GSK126 - CAS GSK126GSK126 is a potent, highly selective, S-adenosyl-methionine- competitive, small-molecule inhibitor of EZH2 methyltransferase.

Slides:

Advertisements

Similar presentations

Retinoic Acid Receptor Alpha and Acute Promyelocytic Leukemia Nidhi Thapar April 1, 2004.

Advertisements

THE WNT SIGNALING PATHWAY AND THE IMPACT LITHIUM HAS ON IT The Pathophysiology of Bipolar Disorder CHELSEA ZAMORA.

CpG hypermethylation Data from literature RESULT: Genes that are hypermethylated at CpG islands in cancer cells (HCT- 116 cell line) are NOT highly.

The Best Selling Chemicals at BOC Sciences BOC Sciences provides a wide scope of chemicals and related custom services. In 2016, the company made a lot.

P57(KIP2) and Beckwith-Wiedemann Syndrome Shannon O’Leary.

Date of download: 9/18/2016 From: The Cardiomyopathy of Overload: An Unnatural Growth Response in the Hypertrophied Heart Ann Intern Med. 1994;121(5):

Beneficial compaction of spinal cord lesion by migrating astrocytes through glycogen synthase kinase ‐ 3 inhibition by Francois Renault ‐ Mihara, Hiroyuki.

School of Pharmacy, Sungkyunkwan University Fri. seminar.

Fig. 1 Expression levels of DNA damage repair genes RAD51 and BRCA1 in fibroids (F) and adjacent myometrial tissues (MyoF) as well as primary cells. Each.

Kui Wang May 6th, 2017.

Leila Kokabee*, Xianhui Wang, Cheryl Eifert, Douglas S. Conklin

JeeHeun Kim (AK).

Training Set Clinicopathological parameters of the training set

GENETIC BIOMARKERS.

Von Hippel-Lindau Syndrome

Fig. 1 Increased MIR155HG expression correlates with glioma grade and mesenchymal transition and confers a poor prognosis in GBM patients. (A) The level.

Developing chemically modified, non-anticoagulant heparin derivatives as galectin-3-targeted novel anti-cancer/anti-metastasis drugs Professor Lu-Gang.

Featured Inhibitors for October-BOC Sciences

Control of Metabolic Pathways (2)

Inhibition of FGFR fusion kinase activity repressed tumor growth in a mouse xenograft model. Inhibition of FGFR fusion kinase activity repressed tumor.

Inhibitor of MAP kinase activation blocks colon cancer growth

Figure 2 Signalling pathways and physiological domains that are

Combined RAF and EGFR inhibition leads to improved in vivo efficacy in BRAF-mutant colorectal cancer. Combined RAF and EGFR inhibition leads to improved.

Lymphoma cells with BCL2/PMAIP1 coamplification are highly sensitive to BCL-2 inhibitor. Lymphoma cells with BCL2/PMAIP1 coamplification are highly sensitive.

Katrin Hoffmeyer, Dirk Junghans, Benoit Kanzler, Rolf Kemler

c-Kit as a Novel Potential Therapeutic Target in Colorectal Cancer

Volume 23, Issue 5, Pages (May 2013)

Therapeutic Suppression of miR-4261 Attenuates Colorectal Cancer by Targeting MCC Guanming Jiao, Qi Huang, Muren Hu, Xuchun Liang, Fuchen Li, Chunling.

C. Allison Stewart, Lauren Averett Byers Cancer Cell

Volume 8, Issue 1, Pages (July 2014)

Gerard L. Brien, Daria G. Valerio, Scott A. Armstrong Cancer Cell

EZH2 Inhibitor EPZ-6438 Synergizes With Anti-Lymphoma Therapies In Preclinical Models by L. Danielle Johnston, Sarah Knutson, Natalie Warholic, Christine.

