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Image Search Results
Journal: Journal of Medicinal Chemistry
Article Title: Discovery of dCDK9-202 as a Highly Potent and Selective PROTAC CDK9 Degrader with Strong In Vivo Antitumor Activity
doi: 10.1021/acs.jmedchem.5c01111
Figure Lengend Snippet: Representative CDK9 inhibitors.
Article Snippet: Various primary antibodies were used to detect
Techniques:
Journal: Journal of Medicinal Chemistry
Article Title: Discovery of dCDK9-202 as a Highly Potent and Selective PROTAC CDK9 Degrader with Strong In Vivo Antitumor Activity
doi: 10.1021/acs.jmedchem.5c01111
Figure Lengend Snippet: Representative CDK9 degraders.
Article Snippet: Various primary antibodies were used to detect
Techniques:
Journal: Journal of Medicinal Chemistry
Article Title: Discovery of dCDK9-202 as a Highly Potent and Selective PROTAC CDK9 Degrader with Strong In Vivo Antitumor Activity
doi: 10.1021/acs.jmedchem.5c01111
Figure Lengend Snippet: Design of the CDK9 degrader. (A) Docking model of CDK9 inhibitor SNS032 to CDK9 enzyme (PDB code 8K5R ). (B) Docking model of CRBN ligand TX-16 to DDB1-CRBN E3 ubiquitin ligase (PDB code 4CI2 ). (C) Structures of the CDK9 inhibitor, degrader, and CRBN ligand.
Article Snippet: Various primary antibodies were used to detect
Techniques: Ubiquitin Proteomics
Journal: Journal of Medicinal Chemistry
Article Title: Discovery of dCDK9-202 as a Highly Potent and Selective PROTAC CDK9 Degrader with Strong In Vivo Antitumor Activity
doi: 10.1021/acs.jmedchem.5c01111
Figure Lengend Snippet: Temporal effect and mechanistic investigation of 14 (dCDK9-202) on CDK9 degradation. (A) CDK9 protein levels in TC-71 cells upon time-course treatment with dCDK9-202 (10 nM). (B) Mechanistic investigation of CDK9 degradation induced by dCDK9-202 in the TC-71 cell line. Cells were pretreated 2 h with CDK9 inhibitor 6 (SNS032, 10 μM), thalidomide (10 μM), (R)-MG132 (5 μM), and MLN4924 (2 μM) followed by 4 h treatment with dCDK9-202 at 20 nM concentration.
Article Snippet: Various primary antibodies were used to detect
Techniques: Concentration Assay
Journal: Journal of Medicinal Chemistry
Article Title: Discovery of dCDK9-202 as a Highly Potent and Selective PROTAC CDK9 Degrader with Strong In Vivo Antitumor Activity
doi: 10.1021/acs.jmedchem.5c01111
Figure Lengend Snippet: Degradation of CDK9 by 13 and 14 (dCDK9-202) across multiple cell lines. (A–D) Examination of dose-dependent CDK9 degradation by 13 and 14 (dCDK9-202) in TC-71, U87, SKUT1, and RH5. Cells were treated with increasing concentrations of indicated compounds for 6 h. (E) Effects of 22 on CDK9 protein. TC-71 cells were treated with the indicated concentration of 22 for 6 h.
Article Snippet: Various primary antibodies were used to detect
Techniques: Concentration Assay
Journal: Journal of Medicinal Chemistry
Article Title: Discovery of dCDK9-202 as a Highly Potent and Selective PROTAC CDK9 Degrader with Strong In Vivo Antitumor Activity
doi: 10.1021/acs.jmedchem.5c01111
Figure Lengend Snippet: Antiproliferative activities of CDK9 degraders 13 and 14 (dCDK9-202) against multiple cancer cell lines. (A) Effect of dCDK9-202 treatment (50 nM, 24 h) on BrdU incorporation by TC-71 cells. Data are presented as mean ± SEM; **, p < 0.01 based on two-tailed t test. (B) Effect of dCDK9-202 treatment (50 nM, 24 h) on caspase-3/7 activity in TC-71 cells. Data are presented as mean ± SEM; ***, p < 0.001 based on two-tailed t test. (C) Effect of dCDK9-202 treatment (24 h) on intracellular levels of CDK9 and apoptotic markers in TC-71 cells. (D) Effect of 13 and 14 (dCDK9-202) treatment on cellular viabilities of indicated cancer cell lines. IC 50 is presented as mean ± SEM with three independent replicates.
