New Ways to Tackle COPD and Other Chronic Pulmonary Diseases


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WEDNESDAY, NOVEMBER 3

12:20 - 1:30 pm Conference Registration

 

New Pathways And Molecular Targets For Treating COPD

1:30 Chairperson’s Remarks

 

1:40 KEYNOTE PRESENTATION: Overcoming Steroid Insensitivity in COPD 

Ian AdcockIan Adcock, Ph.D., Professor, Respiratory Cell & Molecular Biology, Airways Disease Section, National Heart and Lung Institute and Faculty of Medicine, Imperial College, London 

COPD is characterized by an enhanced and uncontrolled inflammatory response. Crucially, COPD is poorly controlled by current anti-inflammatory therapies including glucocorticoids. Elevated lung oxidant burden and activation of key pathways that impinge upon GR function such as p38 MAPK, NF-κB and IL-17 may drive this insensitivity. In addition, the expression and activity of the GR co-repressor protein histone deacetylase 2 (HDAC2) is reduced in COPD in response to oxidative stress possibly due to elevation of the phosphoinositol 3-kinase (PI3K)δ signaling pathway. Importantly, blockade of PI3Kδ or p38 MAPK in primary cells from disease or in disease models restores glucocorticoid function. Selective inhibition of these pathways may provide a therapeutic strategy in COPD both as a novel anti-inflammatory and as a combinatorial therapy with glucocorticoids.

2:40 Autophagy in COPD 

Augustine Choi, M.D., Department of Medicine, Harvard Medical School and Chief, Pulmonary and Critical Care Medicine, Brigham And Women’s Hospital

Chronic obstructive pulmonary disease (COPD) is a debilitating disease caused by chronic exposure to cigarette smoke (CS), which involves airways obstruction and alveolar loss (emphysema). Our previous studies demonstrated elevated autophagy in human COPD lung, and as a cellular and tissue response to CS exposure in experimental model of emphysema in vivo. We identified the autophagic protein microtubule associated protein-1 light chain-3B (LC3B) as a positive regulator of CS-induced lung epithelial cell death. We now extend these initial observations to explore the mechanism by which LC3B mediates CSinduced apoptosis and emphysema development in vivo. Here, we observed that LC3B-/- mice demonstrated significantly decreased levels of apoptosis in the lungs after CS exposure, and displayed resistance to CS-induced airspace enlargement, relative to wild-type littermate mice. We found that LC3B associated with the extrinsic apoptotic factor Fas in lipid rafts in an interaction mediated by caveolin-1 (Cav-1). The siRNA-dependent knockdown of Cav-1 sensitized epithelial cells to CS-induced apoptosis, as evidenced by enhanced DISC formation and caspase activation. In conclusion, we demonstrate a pivotal role for the autophagic protein LC3B in CS-induced apoptosis and emphysema, suggestive of novel therapeutic targets for COPD treatment.    

3:10 Networking Refreshment Break in the Exhibit Hall
**Drop off a business card at CHI’s Sales Booth in the Exhibit Hall for a chance to win an iPod®!

3:45 Talk Title to be Announced

J. David Farrar, Ph.D., Associate Professor, Department of Immunology, University of Texas Southwestern Medical Center

4:15 Sponsored Presentation (Opportunity Available)

4:45 A Decoy CXCL8 Shows Potent Anti-Inflammatory Activity in Murine Lung Inflammation Models of COPD

Andreas J. Kungl, Ph.D., CSO, ProtAffin Biotechnologie AG

Neutrophils play a fundamental role in several chronic lung diseases including COPD and cystic fibrosis. Among the mediators of neutrophil recruitment into the lung, the chemokine CXCL8 is considered to be the major player. CXCL8 exerts its chemotactic activity by binding to its GPCR receptors located on the neutrophils, as well as through interactions with co-receptors located on the inflamed endothelium, the socalled glycosaminoglycans (GAGs). We have engineered higher affinity for GAG binding into human CXCL8 thereby obtaining a protein-based inhibitor for the CXCL8/GAG interaction. By additionally knocking-out the GPCR domain of the chemokine, we obtained a decoy protein (termed PA401) with potent anti-inflammatory characteristics. PA401 has been tested in murine models of lung inflammation induced by lipopolysaccharide and tobacco smoke in which the compound showed strong dose-dependent reduction of BAL neutrophils after intravenous and subcutaneous administration at doses of 40 and 400μg/kg. PA401 is therefore considered a new promising biologic therapeutic with a novel mechanism of action for interfering with lung inflammation.    

5:15 PANEL DISCUSSION: What Are the Biggest Challenges in COPD Over the Next Decade?

Moderator: Augustine Choi, M.D., Department of Medicine, Harvard Medical School and Chief, Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital

5:45 End of Day


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SPONSORSHIPS & EXHIBITS 

The exhibit hall was sold out in 2014, so please contact us early to reserve your place. To customize your sponsorship or exhibit package for 2015, contact:

Jon Stroup
Sr. Business Development Manager
781-972-5483
jstroup@healthtech.com 


 

September 21 

Next-Generation Histone Deacetylase Inhibitors Symposia 

Strategies for Rare Diseases Symposia 

September 22 

Developing CRISPR-Based Therapies Symposia 

September 22 - 23 

Targeting Epigenetic Readers and Chromatin Remodelers 

Targeting the Ubiquitin Proteasome System 

Targeting the Microbiome 

GPCR - Based Drug Discovery - Part 1 

Antibodies Against Membrane Protein Targets - Part 1 

RNAi for Functional Genomics Screening 

Gene Therapy Breakthroughs 

Targeting Ocular Disorders 

September 23 - 24 

Targeting Histone Methyltransferases and Demethylases 

Targeting the Unfolded Protein Response 

Kinase Inhibitor Discovery 

GPCR-Based Drug Discovery - Part 2 

Antibodies Against Membrane Protein Targets - Part 2 

New Frontiers in Gene Editing 

Quantitative Systems Pharmacology 

Short Courses 

SC1: Cancer Metabolism: Pathways, Targets and Clinical Updates 

SC2: Leveraging Data and Analytics for Drug DiSCovery 

SC3: Setting Up Effective Rnai SCreens: From Design to Data to Validation 

SC4: Phenotypic SCreening and Chemical Probe Development 

SC5: GPCR Structure-based Drug Discovery 

SC6: Targeting of GPCRs with Monoclonal Antibodies 

SC7: Setting Up Effective Functional SCreens Using 3D Cell Cultures 

SC8: Targeting Protein-protein Interactions: Biophysical Approaches 

SC9: Preclinical Animal Models for Ocular Indications 

SC10: Introduction to Allosteric Modulators and Biased Ligands of GPCRs 

SC11: Introduction to Targeted Covalent Inhibitors 

SC12: Assays and High-throughput SCreening for Novel Epigenetic Inhibitors 

SC13: Gamification and Drug Target Challenges 

SC14: A Primer to Gene Editing: Tools and Applications 

SC15: Using Mechanistic Physiological Models In Drug Development