7 gpcr-based drug discovery · 2018-02-03 · 3 ubiquitin pathway 8 functional genomics 4 histone...

Sunday, September 3012:00 - 3:00 pm• UnderstandingStructure- andFragment-BasedDrug Discovery:ToolsandTechniques

3:30 - 6:30 pm• Pre-ClinicalToxicity

• UnderstandingandTargeting Protein-ProteinInteractions

Tuesday, October 2 6:30 - 9:00 pm•AllostericModulators: PuttingTheorytoPractice

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GPCR-BasedDrugDiscovery


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TargetingCancerCellMetabolism

Sunday, September 30

12:00 - 3:00 pmUnderstanding Structure- and Fragment- Based Drug Discovery: Tools and Techniques (SC1)Course Instructor:Daniel A. Erlanson, Ph.D.,Co-Founder, Carmot Therapeutics, Inc. Alex Burgin, Ph.D., CSO, Emerald BiostructuresAdditional Instructors to be Announced

3:30 - 6:30 pmPre-Clinical Toxicity (SC2)Course Instructor:James Dykens, Ph.D., CEO, Eyecyte TherapeuticsAdditional Instructors to be Announced

Understanding and Targeting Protein-Protein Interactions (SC4)Course Instructors:Sandor Vajda, Ph.D., Professor, Biomedical Engineering and Chemistry, Boston UniversityAdrian Whitty, Ph.D., Associate Professor, Chemistry, Boston University

tueSday, OctOber 2

6:30 - 9:00 pmDINNER SHORT COURSE: Allosteric Modulators: Putting Theory to Practice (SC6)Course Instructors: Arthur Christopoulos, Ph.D., Professor, Department of Pharmacology, Monash UniversityAnnette Gilchrist, Ph.D., Assistant Professor, Pharmaceutical Sciences, Midwestern University

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October 31 GPCR-Based Drug Discovery 6 Allosteric Modulators

2 Kinase Inhibitors 7 PI3K Pathway

3 Ubiquitin Pathway 8 Functional Genomics

4 Histone Deacetylases 9 Histone Methyltransferases and Demethylases

5 Cancer Cell Metabolism 10 Diabetes Targets

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GPCR-BasedDrugDiscoveryProgressing through Signaling Complexities

mOnday, OctOber 1

7:00 am Conference Registration and Morning Coffee

New Structural Insights8:30 Chairperson’s Opening Remarks

8:40 FEATURED PRESENTATION

Crystal Structure of a Lipid G Protein-Coupled ReceptorMichael Hanson, Ph.D., Director, Structural Biology, Receptos

9:10 Nanobodies for the Structural Analysis of GPCR Transmembrane SignalingJan Steyaert, Ph.D., Professor, Structural Biology Department, Vrije University of BrusselsNanobodies are small (15 kDa) and stable single domain fragments harboring the full antigen-binding capacity of the original heavy chain only antibodies that naturally occur in Camelids. Because of their unique three-dimensional structure, nanobodies have access to cavities or clefts on the surface of proteins. We identified nanobodies thatstabilizetheb2AR•Gscomplex.Oneofthesenanobodieswasused to obtain the high-resolution crystal structure of this complex, providing the first view of transmembrane signaling.

9:40 How Drugs Bind and Control Their Targets: Characterizing GPCR Signaling through Long-Timescale SimulationRon Dror, Ph.D., Senior Research Scientist, D. E. Shaw ResearchWe report on GPCR-related results from our special-purpose machine that accelerates molecular dynamics simulations of biomolecular systems. Unbiased simulations in which drugs spontaneously associate with GPCRs to achieve bound conformations that match crystal structures almost perfectly are now possible (Nature 482:552-6, 2012). Simulations have also captured transitions of the β2-adrenergic receptor between its active and inactive states, allowing us to characterize the mechanism of receptor activation.

10:10 Coffee Break in the Exhibit Hall with Poster Viewing

Screening Strategies10:40 TECHNOLOGY PANEL: Tools and Assays for Probing Orphan and Non-Orphan GPCRsModerator: Neil Burford, Senior Research Investigator II, Lead Discovery & Profiling, Molecular Sciences and Candidate Optimization, Bristol-Myers Squibb Company

(Sponsored panel opportunities available)

11:10 Optical Micro-Spectroscopy Sponsored by Instrumentation and its Application to the Determination of the Quaternary Structure and Distribution in Living Cells of GPCR Homo-OligomersValerica Raicu, Ph.D., Associate Professor, Physics, University of Milwaukee Wisconsin

This presentation will introduce a novel micro-spectroscopic technique for FRET-based determination of the quaternary structure and localization in living cells of membrane protein complexes and will review results obtained from our recent studies of several G protein-coupled receptors (GPCRs) in living cells.

11:25 Sponsored Presentations (Opportunities Available)11:40 Screening Case Studies Using Label Free ApproachesHong Xin, Ph.D., Scientist/Technologist, Lead Generation, Johnson & Johnson PRD

12:10 pm Presentation to be Announced12:40 LUNCHEON PRESENTATION Sponsored by Investigating Receptor Biology Using PathHunter® Technology: Application to GPCR Trafficking and InternalizationLiz Quinn, Ph.D., Marketing Director, LeadHunter Discovery Services, DiscoveRxThe PathHunter system has been employed to monitor protein interactions and translocation in a cell-based, HTS-friendly format. This technology enables the generation of cellular assays for intractable targets and simplifies detection of cellular signaling events using a simple, one-step chemiluminescent protocol. We previously commercialized >220 GPCR targets that monitor receptor activity through Arrestin recruitment. Here, we discuss the application of the technology to receptor trafficking in response to pharmacochaperone activity and receptor internalization in response to agonist activation.

GPCR-Targeted Drug Candidates2:20 Chairperson’s Remarks2:25 Discovery of an Orally Available Prostacyclin (PGI2) Receptor Agonist for the Treatment of Pulmonary Arterial HypertensionGraeme Semple, Ph.D., Vice President, Discovery Chemistry, Arena Pharmaceuticals, Inc.The design and optimization of new prostacyclin receptor agonists with oral activity in rat models of pulmonary arterial hypertension will be described. As well as in vitro and in vivo potency, special attention was paid to pharmacokinetic parameters eventually resulting in the discovery of the clinical candidate, APD811.