Article Snippet: Various primary antibodies were used to detect
Techniques: BrdU Incorporation Assay, Two Tailed Test, Activity Assay
Journal: Journal of Medicinal Chemistry
Article Title: Discovery of dCDK9-202 as a Highly Potent and Selective PROTAC CDK9 Degrader with Strong In Vivo Antitumor Activity
doi: 10.1021/acs.jmedchem.5c01111
Figure Lengend Snippet: Compound 14 (dCDK9-202) selectively proteolyzes CDK9 to impair Pol2 function and cancer-addicted transcriptome. (A) Temporal effect of dCDK9-202 treatment on CDK and IKZF proteins in TC-71 cells. (B, C) Effect of 14 (dCDK9-202) and 6 (SNS032) treatment on Rpb1, phosphorylation of Rpb1 CTD ser2 , and key targets in downstream signaling pathways. (D, E) RNA-seq analysis of TC-71 cells upon dCDK9-202 (10 nM, 8 h) and SNS032 (10 nM, 8 h) treatments. (F) GSEA showing representative biological pathways affected by dCDK9-202 treatment in TC-71.
Article Snippet: Various primary antibodies were used to detect
Techniques: Phospho-proteomics, Protein-Protein interactions, RNA Sequencing
Journal: Journal of Medicinal Chemistry
Article Title: Discovery of dCDK9-202 as a Highly Potent and Selective PROTAC CDK9 Degrader with Strong In Vivo Antitumor Activity
doi: 10.1021/acs.jmedchem.5c01111
Figure Lengend Snippet: Pharmacodynamic analysis of 14 (dCDK9-202) in the TC-71 xenograft model. (A) In vivo PK of compound 14 in mice. (B) Western blotting analysis of CDK9 protein in the TC-71 xenograft lysate. Immunocompromised mice bearing subcutaneous TC-71 tumors were treated with a single IV administration of 14 (dCDK9-202) at a dose of 10 mg/kg. Mice were euthanized at indicated time points for collection of tumor tissues for analysis. (C) Western blotting analysis of CDK9 protein in the spleens of mice receiving a single IV administration of 14 (dCDK9-202) at 10 mg/kg.
Article Snippet: Various primary antibodies were used to detect
Techniques: In Vivo, Western Blot
Journal: Journal of Medicinal Chemistry
Article Title: Discovery of dCDK9-202 as a Highly Potent and Selective PROTAC CDK9 Degrader with Strong In Vivo Antitumor Activity
doi: 10.1021/acs.jmedchem.5c01111
Figure Lengend Snippet: Antitumor activity of 14 (dCDK9-202) in the TC-71 xenograft model in immunocompromised mice. (A) Changes in tumor volume during dCDK9-202, 6 (SNS032), or 10 (THAL-SNS032) treatments (10 mg/kg, i.v., qod). (B) Tumor weight at the end point of experiment. (C) Image of subcutaneous TC-71 xenograft tumors harvested at the end point of experiment. (D) Body weight of recipient mice during treatments. (E) Western blot analysis of CDK9 protein levels in tumor lysates harvested 4 h after final treatment (representative samples shown). Data in panels A, B, and D are presented as mean ± SD and were analyzed by one-way ANOVA (significance denoted as n.s., not significant; *, p < 0.05; **, p < 0.01; ***, p < 0.001).
