Targeting Autophagy


Cambridge Healthtech Institute 第1届
自体吞噬的标靶化
病体内药物调节自体吞噬的技术进步

第15届Discovery on Target其中一环

本座谈会以自体吞噬标靶为主题,研究机构及药厂居指导地位的研究人员将齐聚一堂,能在拓展人脉、建立合作关系的同时,讨论该领域的研究发展。

Final Agenda


RECOMMENDED ALL ACCESS PACKAGE:

· September 25 Symposium: Targeting Autophagy

· September 25 Short Course: Covalent Fragments: Applications in Target-Based and Phenotypic Screens

· September 26-27 Conference: Targeting the Ubiquitin Proteasome System

· September 27-28 Conference: Kinase Inhibitor Discovery

· September 27 Short Course: Introduction to Targeted Covalent Inhibitors

· September 28-29 Symposium: CNS and Neurodegenerative Targets


Monday, September 25

7:00 am Registration Open and Morning Coffee

ADVANCES IN OUR UNDERSTANDING OF AUTOPHAGY IN DISEASE

7:55 Welcome Remarks

Kip Harry, Senior Conference Director, Cambridge Healthtech Institute

8:00 Chairperson's Opening Remarks

Nicholas Cosford, Ph.D., Associate Director, Translational Research & Professor, Cancer Metabolism and Signaling Networks Program, NCI-Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute

8:10 KEYNOTE PRESENTATION: Targeting Autophagy in Cancer

Eileen White, Ph.D., CSO, Deputy Director & Associate Director, Basic Science, Rutgers Cancer Institute of New Jersey

Macroautophagy (autophagy) degrades proteins, other macromolecules, and organelles, in lysosomes and recycles the breakdown products to promote survival in stress and starvation. Autophagy is upregulated in some cancers and promotes survival and malignancy, suggesting that targeting autophagy in cancer may be therapeutically advantageous. Autophagy promotes tumor cell autonomous cancer in preclinical models by suppressing p53, apoptosis, senescence, and immune responses, and also by promoting metabolism and proliferation.

9:10 Context-Specific Regulation and Function of Autophagy, Therapeutic Food for Thought

Eric H. Baehrecke, Ph.D., Professor, Department of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School

Autophagy is an important cellular response to stress, and plays essential roles in development, immunity, cancer and neurodegeneration. Thus, autophagy is considered a promising target for disease therapies. Pioneering studies of yeast led to the identification of conserved core factors that regulate autophagy, but the role of autophagy in specific cell contexts within multi-cellular organisms has not been rigorously studied. Recent studies of how autophagy is regulated and contributes to distinct cell fates will be presented.

9:40 Networking Coffee Break with Poster Viewing

10:10 Regulation of Pexophagy

Vlad Denic, Ph.D., Professor, Molecular and Cellular Biology, Harvard University

10:40 FEATURED PRESENTATION: Autophagy, Metabolism and Cancer

Alec C. Kimmelman, M.D., Ph.D., Professor and Chair, Radiation Oncology, NYU Langone Medical Center

11:10 Sponsored Presentation (Opportunity Available)

11:40 Enjoy Lunch on Your Own

THERAPEUTICALLY MODULATING AUTOPHAGY

1:10 pm Chairperson's Remarks

Eric H. Baehrecke, Ph.D., Professor, Department of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School

1:20 The Investigation of Autophagy in Cancer Using Chemical Biology

Nicholas Cosford, Ph.D., Associate Director, Translational Research & Professor, Cancer Metabolism and Signaling Networks Program, NCI-Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute

Despite recent breakthroughs in the understanding of how ULK1 is activated by nutrient deprivation, how ULK1 promotes autophagy remains poorly understood. Using various chemical biology approaches, we identified and characterized a potent ULK1 small molecule inhibitor. The compound SBI-0206965 is a highly selective ULK1 kinase inhibitor in vitro and suppresses ULK1-mediated phosphorylation events in cells, regulating autophagy and cell survival. This presentation will describe our efforts to date on the validation of autophagy inhibition.

1:50 Targeting Autophagy in Cancer

Jeff MacKeigan, Ph.D., Professor, College of Human Medicine, Michigan State University

In recent years, autophagy has emerged as an important therapeutic target. In response to environmental, therapeutic, and oncogenic stress, cancer cells upregulate autophagy and also demonstrate an increased dependence upon this intracellular recycling process. Many cancers still lack targeted therapeutic options, and autophagy inhibitors are a promising and emerging anti-cancer target. We present the therapeutic development of autophagy inhibitors from early lysosomotropic agents to next-generation lysosome-targeted drugs to kinase-directed targets.

2:20 Targeting the Lysosome in Cancer

Ravi Amaravadi, M.D., Associate Professor, Medicine, University of Pennsylvania

The anti-tumor efficacy of the second-generation dimeric chloroquine Lys05 has now been demonstrated by a number of laboratories. A new series of third-generation longer linkered dimeric chloroquines such as DC661 demonstrate substantial improvements in potency compared to Lys05. Finally the dimeric quinacrine DQ661 concurrently inhibits mTOR and autophagy. The molecular target of dimeric chloroquine derivatives was pulled down using multiple DC and DQ-photoaffinity probes. This lysosomal enzyme could play a critical role in multiple oncogenic pathways.

2:50 Networking Refreshment Break with Poster Viewing

3:30 Inhibitors of Vps34 in Cancer Treatment

Jessica Martinsson, Ph.D., Vice President, Medicinal Chemistry, Sprint Bioscience AB

We have developed potent and selective inhibitors of Vps34 with excellent drug properties. The compounds are potent inhibitors of autophagy, affecting cellular metabolism and oxygen consumption. With these compounds, we have shown the relevance of autophagy inhibition in TNBC and investigated its role in immune response.

4:00 Discovery of Novel TAOK2 Inhibitor Scaffolds from High-Throughput Screening

Malia B. Potts, Ph.D., Assistant Member, Cell and Molecular Biology, St. Jude Children's Research Hospital

A synthetic lethal screen performed using a NSCLC (non-small cell lung cancer) cell line, and a second screen identifying potential modulators of autophagy have implicated TAOK2 as a potential cancer therapeutic target. Using a 200,000 compound high throughput screen, we identified three specific small molecule compounds that inhibit the kinase activity of TAOK2. These compounds also showed inhibition of autophagy. Based on SAR (structure-activity relationship) studies, we have predicted the modifications on the reactive groups for the three compounds.

4:30 Targeting Autophagy for Cancer Therapy

Johara Chouitar, Ph.D., Scientist, Millennium Pharmaceuticals, The Takeda Oncology Company

5:00 Close of Symposium

5:00 Pre-Conference Dinner Short Course Registration

Click here for details on short courses offered.

* 活动内容有可能不事先告知作更动及调整。

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