2:55 Case Study in Quantifying Potency and Mode of Action of a Small Molecule Antagonist of a Class B Receptor, CRF1Simeon Ramsey, Ph.D., Senior Principal Scientist, Inflammation, PfizerThis presentation will highlight the utility of a non-equilibrium receptor-ligand binding assay to quantify the binding kinetics of small molecule antagonists to the CRF1 receptor and how data from this platform was used to explain apparent non-competitive, insurmountable antagonism observed in cell based functional assays. It also demonstrates how these kinetic data can be used to design, interpret and predict in vivo receptor occupancy.

3:25 Refreshment Break in the Exhibit Hall with Poster Viewing


4:05 Orexin Receptors and the Physiology/Pharmacology of SleepTimothy Lovenberg, Ph.D., Senior Research Fellow, Neuroscience, Johnson & Johnson La JollaThis talk will cover the distinct roles of Orexin-1 and Orexin-2 receptors in the sleep-inducing effects of Orexin receptor antagonists.

4:35 Targeting Novel Regulatory Mechanisms of PDE4 as Potential New Treatments for Mood DisordersJames A. Bibb, Ph.D., Associate Professor, Departments of Psychiatry, Neurology and Neurotherapeutics, University of Texas Southwestern Medical CenterA new regulatory mechanism by which PDE4 is activated in brain will be presented as a novel target for therapy development. We will demonstrate the antidepressant effects of disrupting this mechanism using small interfering peptides in animal paradigms modeling depression. This may be the first demonstration that it is sufficient to target cAMP/PKA activity in the nucleus accumbens to achieve antidepressant-like effects. Our results underscore the potential of selectively targeting intracellular signaling mechanisms for drug development.

5:05 Interactive Breakout Discussion GroupsSharing Orphan Receptor StrategiesModerator: Neil Burford, Senior Research Investigator II, Lead Discovery & Profiling, Molecular Sciences and Candidate Optimization, Bristol-Myers Squibb Company

Exploiting Ligand-Biased SignalingModerator to be Announced

Using Native Cell LinesModerator to be Announced

6:15 – 7:30 Welcome Reception in the Exhibit Hall with Poster Viewing

tueSday, OctOber 2

7:30 am Breakfast Presentation (Sponsorship Opportunity Available) or Morning Coffee

GPCR-Targeted Drug Candidates (Continued)8:15 Chairperson’s Opening Remarks8:20 Pimavanserin – a 5-HT2A Inverse Agonist with Large Potential Therapeutic UtilityUli Hacksell, Ph.D., CEO, Acadia PharmaceuticalsWhen investigating what GPCR receptors were blocked or activated by existing CNS drugs and their metabolites, we discovered that all modern (atypical) antipsychotic drugs were acting as inverse agonists on 5-HT2A receptors, a receptor activity not shared by the less well tolerated older (typical) antipsychotics. Having established this key role of 5-HT2A inverse agonism, we decided to develop a selective 5-HT2A inverse agonist. Optimization of the lead compound identified by uHTS led to the discovery of pimavanserin. This drug candidate is currently in Phase III development for Parkinson’s disease psychosis. Pimavanserin has also demonstrated impressive clinical efficay in sleep maintenance and schizophrenia. Throughout 15 completed clinical trials, pimavanserin has demonstrated an attractive safety and tolerability profile.

8:50 Examining the Therapeutic Potential of CCR1 Antagonists for Multiple MyelomaAnnette Gilchrist, Ph.D., Assistant Professor, Pharmaceutical Sciences, Midwestern UniversityAntagonists for chemokine receptor CCR1 were developed for rheumatoid arthritis and multiple sclerosis. However, we hypothesize they might also be useful for multiple myeloma (MM). MM results from malignant plasma cell growth, with abnormal plasma cells accumulating in the bone marrow resulting in increased osteoclastactivity and osteolytic bone disease. Using a variety of assays including osteoclast differentiation, metabolism, interleukin-6 production, and ability to induce myeloma cell migration, we have evaluated several chemokine CCR1 antagonists.

9:20 Sponsored Presentation (Opportunity Available)9:50 Coffee Break in the Exhibit Hall with Poster Viewing10:40 Mechanisms Underlying Antagonism of the Glucagon Receptor by Therapeutic AntibodiesChristopher Koth, Ph.D., Scientist, Structural Biology, GenentechInhibitors of the glucagon receptor (GCGR) are of considerable therapeutic interest as elevated glucagon levels promote hyperglycemia in diabetes. We report the crystal structure of the GCGR ectodomain (ECD) in complex with the Fab fragment of an inhibitory antibody, providing a unique insight into its mechanism of action. We also elucidated the mechanisms of action of two additional antibodies, including one with inverse agonist activity.

11:10 GPR119: Expanding Your Lead Options by Changing the ConstantKim McClure, Ph.D., Senior Principal Scientist, PfizerThis presentation provides an example of lead expansion in the highly competitive GPR119 agonist area. It emphasizes the potentially greater value obtained in replacing the more prevalent region of the pharmacophore to known agonists. The talk also details the use of conformation vs. pharmacology as a means of guiding the structural differentiation. The synthesis and pharmacology of 2,6-diazatricyclo[3.3.1.13,7]decane based GPR119 agonists is described.

11:40 Label-Free Assays to Discover and Characterize Small Neutralizing Molecules Targeting Chemokines/Cytokines that Bind to GPCRsJean Luc Galzi, Ph.D., Research Director, School of Biotechnology, CNRS, University of StrasbourgChemokines and cytokines are small signaling proteins, many which act on GPCRs, with sufficiently rigid structures to harbor binding sites for small chemical ligands. Chemical libraries can be successfully screened to identify ligands that bind to chemokines or cytokines and block their binding to their receptors through a mechanism of action that is reminiscent of many human pathogens including viruses, bacteria and parasites. The presentation will describe the discovery of such neutralizing molecules, also named neutraligands, and their usefulness for in vitro and in vivo studies of allergic diseases, carcinogenesis, or susceptibility to parasite infections. The targeting of ligands, rather than receptors, by chemical compounds, is complementary to the traditional anti-receptor strategy.