Article Snippet: Various primary antibodies were used to detect
Techniques: Activity Assay, Western Blot
Journal: Journal of Medicinal Chemistry
Article Title: Discovery of dCDK9-202 as a Highly Potent and Selective PROTAC CDK9 Degrader with Strong In Vivo Antitumor Activity
doi: 10.1021/acs.jmedchem.5c01111
Figure Lengend Snippet: Compound 14 (dCDK9-202) selectively proteolyzes CDK9 to impair Pol2 function and cancer-addicted transcriptome. (A) Temporal effect of dCDK9-202 treatment on CDK and IKZF proteins in TC-71 cells. (B, C) Effect of 14 (dCDK9-202) and 6 (SNS032) treatment on Rpb1, phosphorylation of Rpb1 CTD ser2 , and key targets in downstream signaling pathways. (D, E) RNA-seq analysis of TC-71 cells upon dCDK9-202 (10 nM, 8 h) and SNS032 (10 nM, 8 h) treatments. (F) GSEA showing representative biological pathways affected by dCDK9-202 treatment in TC-71.
Article Snippet: Various primary antibodies were used to detect CDK9 (Cell Signaling Technology, 2316), CDK9 (Santa Cruz, sc-13130), ACTIN (Proteintech, 66009-1-Ig), GAPDH (Cell Signaling Technology, 2118), CDK1/2 (Santa Cruz, sc-53219), CDK4 (Cell Signaling Technology, 12790), CDK5 (Santa Cruz, sc-173), CDK6 (Cell Signaling Technology, 13331), CDK7 (Bethyl Laboratories, A300-405A), CDK8 (Santa Cruz, sc-13155), CDK11 (Abclonal, A12830), CDK12 (Cusabio, CSB-PA882147LA01HU), cleaved caspase-3 (Diagbio, db15982), cleaved PARP (Cell Signaling Technology, 5625), BCL-xL (Santa Cruz, sc-8392), E2F1 (Cell Signaling Technology, 3742), IKZF1 (Genetex, GTX124438), IKZF3 (Cell Signaling Technology, 15103), MCL1 (Diagbio, db11616), MYC (Cell Signaling Technology, 5605), RNA polymerase II Rpb1 (Cell Signaling Technology, 14958), and
Techniques: Phospho-proteomics, Protein-Protein interactions, RNA Sequencing
Journal: Journal of Medicinal Chemistry
Article Title: Discovery of dCDK9-202 as a Highly Potent and Selective PROTAC CDK9 Degrader with Strong In Vivo Antitumor Activity
doi: 10.1021/acs.jmedchem.5c01111
Figure Lengend Snippet: Compound 14 (dCDK9-202) selectively proteolyzes CDK9 to impair Pol2 function and cancer-addicted transcriptome. (A) Temporal effect of dCDK9-202 treatment on CDK and IKZF proteins in TC-71 cells. (B, C) Effect of 14 (dCDK9-202) and 6 (SNS032) treatment on Rpb1, phosphorylation of Rpb1 CTD ser2 , and key targets in downstream signaling pathways. (D, E) RNA-seq analysis of TC-71 cells upon dCDK9-202 (10 nM, 8 h) and SNS032 (10 nM, 8 h) treatments. (F) GSEA showing representative biological pathways affected by dCDK9-202 treatment in TC-71.
Article Snippet: Various primary antibodies were used to detect CDK9 (Cell Signaling Technology, 2316), CDK9 (Santa Cruz, sc-13130), ACTIN (Proteintech, 66009-1-Ig), GAPDH (Cell Signaling Technology, 2118), CDK1/2 (Santa Cruz, sc-53219), CDK4 (Cell Signaling Technology, 12790), CDK5 (Santa Cruz, sc-173), CDK6 (Cell Signaling Technology, 13331), CDK7 (Bethyl Laboratories, A300-405A), CDK8 (Santa Cruz, sc-13155), CDK11 (Abclonal, A12830), CDK12 (Cusabio, CSB-PA882147LA01HU), cleaved caspase-3 (Diagbio, db15982), cleaved PARP (Cell Signaling Technology, 5625), BCL-xL (Santa Cruz, sc-8392), E2F1 (Cell Signaling Technology, 3742), IKZF1 (Genetex, GTX124438), IKZF3 (Cell Signaling Technology, 15103), MCL1 (Diagbio, db11616), MYC (Cell Signaling Technology, 5605),
Techniques: Phospho-proteomics, Protein-Protein interactions, RNA Sequencing