Select Conferences | Ion Channel Targets 2008

Agenda

Day One - 9 September

8:55am	Welcome
	Calcium Channels Chaired by David Triggle, New York State University at Buffalo
9:00am	Calcium Channels as Drug Targets. Plus Ca Change, Plus c’est la Meme Chose David Triggle, Professor, New York State University at Buffalo Calcium channel antagonists, including the prototypical diltiazem, nifedipine and verapamil, targeting specific sites on the L-type VGCC, have been widely employed as cardiovascular drugs for over 25 years. However, success in discovering equivalent small molecules that target the other classes of VGCC – T, P/Q, N and R – has been minimal. Does the problem lie with the target(s) or the molecules selected, or both?
9:30am	Functional Characterization of Store-Operated Calcium Channels in Primary Immune Cells by Automated Planar Patch-Clamp Peter Miu, Senior Scientist, Amgen The calcium release activated calcium channel plays an important role in immune cells. Amgen have characterized the native CRAC channels in primary immune cells using a planar patch-clamp instrument. The CRAC currents recorded by the planar patch-clamp instrument are comparable to those recorded by conventional patch-clamp method.
10:00am	Electrophysiological Characterization of Novel P2X₇ Antagonists Michelle Dourado, Senior Scientist, Evotec The P2X₇ receptor is expressed in cells of the immune system where it acts to promote release of pro-inflammatory cytokines. As a result it is a promising target for the treatment of inflammation and pain. Electrophysiological techniques have been used along with ligand binding and Calcium influx assays to characterize novel P2X₇ antagonists.
10:30am	Coffee Break and Networking in the Exhibition Hall
	Sodium Channels Chaired by David Triggle, New York State University at Buffalo
11:15am	Inhibitory Antibodies Targeting Nav1.8 Sodium Channels James Miller, Principal Scientist, Elan Pharmaceuticals Nav1.8 is a voltage-gated sodium channel expressed exclusively in nociceptive sensory neurons of dorsal root and trigeminal ganglia that participates in the transmission of nociceptive information. As such, this channel has attracted considerable attention as a target for analgesic therapeutics.
11:45am	Influence of Lipid Soluble Gating Modifier Toxins on Sodium Influx in Neocortical Neurons Thomas Murray, Professor/Chair of Pharmacology, Creighton University School of Medicine Recent work has focused on sodium channel gating modifiers, and their capacity to trigger sodium influx in cerebrocortical neurons. These studies utilize the sodium-sensitive dye SBFI and a FLEX station. Complimentary studies have assessed the influence of the same compounds on membrane potential using FMP Blue with the FLEX station.
12:15pm	Hypertension in P2Y₂ Receptor-Deficient Mice is Caused by Constitutive Activation of ENaC James Stockand, Associate Professor, University of Texas Health Science Center at Houston ENaC activity in the distal nephron controls blood pressure. ATP, acting in a paracrine manner via purinergic receptors, promotes tonic PI(4,5)P₂ metabolism to mitigate inappropriate increases in ENaC open probability. Loss of this purinergic regulation of ENaC leads to hypertension.
12:45pm	Lunch and Networking in the Exhibition Hall
1:45pm	Poster Viewing
	Therapeutics Chaired by Chuan-Chu Chou, Schering-Plough Research Institute
2:30pm	Ion Channel Panels for Safety Assessment and Drug Discovery Arthur "Buzz" Brown, President & CEO, ChanTest Corporation ChanTest have developed a library of ion channel-expressing cell lines. They assemble the “books” by tissue, disease or family into channel panels and use automated patch clamp to screen panels for drug safety and efficacy. Case studies are presented.
3:00pm	Ion Channel-Based Drug Discovery: Opportunities and Challenges Chuan-Chu Chou, Fellow, Schering-Plough Research Institute This presentation will address the issues that concerned pharmaceutical companies about ion channel-based drug discovery that are fact-based and perception-based. Examples will be used to support the value and the practicality of re-positioning ion channels to a favorable class of therapeutic targets.
3:30pm	Coffee Break and Networking in the Exhibition Hall
	Potassium Channels Chaired by Chuan-Chu Chou, Schering-Plough Research Institute
4:15pm	Kv1.3 Channels in T Cells: Therapeutic Target for Autoimmune Diseases George Chandy, Professor, University of California Irvine & Founder of Airmid Kv1.3 channels, ShK peptides, effector/memory T cells, and autoimmune diseases.
4:45pm	Retigabine and Therapeutic Indications of Activating Neuronal KCNQ Voltage-Gated Potassium Ion Channels Jim Wu, Head of Discovery Biology, Roche R&D Center Retigabine is an investigational drug currently in phase III trials for refractory partial epilepsy. It is a novel potassium channel opener and acts by enhancing M-current and suppressing neuronal hyperexcitability. The presentation will cover its mechanism of action and preclinical profile in seizure/epilepsy as well as non-epilepsy disease models.
5:15pm	Drinks Reception in the Exhibition Hall