12:10 pm Close of Conference




TargetingCancerCellMetabolismStrategies for Starving a Tumor

mOnday, OctOber 1

7:00 am Conference Registration and Morning Coffee

Perspectives and Progress8:30 Chairperson’s Opening Remarks

» 8:40 KeynOte preSentatIOnIntegrating Cancer Metabolism, Autophagy, and the Tumor Microenvironment to Achieve Personalized Cancer TreatmentMichael P. Lisanti, M.D., Ph.D., Director and Chair, Stem Cell Biology and Regenerative Medicine Center; Landenberger Endowed Professor in Breast Cancer Research; Professor of Cancer Biology, Medical Oncology, and Biochemistry, Kimmel Cancer Center, Thomas Jefferson UniversityDr. Lisanti will discuss a new model of cancer metabolism, which is paradigm shifting.

9:10 Metabolism as a Key Component of Systems Biology for Targeting CancerMichael Su, Ph.D., Senior Vice President, R&D, Agios PharmaceuticalsThis presentation provides a better understanding of the pioneering research being conducted in the space and the first-in-class anticancer drugs that will “starve” cancer cells by interrupting the metabolic processes that fuel their growth. It will be presented how this new frontier of boundary-breaking science has the potential to uncover treatments with the potential to change patients’ lives.

9:40 A New View of CancerDavid W. Moskowitz, M.D., M.A., FACP, CEO, GenoMed, Inc.The prevailing view of sporadic cancer is that it arises from mutations in somatic cells, and that the secret to curing cancer lies in the tumor. We have found thousands of cancer-associated SNPs in the germline of cancer patients. This suggests that cancer arises when tissue stem cells, sensing tissue atrophy, begin proliferating but fail to differentiate properly. Differentiation within the adult organism is more difficult than in the embryo because of the absence of fields of transcription factors. Our SNPs provide targets for non-toxic differentiation therapy.


Targeting Glucose Metabolism10:40 Glucose Metabolism in Human Brain TumorsElizabeth Maher, M.D., Ph.D., Associate Professor, Theodore H. Strauss Professorship in Neuro-Oncology, Southwestern Medical Center

11:10 Multiplex Analysis of Cellular Sponsored by Metabolism Pathways Using MILLIPLEX® MAP PanelsKelly Barrett, Field Application Scientist, EMD Millipore Corporation Cellular metabolism is the set of processes that convert biochemical energy into ATP. Significant progress has been made in understanding links between cellular metabolic pathways and diverse conditions (i.e. diabetes, AD, PD, cancer, aging). These pathways have drawn renewed interest in the research community. EMD Millipore has developed a series of innovative multiplex immunoassay panels based on the Luminex® xMAP® platform. These panels enable quantitative detection of multiple proteins simultaneously and are valuable tools in the study of diverse biological processes. We will provide an overview of the multiplex technology and present application data from selected MILLIPLEX® MAP Cellular Metabolism panels, such as PDH Complex, FAO, and OXPHOS.

11:25 Sponsored Presentations (Opportunity Available)

11:40 Chloroacetaldehyde, an Ifosfamide Metabolite, Inhibits Cell Proliferation and Glucose Metabolism without Decreasing Cellular ATP Content in Human Breast Cancer Cells MCF7Gabriel Baverel, Ph.D., Professor, CEO, CSO, Metabolomics, Metabolys, Inc.Chloroacetaldehyde, a metabolite of the widely used anticancer drug ifosfamide, inhibits cell proliferation and specific steps of glucose metabolism but does not decrease cellular ATP content in human breast cancer cells MCF7.

12:10 pm Glycolytic Cancer Cells Lacking 6-Phosphogluconate Dehydrogenase Metabolize Glucose to Induce SenescenceBarden Chan, Ph.D., Instructor, Medicine, Beth Israel Deaconess Medical CenterWe show that knockdown of 6-phosphogluconate dehydrogenase (6PGD) of the pentose phosphate pathway (PPP) inhibits growth of gefitinib-resistant lung cancer cells (H1975) by senescence induction. This inhibition is not due to a defect in the oxidative PPP per se. Significantly, G6PD knockdown rescues proliferation of cells lacking 6PGD, suggesting accumulation of growth inhibitory glucose metabolics in cells lacking 6PGD. Therefore, 6PGD inhibition may provide a novel strategy to treat glycolyic tumors such as lung cancer.

12:40 Luncheon Presentation (Sponsorship Opportunity Available) or Lunch on Your Own

The Warburg Effect2:20 Chairperson’s Remarks


2:25 The Use of Warburg Effect Indicators Such as FDG PET Avidity to Identify Lymphoma Patients Who May Be Candidates for Definitive Ultra Low Dose (2 Gy X 2) RadiotherapyRoger Macklis, M.D., Professor of Medicine, Radiation Oncology, Cleveland ClinicThe absence of the Warburg switchover in cell metabolism is an indicator of potentially intact p53 status and may thus be a proxy for high cellular radiosensitivity and immunoresponsiveness in patients with sensitive disease.

Targeting the Mitochondrial Metabolism

2:55 Targeting Mitochondrial Bioenergetics Potently Induces Cell Death in Stem-Like Ovarian Cancer CellsAyesha B. Alvero, M.D., M.S., Associate Research Scientist, Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of MedicineOvarian tumors are comprised of a heterogenous population of cells with distinct growth and survival requirements as well as unique chemoresistant characteristics. CD44+ ovarian cancer cells exhibit stem-like properties and are inherently chemoresistant to currently available agents. Elaboration of a unique mitochondrial and metabolic profile in these cells identifies a novel therapeutic option.

3:25 Refreshment Break in the Exhibit Hall with Poster Viewing4:05 Targeting Mitochondria for Cancer Therapy: Exploiting Cancer Cell Metabolism to Develop Combination TherapyCharles E. Wenner, Ph.D., Professor, Member, Molecular and Cellular Biology, Roswell Park Cancer InstituteRecent advances in the understanding of the role of sirtuins in metabolic diseases such as cancer offer new opportunity to develop therapeutic approaches which are based on reprogramming of the Warburg Effect.

