors, small interfering RNA (siRNA), and small molecules targeting other pathways. (D) Polymerase chain reaction (PCR)-based amplicon assay to confirm binding of γPNA1 to the target site in U2932 cells. Amplicon assay after treatment of γPNA1 and ScR-γPNA2 with HDACi. (E) The graph represents quantification of γPNA1 and ScR-γPNA2 amplicon in combination with HDACi. (F) The graph represents the quantification of amplicon assay from class I HDACi with γPNA1. Results are presented as mean ± SEM. One-way ANOVA was used to determine the statistically significant difference between groups.

Article Snippet: Cells were cotreated with 1:2 dilutions of MYC/MAX inhibitors (Myci975 [Selleckchem, #S8906]), EN4 (MedChemExpress, #HY-134761), 10058-F4 (MedChemExpress, #HY-12702), SAJM589 (MedChemExpress, #HY-122683), and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. Cells were cotreated with 1:10 dilutions of small molecule inhibitors (JQ1 [MedChemExpress, #HY-13030]), sapanisertid (MedChemExpress, #HY-13328), and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. MDA-MB 231 cells were cotreated with dinaciclid (MedChemExpress, #HY-10492) and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. MDA-MB-231 and HeLa cells were cotreated with c-Myc siRNA (50 nM) and γPNA1 and ScR-γPNA2 for 48 h. At 0 μM concentration, cells were treated only with PBS and not treated with MYC/MAX inhibitors, HDAC inhibitors, small molecule inhibitors, or γPNA1.

Techniques: Inhibition, Control, Histone Deacetylase Assay, Small Interfering RNA, Polymerase Chain Reaction, Amplification, Binding Assay

Journal: Molecular Therapy. Nucleic Acids

Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

doi: 10.1016/j.omtn.2025.102804

Figure Lengend Snippet: Cell viability of Histone deacetylase inhibitors in combination with γPNA1 (A) Cell viability of U2932 cells treated with increasing doses of HDACi (romidepsin, entinostat, vorinostat, panobinostat, and belinostat) alone and in combination with γPNA1 and ScR-γPNA2 (8 μM) for 48 h. Results are presented as mean ± SEM. (B) The IC 50 ± SEM values of HDACi and combination treatment of HDACi with γPNA1 in U2932 cells. (C) Cell viability of Raji cells treated with increasing doses of HDACi (romidepsin, entinostat, vorinostat, panobinostat, and belinostat) alone and in combination with γPNA1 and ScR-γPNA2 (8 μM) for 48 h. Results are presented as mean ± SEM. (D) The IC 50 ± SEM values of HDACi and combination treatment of HDACi with γPNA1 in Raji cells.

Article Snippet: Cells were cotreated with 1:2 dilutions of MYC/MAX inhibitors (Myci975 [Selleckchem, #S8906]), EN4 (MedChemExpress, #HY-134761), 10058-F4 (MedChemExpress, #HY-12702), SAJM589 (MedChemExpress, #HY-122683), and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. Cells were cotreated with 1:10 dilutions of small molecule inhibitors (JQ1 [MedChemExpress, #HY-13030]), sapanisertid (MedChemExpress, #HY-13328), and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. MDA-MB 231 cells were cotreated with dinaciclid (MedChemExpress, #HY-10492) and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. MDA-MB-231 and HeLa cells were cotreated with c-Myc siRNA (50 nM) and γPNA1 and ScR-γPNA2 for 48 h. At 0 μM concentration, cells were treated only with PBS and not treated with MYC/MAX inhibitors, HDAC inhibitors, small molecule inhibitors, or γPNA1.

Techniques: Histone Deacetylase Assay

Journal: Molecular Therapy. Nucleic Acids

Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

doi: 10.1016/j.omtn.2025.102804

Figure Lengend Snippet: MYC/MAX inhibitors in combination with anti-transcription γPNA1 Cell viability of (A) U2932 and (B) Raji cells treated with increasing doses of MYC/MAX inhibitors (Myci975, EN4, 10058-F4, and sAJM589) alone and in combination with γPNA1 and ScR-γPNA2 (8 μM) for 72 h. Results are presented as mean ± SEM. The IC 50 (95% CI) values of MYC/MAX inhibitors alone and combination treatment of MYC/MAX with γPNA1 in (C) U2932 and (D) Raji cells. (E) Cell viability of γPNA1-treated U2932 and Raji cells at 8 μM concentration. Western blot analysis representing the change in c-MYC protein 72 h after treatment with γPNA1 and ScR-γPNA2 in combination with (F) Myci975, (G) EN4, (H) 10058-F4, and (I) sAJM589. ∗∗(F–I) Cyclophilin B was used as an endogenous control, and the same blots are presented in A–S7D. c-MYC, EZH2, and cyclophilin B were probed from the same blot. Results are presented as mean ± SEM, p value for one-way ANOVA.