A Mitochondrial Power Play in Lymphoma

Figure 1 Exosomes with siRNAs targeting

INTERLEUKIN 10 (IL-10) CATEGORY: RECEPTORS & MOLECULES

RORα inhibits cell proliferation and expression of the E2F1-targeted genes. RORα inhibits cell proliferation and expression of the E2F1-targeted genes.

Volume 23, Issue 6, Pages (June 2013)

Volume 155, Issue 4, Pages (October 2018)

Epigenomics: Analysis of Epigenetic Therapy to Treat Cancer

Volume 8, Issue 5, Pages (May 2017)

Volume 11, Issue 6, Pages (December 2018)

Epigenetics modification

Histone H3.3 Mutations: A Variant Path to Cancer

C. Allison Stewart, Lauren Averett Byers Cancer Cell

Volume 22, Issue 5, Pages (May 2014)

Volume 25, Issue 10, Pages e4 (December 2018)

Volume 20, Issue 11, Pages (November 2013)

Supplementary Materials DNMT1-shRNA’ DNMT1-shRNA control DNMT1 DNMT3a

Long Noncoding RNAs in Cell-Fate Programming and Reprogramming

Targeting Apoptosis in AML

Volume 20, Issue 2, Pages (August 2011)

Smoothing Out Drug Resistance

Fig. 3. Inactivation of the Wnt/β-catenin signaling pathway inhibited cell proliferation and induced apoptosis in A549 and SPC-A-1 cells. Inactivation.

Deubiquitinating activity, but not HCF-1 binding, is required for BAP1 function in thymocytes. Deubiquitinating activity, but not HCF-1 binding, is required.

Hypothetical model of HvAP2 control of stem elongation.

LSD1, a histone demethylase, is required for the assembly of the Notch repressor complex. LSD1, a histone demethylase, is required for the assembly of.

Nat. Rev. Rheumatol. doi: /nrrheum

The Angiogenesis Inhibitor Vasostatin does not Impair Wound Healing at Tumor- Inhibiting Doses Bernhard Lange-Asschenfeldt, Paula Velasco, Michael Streit,

Volume 14, Issue 8, Pages (March 2016)

The SFKs confer BRAF inhibitor resistance in BRAF-mutant melanoma cells. The SFKs confer BRAF inhibitor resistance in BRAF-mutant melanoma cells. A, phospho-protein.

Small-molecule EZH2 inhibitor development.

PRIMA-1Met inhibits the growth of multiple myeloma tumors with mutant p53 in vivo. PRIMA-1Met inhibits the growth of multiple myeloma tumors with mutant.

Epigenetic factors influencing resistance to nuclear reprogramming

Antitumor effects of celastrol in vitro and in vivo.

THE GROWTH ENVIRONMENT.

Loss of HDAC3 inhibits CREBBP-mutant lymphoma growth in vitro and in vivo. Loss of HDAC3 inhibits CREBBP-mutant lymphoma growth in vitro and in vivo. A,

Targeting GAPLINC decreased CD44 expression and tumor growth in vivo.

Both TKI and EZH2i upregulate H3K27me3 targets, and combined treatment potentiates loss of LSCs. A, summary of global mean mRNA expression changes found.

BH3-targeted inhibitors drive specific resistance in human cell lines, which can be overcome with alternating or combining inhibitors. BH3-targeted inhibitors.

Tackling Resistance to PI3K Inhibition by Targeting the Epigenome

Presentation transcript:

GSK126 - CAS GSK126GSK126 is a potent, highly selective, S-adenosyl-methionine- competitive, small-molecule inhibitor of EZH2 methyltransferase activity. GSK126 decreases global H3K27me3 levels and reactivates silenced PRC2 target genes. GSK126 effectively inhibits the proliferation of EZH2 mutant DLBCL cell lines and markedly inhibits the growth of EZH2 mutant DLBCL xenografts in mice. Together, these data demonstrate that pharmacological inhibition of EZH2 activity may provide a promising treatment for EZH2 mutant lymphoma.