4:35 Lipoate Analogs: Powerful Chemotherapeutic Agents Attacking Cancer Cell MetabolismPaul M. Bingham, Ph.D., Vice President, Research, Cornerstone Pharmaceuticals; Professor, Biochemistry and Cell Biology, Stony Brook UniversityLipoate is a uniquely pivotal molecule, having both indispensable catalytic and regulatory functions in mitochondrial metabolism. These regulatory functions include components systematically reconfigured during malignant transformation, allowing analogs of lipoate to selectively attack tumor cell metabolism. I will discuss progress on the mechanism and clinical efficacy of this novel drug family.

5:05 Interactive Breakout Discussion GroupsStrategic Planning of How to Starve a TumorModerator: Michael Su, Ph.D., Senior Vice President, R&D, Agios PharmaceuticalsChallenges of Targeting the Mitochondrial MetabolismModerator: Paul M. Bingham, Ph.D., Vice President, Research, Cornerstone Pharmaceuticals; Professor, Biochemistry and Cell Biology, Stony Brook UniversityUnderstanding the “Biology” of Novel Ligand Binding SitesModerator: Marc O’Reilly, Ph.D., Associate Director, Structural Biology, Astex Pharmaceuticals

6:15 – 7:30 Welcome Reception in the Exhibit Hall with Poster Viewing

tueSday, OctOber 2

7:30 am Breakfast Presentation (Sponsorship Opportunity Available) or Morning Coffee

Strategies to Inhibit Cell Proliferation8:15 Chairperson’s Opening Remarks

8:20 The Histone Deacetylase SIRT6 Modulates Glucose Homeostasis and Cancer MetabolismRaul Mostoslavsky, M.D., Ph.D., Assistant Professor, The Massachusetts General Hospital Cancer Center, Harvard Medical SchoolOur work demonstrated that the chromatin deacetylase SIRT6 functions to inhibit expression of glycolytic genes, in this way controlling glucose utilization in cells. Cancer cells appear to inhibit SIRT6 expression, and such inhibition plays a critical role, allowing tumor cells to switch towards aerobic glycolysis, as described by Otto Warburg years ago. Our studies provide direct evidence that SIRT6 functions as a tumor suppressor, modulating glucose utilization and protecting against the Warburg effect.

8:50 Molecular Therapy for Liver Cancer by Targeting GAPDH: Thinking the UnthinkableJean-Francois Geschwind, M.D., Professor, Director, Interventional Radiology Division, Radiology & Radiological Sciences, Johns Hopkins University School of MedicineTargeting tumor metabolism has long been considered a potential effective therapeutic strategy for cancer. We have identified the glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as the principal target of the antiglycolytic agent, 3-bromopyruvate (3-BrPA). Furthermore, targeting GAPDH is sufficient to block tumor progression. As GAPDH is present ubiquitously, we demonstrated that targeted-delivery of GAPDH antagonists directly into the tumor under image guidance destroyed the tumor without causing systemic toxicity.

9:20 Sponsored Presentation (Opportunity Available)


10:40 Presentation to be Announced

11:40 The Use of Fragment Based Screening to Identify Novel Modulators of Human PKM2 ActivityMarc O’Reilly, Ph.D., Associate Director, Structural Biology, Astex PharmaceuticalsThis talk provides insights into how to prosecute a fragment based screen versus a highly challenging and biologically complex target.

12:10 pm Close of Conference


TUESDAY, OCTOBER 2

12:30 pm Conference Registration

Targets for New Diabetes Therapies1:30 Chairperson's RemarksClaire Steppan, Ph.D., Associate Research Fellow, Diabetes, Pfizer


Targeting Diabetes via Glucocorticoid Modulation: The Identification of Advanced 11b-HSD-1 InhibitorsJeffrey A. Robl, Ph.D., Executive Director, Metabolic Diseases R&D, Bristol-Myers Squibb

Preventing excess glucocorticoid tone in metabolically active tissues such as the liver and adipose may be beneficial in addressing glucose homeostasis and hyperglycemia in patients with type 2 diabetes. We have optimized a series of triazolopyridine based inhibitors resulting in the advancement of BMS-770767 to phase 2 clinical trials. The discovery of BMS-770767 will be presented as well as a description of its development properties, pharmacokinetics, and pre-clinical pharmacology profile.

2:10 Dyslipidemia Targets and DiabetesRebecca Taub, M.D., CEO, Madrigal Pharmaceuticals

2:40 Effects of PF-04620110, a Novel Diacylglycerol Acyl-Transferase 1 (DGAT1) Inhibitor on Healthy-Obese Volunteers and Type 2 Diabetic SubjectsClaire Steppan, Ph.D., Associate Research Fellow, Diabetes, PfizerInhibition of DGAT1, the terminal enzyme in the synthesis of triglycerides (TG), has been proposed for the treatment of type 2 diabetes (T2DM). We sought to examine the effects of a potent and selective DGAT1 inhibitor, PF-04620110, on vitamin A absorption, TG, glucose, insulin and total amide glucagon-like peptide-1 (GLP-1) levels in both healthy-obese volunteers and Type 2 Diabetic subjects. The results of these studies will be presented.


3:45 Pharmacological Manipulation of Diacyl Glycerol Acyl Transferase 1 Using Pre-Clinical ModelsShirly Pinto, Ph.D., CVD - Atherosclerosis Team Lead, Merck

Research Laboratories

4:15 Targeting the Ileal Brake with an Oral Mimetic of RYGBJerome J. Schentag, PharmD, Professor of Pharmaceutical Sciences, University at BuffaloReports of putative cures of T2D by RYGB surgery has led to a search for oral mimetics of these beneficial properties. T2D is controlled even before weight loss occurs, and even more surprisingly, it now seems clear that beneficial effects occur after RYGB even in patients without obesity. As an oral mimetic of RYGB surgery, Brake™ specifically targets the ileal Brake. When taken once daily, oral Brake™ treatment elicits the full range of hormonal mediator outputs and controls hyperglycemia, hyperlipidemia, and obesity. There was resolution of hepatic steatosis and NAFLD as added benefit.