Article Snippet: Cells were cotreated with 1:2 dilutions of MYC/MAX inhibitors (Myci975 [Selleckchem, #S8906]), EN4 (MedChemExpress, #HY-134761), 10058-F4 (MedChemExpress, #HY-12702), SAJM589 (MedChemExpress, #HY-122683), and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. Cells were cotreated with 1:10 dilutions of small molecule inhibitors (JQ1 [MedChemExpress, #HY-13030]), sapanisertid (MedChemExpress, #HY-13328), and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. MDA-MB 231 cells were cotreated with dinaciclid (MedChemExpress, #HY-10492) and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. MDA-MB-231 and HeLa cells were cotreated with c-Myc siRNA (50 nM) and γPNA1 and ScR-γPNA2 for 48 h. At 0 μM concentration, cells were treated only with PBS and not treated with MYC/MAX inhibitors, HDAC inhibitors, small molecule inhibitors, or γPNA1.

Techniques: Concentration Assay, Western Blot, Control

Journal: Molecular Therapy. Nucleic Acids

Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

doi: 10.1016/j.omtn.2025.102804

Figure Lengend Snippet: Efficacy of small molecules targeting other pathways with anti-transcription γPNA1 (A) Cell viability of U2932 and Raji cells treated with increasing doses JQ1 (BRD4 inhibitor) alone and with γPNA1 and ScR-γPNA2 for 48 h. (B) Cell viability of U2932 and Raji cells treated with increasing doses of sapnisertid (mTOR inhibitor) alone and with γPNA1 and ScR-γPNA2 for 48 h. (C) Cell viability of MDA-MB-231 cells treated with increasing doses of dinaciclib (CDK inhibitor) alone and with γPNA1 and ScR-γPNA2 for 48 h. (D) The IC 50 (95% CI) values of small molecule inhibitors alone and in combination with γPNA1. (A–C) Results are presented as mean ± SEM.

Article Snippet: Cells were cotreated with 1:2 dilutions of MYC/MAX inhibitors (Myci975 [Selleckchem, #S8906]), EN4 (MedChemExpress, #HY-134761), 10058-F4 (MedChemExpress, #HY-12702), SAJM589 (MedChemExpress, #HY-122683), and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. Cells were cotreated with 1:10 dilutions of small molecule inhibitors (JQ1 [MedChemExpress, #HY-13030]), sapanisertid (MedChemExpress, #HY-13328), and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. MDA-MB 231 cells were cotreated with dinaciclid (MedChemExpress, #HY-10492) and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. MDA-MB-231 and HeLa cells were cotreated with c-Myc siRNA (50 nM) and γPNA1 and ScR-γPNA2 for 48 h. At 0 μM concentration, cells were treated only with PBS and not treated with MYC/MAX inhibitors, HDAC inhibitors, small molecule inhibitors, or γPNA1.

Techniques:

Journal: bioRxiv

Article Title: Functional and sensitivity profiling of the KIT Mutation Landscape in Melanoma

doi: 10.64898/2026.02.18.706482

Figure Lengend Snippet: KIT mutations shows differential responses towards common KIT inhibitors in vitro. (A) Western Blot analysis revealed changes in cell growth and proliferation pathways upon expression of KIT mutants in MeWO melanoma cells. (B) Upper panel: Monitoring relative growth of melanoma cell spheroids expressing KIT mutants using high-content microscopy. Lower panel: Representative image depicting spheroid size after 8 days of growth in 3D environment. (C) Western Blot demonstrating the expression of KIT in Ba/F3 cells. (D) Assessment of relative growth of Ba/F3 cells expressing different KIT mutants following withdrawal of IL-3 from the culture medium, measured using cell-titre glo assay. (E) Heatmap shows the relative IC50 of Ba/F3 cell with KIT mutants against KIT inhibitors. (F) Violin plot illustrating the IC50 values of MeWo cells expressing KIT mutants when treated with various KIT inhibitors. Results were obtained from three independent experiments. The horizontal line represents the mean, and statistical analysis was performed using one-way ANOVA.

Article Snippet: Small molecule inhibitors (Imatinib, Sunitinib, Nilotinib, Nintedanib, and Ripretinib) were purchased from MedChemExpress, dissolved in DMSO to a 10 mM stock, and stored at −80°C.

Techniques: In Vitro, Western Blot, Expressing, Microscopy, Glo Assay

Journal: bioRxiv

Article Title: Functional and sensitivity profiling of the KIT Mutation Landscape in Melanoma

doi: 10.64898/2026.02.18.706482

Figure Lengend Snippet: In vivo anti-tumor efficacy of KIT inhibitors against MeWo cells expressing KIT WT/mutants in a mouse xenograft model. (A-C) Response of MeWO-KIT-WT, MeWo-KIT p.L576P, and MeWo-KIT-p.N822K mouse xenograft models to Imatinib, Sunitinib, Nilotinib, and Nintedanib, respectively (n = 3 independent experiments). (D-F) Response of MeWO-KIT-WT, MeWo-KIT p.L576P, and MeWo-KIT-p.N822K mouse xenograft models to Ripretinib (n = 3 independent experiments). Fraction of tumor growth represents the change in tumor volume normalized to day 0 of treatment.

Article Snippet: Small molecule inhibitors (Imatinib, Sunitinib, Nilotinib, Nintedanib, and Ripretinib) were purchased from MedChemExpress, dissolved in DMSO to a 10 mM stock, and stored at −80°C.

Techniques: In Vivo, Expressing