Day Two - 10 September

	Potassium Channels (continued) Chaired by Min Li, Johns Hopkins School of Medicine
8:30am	Chemical Activation of Voltage-Gated Potassium Channels Min Li, Professor, Department of Neuroscience & High Throughput Biology Center, Johns Hopkins School of Medicine The presentation will cover a series of studies on chemical modulators for voltage-gated potassium channels with special emphasis on newly identified channel openers, their mechanisms of action and potential utilities in therapeutics.
9:00am	Kv1.3 and Synaptotagmin-7 Regulates Calcium-Dependent GUT4 Traffic Gary Desir, Professor, Yale School of Medicine The voltage-gated K channel Kv1.3 interacts with the calcium sensor synaptotagmin-7 (Syt-7) to regulate insulin sensitivity and GLUT4 traffic. Kv1.3 knockout are more insulin sensitive than control animals. Syt-7 deletion impairs glucose-stimulated insulin secretion. The role of Kv1.3 and Syt-7 in glucose metabolism will be discussed.
9:30am	Kv3.3 Potassium Channels and Spinocerebellar Ataxia Type 13 Diane Papazian, Professor, University of California at Los Angeles Spinocerebellar Ataxia Type 13 is caused by mutations in Kv3.3. The disease occurs in two allelic forms with significantly different clinical presentations. The group is studying the molecular and cellular basis of SCA13 using expression systems, mammalian neurons, and the zebrafish, Danio rerio.
10:00am	Coffee Break and Networking in the Exhibition Hall
10:45am	Novel Recombinant Peptide Toxin Fusion Proteins as Potential Therapeutics for the Treatment of Autoimmune Disease Hung Nguyen, Principal Scientist, Amgen Peptide toxins have evolved unique abilities to potently block ion channels. Sea anemone toxin ShK and scorpion peptide toxin OSK1 block voltage-gated potassium channel, Kv1.3. The presentation will describe the engineering of novel peptide toxins to block Kv1.3 as autoimmune disease treatments.
11:15am	Novel Activators of Small- and Intermediate-Conductance Calcium-Activated Potassium Channels Based on the Neuroprotectant Riluzole Heike Wulff, Associate Professor, University of California, Davis The neuroprotectant riluzole activates small- and intermediate-conductance Ca2+-activated K+ channels at 2 to 20 microM. Based on rilzuole the group designed the more potent and selective KCa2/3 channel activator SKA-31, which lowers blood pressure by increasing the EDHF response and exhibits anticonvulsant properties.
	Target Opportunities Chaired by Min Li, Johns Hopkins School of Medicine
11:45am	The Use of Automated Platforms for Developing Improved Throughput Electrophysiology Assays for Ligand-Gated Ion Channels Jeff Clare, Director of R&D, Ion Channel Group, Millipore Development of compound screening assays for several ligand-gated channels using two automated platforms will be presented. The presentation will show that these assays can detect ligands with differing subtype selectivity and mechanisms of action with comparable fidelity to conventional patch clamp.
12:15pm	Lunch and Networking in the Exhibition Hall
1:15pm	Poster Viewing
	Target Opportunities (continued) Chaired by Merritt Maduke, Stanford University School of Medicine
2:00pm	What Constitutes a High Quality Patch-Clamp Recording? Mats Holmqvist, Labhead, Novartis Institute for Biomedical Research This presentation will describe a systematic analysis and characterization of electrophysiological parameters and assay performance from thousands of cells recorded on the QPatch.
2:30pm	CLC Chloride Channel Inhibitors Merritt Maduke, Assistant Professor, Stanford University School of Medicine CLC chloride channels are potential targets for diverse therapies, yet no specific, high-affinity modulators have yet been identified. Recently, the group has discovered that hydrolysis products of the non-specific anion-transport inhibitor DIDS are the most potent CLC inhibitors yet reported.
3:00pm	Poster Award
3:10pm	Coffee Break and Networking in the Exhibition Hall
3:50pm	Mechanosensitivity, A Wide Open Field Frederick Sachs, Distinguished Professor, New York State University at Buffalo Mechanosensitive ion channels are ubiquitous and associated with a variety of pathologies ranging from dystrophy to cardiac fibrillation. There is a specific blocker for these channels. No drug company has an R&D program in the area.
4:20pm	Close of Conference