4:45 Beneficial and Adverse Effects of Glucokinase Activators on Glucose Metabolism in Rat Liver CellsGabriel Baverel, Ph.D., CEO and CSO, Metabolomics, Metabolys, Inc.Using a metabolic flux approach, we show the potential beneficial and adverse effects of three gluco-kinase activator drug candidates for type2 diabetes. We report the gluco-kinase activators’ effects on glucose utilization and production, glycogen synthesis and degradation, lactic acid and triglyceride accumulation and on the citric acid cycle during glucose metabolism in rat liver cells. Our work illustrates the advantage of metabolic flux analysis for predicting early during the drug development process, both the efficacy and safety of very small amounts of antidiabetic drug candidates.

5:15 Connecting Mitochondrial Dysfunction and DiabetesJames Dykens, CEO, Eyecyte TherapeuticsMitochondrial dysfunction contributes via bioenergetic and oxidative mechanisms to a host of degenerative and metabolic diseases, including diabetes. Mitochondrial Ca2+ dynamics alter insulin release, while production of free radicals yields dysregulation of glycolysis. Importantly, xenobiotic therapies for diabetes, e.g., biguanides and thiazolidinediones, directly undermine mitochondrial function thereby lowering blood glucose, albeit via an untoward mechanism. The latter results from cell culture conditions that model diabetes and anaerobic poise, not normal aerobic physiology.

5:45 End of Day


Diabetes Drug Discovery and BeyondTherapeutic Targets for Diabetes and Related Metabolic Disorders


Media Partners


WedneSday, OctOber 3

8:00 am Interactive Breakfast Breakout Discussion Groups

Targeting GPCRsModerator: Peter Cornelius, Ph.D., Director of Metabolic Diseases, SystaMedic, Inc.

Cardiovascular ChallengesModerator: Rebecca Taub, CEO, Madrigal Pharmaceuticals

Better Diabetes Models and MarkersModerator: Jerome J. Schentag, PharmD, Professor of Pharmaceutical Sciences, University at Buffalo

Targeting Membrane Proteins for Type2 Diabetes

9:05 Chairperson's RemarksPeter Cornelius, Ph.D., Director of Metabolic Diseases, SystaMedic Inc.


Discovery of Ertugliflozin: An Anti-Diabetic Agent from a New Class of SGLT2 InhibitorsVincent Mascitti, Ph.D., Senior Director, Pfizer Global R&D

Inhibition of sodium-dependent glucose co-transporter 2 (SGLT2), located in the kidney, promotes reduction of plasma glucose concentration. The medicinal and synthetic organic chemistry rationale that led to the rapid identification of Ertugliflozin (PF-04971729), an anti-diabetic agent currently in development and belonging to a new class of SGLT2 inhibitors bearing a dioxa-bicyclo[3.2.1]octane bridged ketal motif, will be presented.

9:40 Targeting FGF21 for Type 2 DiabetesAndrew C. Adams, Ph.D., Post-Doctoral Research Fellow, Diabetes Research, Lilly Research Laboratories


10:55 Update on the Clinical Candidate ARRY-981: A GPR119 AgonistBrad Fell, Senior Research Investigator, Medicinal Chemistry, Array BioPharmaGPR119 is a promising new target for the treatment of type 2 diabetes. Agonists of this GPCR, which promote insulin secretion from pancreatic ß-cells and GLP-1 release from enteroendocrine L-cells, provide a unique opportunity for a single drug to elicit insulin secretion via two distinct pathways. However, several GPR119 agonists have recently demonstrated poor clinical efficacy. We will discuss our novel GPR119 clinical candidate, ARRY-981, that has shown meaningful and durable glucose control in preclinical models of diabetes.

11:25 Inflammation, Obesity and Diabetes: Pre-Clinical Investigations of a CCR2 AntagonistDana Johnson, Ph.D., Senior Scientific Director, Drug Discovery, Janssen Pharmaceuticals, Johnson & JohnsonWith the growing idea of insulin resistance due, in part, to low grade systemic inflammation, mechanistic investigations aimed at altering inflammatory tone have been undertaken by us as well as others. Recruitment of the macrophage and continued activity in the adipose tissue appears to drive insulin resistance, in part, via the secretion of Moncocyte Chemoattractant Protein 1 (MCP-1) and its cognate receptor C-C Chemokine Receptor-2 (CCR2). Our efforts in disrupting the macrophage recruitment via the use of CCR2 antagonists will be presented.

11:55 Monoclonal Antibody Antagonists of the Glucagon Receptor as Therapeutic AgentsBernard B. Allan, Ph.D., Scientist, Department of Molecular Biology, Genentech, Inc.Excess glucagon signaling plays a key role in the development of hyperglycemia in type 1 and type 2 diabetic patients. We have generated potent anti-glucagon receptor antagonist antibodies and will present the mechanisms underlying their anti-diabetic activities in pre-clinical models, including their direct effects on hepatic glucose metabolism and indirect effects on beta-cell mass.

12:25 pm Sponsored Presentation (Opportunity Available)

12:40 Luncheon Presentation (Sponsorship Opportunity Available) or Lunch on Your Own

New Therapeutic Approaches1:55 Chairperson's RemarksJesper Gromada, Ph.D., Executive Director, Cardiovascular and Metabolic Diseases, Novartis Institutes for BioMedical Research

2:00 XMetA, an Allosteric Agonist Antibody to the Insulin Receptor that Selectively Activates Insulin Receptor Metabolic Signaling and Restores Glycemic Control in Mouse Models of DiabetesJohn Corbin, Ph.D., Associate Director, Molecular Interactions and Biophysics, Pre-Clinical Research, XOMAThe XMetA antibody represents novel drug class for the treatment of diabetes. XMetA has unique properties including selective partial agonism of insulin receptor metabolic signaling resulting in improvements in the disease state of both hyperinsulinemic insulin resistant and insulinopenic diabetic animals. The in vitro and in vivo data to be presented for XMetA will provide a clear demonstration of how allosteric modulation of the insulin receptor with a monoclonal antibody can translate to improvements in disease.


2:30 Phenotype-Driven Approaches towards Novel Beta-Cell Proliferative and Protective TherapiesBryan Laffitte, Ph.D., Associate Director, Genomics Institute of the Novartis Research FoundationType 1 and type 2 diabetes are characterized by a loss of beta cell mass. However, therapeutic options aimed at preservation or restoration of endogenous beta cell mass, are not currently available. We used phenotypic screening approaches for both small molecule and biologic agents to identify regulators of beta cell survival and beta cell proliferation. We report on several series of small molecules that induce beta cell proliferation and/or protect beta cells from various forms of stress and have potential as therapeutic options for both type 1 and type 2 diabetes.


3:40 Gastric Bypass in Mice as a Model for Target IdentificationVincent Aguirre, M.D., Ph.D., Assistant Professor, Internal Medicine, University of Texas Southwestern Medical CenterWe will discuss a mouse model of gastric bypass, which recapitulates effects of this procedure on body weight, body composition, glucose homeostasis, and stool energy observed in humans. The reproducibility of this model allows high-resolution comparison of effects of gastric bypass across genetic models using advanced methodologies, such as MRS metabolic flux, proteo metabolomics, and deep sequencing. As such, it enables targeted investigation of bypass-induced biological pathways and refined identification of novel pharmaceutical targets capable of mimicking beneficial effects of bariatric surgery.

4:10 Cell-Based Therapies to Treat DiabetesNorma Kenyon, Ph.D., Professor of Surgery, Microbiology and Immunology and Biomedical Engineering; Executive Director of the Wallace H. Coulter Center for Translational Research; School of Medicine, University of MiamiThis presentation will focus on the role of stem cell-based therapies to treat diabetes, highlighting the therapeutic potential of mesenchymal stem cells in diabetes. Our research group’s focus is on ways to transplant islet cells without the need for anti-rejection drugs, including the incorporation of stem cells into transplant protocols.

4:40 Discovery of Lorcaserin: A Selective5-HT2C Agonist for Weight ManagementGraeme Semple, Ph.D., Vice President, Discovery Chemistry, Arena Pharmaceuticals, Inc.Compelling evidence suggests that drugs which activate the 5-HT2C receptor cause weight loss and thus have potential for use as weight management agents. Because serotonin elicits a number of biological responses through modulation of other 5HT-related proteins, selectivity was a critical challenge particularly with respect to the closely related 5-HT2A and 5-HT2B receptors. This presentation outlines some of events, challenges and achievements that led to the discovery and development of lorcaserin.

5:10 Close of Conference

Hotel & Travel Information

conference Venue and Host Hotel: Boston Marriott Copley Place110 Huntington Ave.Boston, MA 02116Tel: 617-236-5800

room rate: $269 s/dreservation cutoff:September 4, 2012

Please visit our conference website to make your reservations online or call the hotel directly to reserve your sleeping accommodations. You will need to identify yourself as a Cambridge Healthtech Institute conference attendee to receive the discounted room rate with the host hotel. Reservationsmadeafterthecut-offdateorafterthegrouproomblockhasbeenfilled(whichevercomesfirst)willbeacceptedonaspace-andrate-availabilitybasis.Roomsarelimited,sopleasebookearly.

Flight discounts:

Special discounts have been established with American Airlines. • Call American Airlines 1-800-433-1790 and use Conference

code 13H2BN• Go to www.aa.com/group and enter Conference code 13H2BN

in promotion discount box• Contact our designated travel agent, Wendy Levine at 1-877-

559-5549 or [email protected]

car rental discounts:

Special rental discounts have been established with Hertz for this conference.• Call Hertz 1-800-654-3131 and use our Hertz Convention Number

(CV): 04KL0003• Go to www.hertz.com and use our Hertz Convention Number

(CV): 04KL0003


mailto:wendy.levine%40protravelinc.com?subject=Discovery%20On%20Target


Allosteric ModulatorsAn Emerging Strategy for Targeting GPCRs

TUESDAY, OCTOBER 2

12:30 pm Conference Registration

Allosteric Modulators of CNS Targets1:30 Chairperson’s RemarksAndrew Alt, Ph.D., Senior Research Investigator, Lead Discovery, Bristol-Myers Squibb

1:40 Development of an Amino-aza-benzimidazolone Class of mGluR2 Positive Allosteric Modulators for the Treatment of SchizophreniaJoseph Pero, Ph.D., Senior Research Chemist, Medicinal Chemistry, MerckUp-regulation of glutamatergic transmission in the forebrain has been associated with the symptomology of schizophrenia. Activation of the metabotropic glutamate receptor 2 (mGluR2) regulates glutamate hyperactivity and represents a novel approach toward the treatment of the disease. Positive allosteric modulators (potentiators) of mGluR2 may offer distinct advantages over orthosteric mGluR2/3 agonists due to their unique mode of action and selectivity. This talk will describe the discovery of a novel class of azabenzimidazolone-derived mGluR2 potentiators.

2:10 Challenges and Opportunities in the Development of Muscarinic Receptor Allosteric Modulators for SchizophreniaChristian Felder, Ph.D., Research Scientist, Neuroscience, Eli Lilly & Co.The development of allosteric modulators and agonists is beginning to solve the pharmacological selectivity challenge for small molecule development at highly homologous receptor families. Positive allosteric modulators (PAMs) have the added benefit of providing physiologic spatial and temporal regulation of natural neurotransmitter action. Though an innovative drug development opportunity, this approach is not without its challenges. Learnings will be discussed from the development of muscarinic small molecule discovery.

2:40 Interactions of Putative Endogenous Ligands with Metabotropic Glutamate (mGlu) Receptors in the BrainThomas E. Salt, Ph.D., Professor, Visual Neuroscience, University College of London Institute of OphthalmologyIn addition to L-glutamate, other endogenous substances (some of which belong to the kynurenine metabolism pathway) have been proposed as ligands (“endocoids”) of mGlu receptors. Disorders of these pathways could thus result in changes in mGlu receptor function contributing to pathophysiology of CNS/neurological disorders such as sensory/pain processes, cognitive processes, schizophrenia, and epilepsy. We have been investigating the

interactions of such endocoids with mGlu-mediated synaptic function and allosteric modulators in vivo and in vitro.


Allosterism by Design

» 3:45 KEYNOTE PRESENTATION: GPCR Allostery in the New Millennium: Lessons, Challenges and OpportunitiesArthur Christopoulos, Ph.D., Professor, Pharmacology, Monash University

It is now well accepted that G protein-coupled receptors (GPCRs) possess allosteric binding sites. However, the myriad behaviors ascribed to allosteric ligands reflect not only molecular drug-receptor properties, but also cell-dependent factors that sculpt the final observed response. This presentation will focus on the minimal expectations of allosteric modulator effects and approaches for differentiating the contributions of the host system to observed allostery in order to facilitate modulator classification, structure-activity relations and translational studies.

4:30 Sponsored Presentation (Opportunity Available)

4:45 Allosteric Modulators for Taste Receptors: A New Paradigm for Flavor DevelopmentGuy Servant, Ph.D., Director, Assay Development and HTS, Senomyx

5:15 Allosterism, Opioid Receptor Heteromers, and AntinociceptionWilliam P. Clarke, Ph.D., Professor, Department of Pharmacology, University of Texas Health Science CenterWe present evidence, from primary cell culture and behavioral experiments, that delta and kappa opioid receptors form functional heterodimers in peripheral sensory neurons and that orthosteric ligands for one receptor of the pair allosterically regulate responses to ligands for the other receptor. Moreover, a heteromer-selective antibody against the delta-kappa heteromer also appears to allosterically regulate the response to orthosteric ligands. Some of this work has been recently published (see Berg et al, Mol Pharm 81(2):264-272, 2012).

5:45 End of Day



WEDNESDAY, OCTOBER 3

8:00 am Interactive Breakfast Breakout Discussion Groups

Determining Selectivity/Ligand BiasModerator: Joseph Pero, Ph.D., Senior Research Chemist, Medicinal Chemistry, Merck

Allosterically Modulating CNS TargetsModerator: Thomas E. Salt, Ph.D., Professor, Department of Visual Neuroscience, University College of London Institute of Ophthalmology

Allosteric Kinase InhibitorsModerator: John Robinson, Ph.D., Senior Scientist, Medicinal Chemistry, Array

Modulation of GPCRs and Other Proteins9:05 Chairperson’s RemarksJoseph Pero, Ph.D., Associate Principal Scientist, Medicinal Chemistry, Merck

9:10 Biophysical Approach to Allosteric Site Discovery and Characterization of KinasesPratul Agarwal, Ph.D., Staff Scientist at Oak Ridge National LaboratoryAllosteric sites are of interest in drug design in discovery due to the potential of increased chemical space and reduction in side-effects. Currently, methodology that systematically identifies these allosteric sites of targets of interest are missing. We have developed a unique biophysics driven computational methodology that allow discovery, ranking and characterization of allosteric sites. This talk will show how we’ve applied the technology to protein kinases.

9:40 Allosteric Inhibitor of Kinesin Spindle Protein / Eg5John Robinson, Ph.D., Senior Scientist, Medicinal Chemistry, ArrayARRY-520 is an allosteric inhibitor of the non-GPCR, Kinesin Spindle Protein / Eg5, which is currently in multiple phase II clinical trials for multiple myeloma. Discovery and optimization of small molecule KSP inhibitors leading to ARRY-520 will be discussed.


10:55 Allosteric Modulators in Endogenous Cells: Effects on Activity and ExpressionJoan Ballesteros, Ph.D., CEO, Vivia Allosterics SLSome benefits from allosteric modulators vs standard agonists have been studied in the biologically relevant context provided by endogenously expressed receptors; pancreatic islet cells, and insulin secreting immortalized cell lines of both rat and human origin. We discovered that glucose upregulated expression of the GLP1 receptor in 50% of these cells. Continuous agonist exposure induced more profound effects on receptor function and internalization than our newly discovered nM potent allosteric compounds.

10:55 Allosteric Modulators in Endogenous Cells: Effects on Activity and ExpressionJoan Ballesteros, Ph.D., CEO, Vivia Allosterics SL

11:25 TECHNOLOGY PANEL: New Technologies and Assays for Probing Allosteric ModulationModerator: Andrew Alt, Ph.D., Senior Research Investigator, Lead Discovery, Bristol-Myers SquibbPanelists:Joan Ballesteros, Ph.D., CEO, Vivia Allosterics SLArthur Christopoulos, Ph.D., Professor, Department of Pharmacology, Monash UniversityChristian Felder, Ph.D., Research Scientist, Neuroscience, Eli Lilly & Co.

12:10 Single Cell Hit Discovery and Endogenous GPCR ValidationJoan Ballesteros, Ph.D., CEO, Vivia Allosterics SL

12:25 Summary from Breakout DiscussionsModerators from morning’s breakout groups

12:40 pm Luncheon Presentation (Sponsorship Opportunity Available) or Lunch on your own

Allosteric Modulators with Therapeutic Potential

1:55 Chairperson's Remarks

2:00 Update on Allosteric Modulators of mGluR4 for Parkinson’s DiseaseCarrie K. Jones, Ph.D., Assistant Professor, Pharmacology, Vanderbilt University Parkinson’s disease (PD) is a debilitating neurodegenerative disorder associated with severe motor impairments caused by the loss of dopaminergic innervation of the striatum. One emerging pharmacologic approach for the symptomatic treatment of PD is the development of selective positive allosteric modulators (PAMs) of the metabotropic glutamate receptor 4 (mGlu₄). This talk will review the recent discovery of a novel class of mGluR4 PAMs that have exciting antiparkinsonian-like effects in preclinical models of PD.

2:30 Generation and Characterization of a GABA BR- Focused Allosteric Modulator LibraryEmmanuel Sturchler, Ph.D., Senior Scientist, Department of Molecular Therapeutics, Scripps Research InstituteImpaired GABAB-R-mediated synaptic transmission underlies various nervous system disorders including addiction, epilepsy and cognitive dysfunction. By modulating the physiological GABA-induced cellular response, GABAB-R allosteric modulators (AMs) provide novel modes of efficacy that may facilitate the development of GABAB-R targeted therapeutic agents. In my presentation I will describe the approach that we employed to generate a GABAB-R- focused AM small molecule library and how this library was characterized using multiple cell-based assays and cell lines expressing either the human GABAB-R or its rat orthologue. The screening strategy presented here not only enables rapid hit expansion but also provides the framework for lead identification, lead confirmation, selectivity, and receptor functional analysis and helps bridge the gap between animal model and human compound efficacy.



3:40 Gevokizumab, a Therapeutic anti-IL- 1b Antibody with a Novel Allosteric Mechanism of ActionMarina Roell, Ph.D., Director, Molecular Interactions and Informatics, XOMAThe clinical-stage molecule gevokizumab has an allosteric MOA uncommon among antibody therapeutics, and unlike classical allosteric modulators, binds a ligand to modulate its receptor interaction kinetics. Furthermore, gevokizumab differentially modulates the affinity of the ligand for two different receptors, which could have implications for its activity in vivo. Its behavior both in binding and functional assays fits well to classic allosteric analyses. Biophysical data and clinical activity will be presented.

4:10 Allosteric Modulation of Cannabinoid Receptor to Produce Biased SignalingDebra Kendall, Ph.D, Professor, Molecular and Cellular Biology, University of ConnecticutThe cannabinoid CB1 receptor, a class A GPCR, binds orthosteric ligands such as CP55940 and ∆9-THC and triggers Gi-mediated

effects. ORG27569 has been identified as a positive allosteric modulator of CP55940 binding to CB1 yet acts as an antagonist of G protein coupling. The ORG27569-induced conformational change of the CB1 receptor leads to cellular internalization and downstream activation of ERK signaling in a G-protein independent manner, providing the first case of allosteric ligand-biased signaling via CB1 in HEK293 and neuronal cells.

4:40 Targeting Obesity with Negative Allosteric Modulators of CB1 Cannabinoid ReceptorGanesh Thakur, Ph.D., Assistant Professor, Pharmaceutical Sciences, Northeastern UniversityThe CB1 cannabinoid receptor is a validated therapeutic target for treating obesity and reducing associated cardiometabolic risk. However CB1 antagonists were withdrawn from the market due to associated undesirable CNS side effects. We are developing negative allosteric modulators of CB1 as a way to achieve greater selectivity and thus fewer side-effects. I present the SAR and lead optimization efforts and in vivo efficacy data of our candidate CB1 negative allosteric molecules.

5:10 Close of Conference

Co-located with

Session Topics:Exploring Translational ApplicationsTroubleshooting RNAi ScreensLeveraging Chemical Genomics Screens

Discussion Groups:• Best Practices in Setting Up siRNA

and shRNA Screens• Best Strategies for Tackling Off-Target Effects• Utilization of RNAi Screens

for Translational Work


Functional Genomics Screening StrategiesEffectively Utilizing RNAi and Chemical Genomics Screens to Drive Drug Discovery

Inaugural | October 1-2, 2012

Targeting the Ubiquitin PathwayDiscovery and Development of Novel Inhibitors

Session Topics:Ubiquitin PerspectivesTargeting the Proteasome SystemUbiquitin LigasesExploring Novel Strategies

Featured Presentation:Ubiquitin and ER Quality ControlHidde Ploegh, Ph.D., Member, Whitehead Institute for Biomedical Research, Professor of Biology, Massachusetts Institute of Technology

Ways toSAVE!

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Suggested Conference Packagesbest Value Includes access to 2 conferences

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Structure/Fragment Based Design + Kinase Structure/Function

Kinase Inhibitors PI3K Pathways

Allosteric Modulators GPCR Allosteric Modulators

Epigenetic Tools HDACs Histone Methyltransferases

Toxicity Cancer Cell Metabolism Allosteric Modulators

Structure/Fragment Based Design + Protein-Protein Interaction

Ubiquitin Allosteric Modulators

Structure/Fragment Based Design + Allosteric Modulators

GPCR Diabetes Targets

Conference DiscountsPRESENT A POSTER AND SAVE $50!Poster abstracts are due by August 24, 2012. Once your registration has been fully processed, we will send an email containing a unique link allowing you to submit your poster abstract. *CHI reserves the right to publish your poster title and abstract in various marketing materials and products.

REGISTER 3 - 4th IS FREE: Individuals must register for the same conference or conference combination and submit completed registration form together for discount to apply.Alumni Discounts (SAVE 20%)

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Each registration includes all conference sessions, posters and exhibits, food functions, and access to the conference proceedings link.

Handicapped Equal Access: In accordance with the ADA, Cambridge Healthtech Institute is pleased to arrange special accommodations for attendees with special needs. All requests for such assistance must be submitted in writing to CHI at least 30 days prior to the start of the meeting.

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Sunday, September 30 Tuesday, October 2

An Understanding of Structure- and Fragment- Based Drug Discovery: Tools and Techniques (SC1)

Setting Up Effective RNAi Screens: Getting from Design to Data (SC5)

Pre-Clinical Toxicity (SC2) DINNER SHORT COURSE: Allosteric Modulators (SC6)

Understanding Protein-Protein Interactions (SC4) DINNER SHORT COURSE: Epigenetic Drug Discovery Tools (SC7)

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October 1-2, 2012 October 2-3, 2012

1 GPCR-Based Drug Discovery 6 Allosteric Modulators

2 Novel Strategies for Kinase Inhibitors 7 Advances in Targeting the PI3K Pathway

3 Targeting The Ubiquitin Pathway 8 Functional Genomics Screening Strategies

4 Next-Generation Histone Deacetylase Inhibitors 9 Targeting Histone Methyltransferases and Demethylases

5 Targeting Cancer Cell Metabolism 10 Diabetes Drug Discovery and Beyond


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7th Annual | October 1-2, 2012GPCR-BasedDrugDiscovery

2nd Annual | October 1-2, 2012TargetingCancerCellMetabolism

5th Annual | October 2-3, 2012DiabetesDrugDiscoveryandBeyond

2nd Annual | October 2-3, 2012AllostericModulators

7 gpcr-based drug discovery · 2018-02-03 · 3 ubiquitin pathway 8 functional genomics 4 histone...

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