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CPN 2010

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Recommended Short Courses*

Monday, June 14
9:00 am – 12:00 pm
(SC2) Animal Models of Pain: Progress and Challenges
(SC1) Reactive Metabolites in Drug Discovery and Development-A Critical Examination of the Issues

2:00 pm – 5:00 pm
(SC5) Dealing with the Blood-Brain Barrier

*Separate Registration Required.



TUESDAY, JUNE, 15


7:00 am Registration and Morning Coffee


Anti Ngf and Trk Inhibition

8:15 Chairperson's Opening Remarks

Ramana Sonty, Ph.D., MBBS, Vice President, Prescient Life Sciences

8:25 KEYNOTE ADDRESS
Pat MantyhAntagonism of NGF-TrkA Signaling and the Relief of Musculoskeletal Pain

Pat Mantyh, Ph.D., J.D., Department of Pharmacology, University of Arizona College of Medicine

Painful musculoskeletal conditions are the most common cause of chronic pain and physical disability in both developing and developed countries. Skeletal pain frequently results in impairment of physical function and long-term disability.  This presentation will focus on the mechanisms by which antagonism of NGF-TrkA signaling attenuates pain and why these therapies may be particularly efficacious in blocking musculoskeletal pain.

8:55 Inhibition of Nerve Growth Factor for Treatment of Pain: Going Beyond Traditional Analgesic Drugs?

Kenneth VerburgKenneth Verburg, Ph.D., Vice President, Development Head, Pfizer’s Pain Portfolio, Pfizer, Inc.

Pharmacological blockade of nerve growth factor (NGF) reduces pain-related behaviors in animal studies leading to interest in translation and clinical utility of this approach for the treatment of pain. Tanezumab is a monoclonal antibody against NGF under investigation to profile the importance of NGF across clinical pain conditions through evaluation of analgesic efficacy, to characterize the safety of NGF inhibition, and thereby optimize further clinical development strategies.


9:25 Small Molecule Trk Inhibitors in Pre-Clinical Models of Pain

Steven W. Andrews, Ph.D., Associate Director, Drug Discovery, Array BioPharma, Inc.

Array has discovered selective inhibitors of the Trk kinase family which have demonstrated good efficacy in multiple animal models of pain and inflammation. This efficacy is peripherally mediated with no observed effects on neuronal health or function. Thus, peripheral inhibition of the Trk pathway through Trk kinase inhibition may represent an important advance in the clinical treatment of inflammatory pain.

9:55 Networking Coffee Break


Leading Edge Case Studies

10:25 Addressing the Challenges of Analgesic Drug Development with Novel Proof-of-Concept Studies

David J. Hewitt, M.D., Senior Director, Clinical Neuroscience, Merck Research Laboratories

10:55 Translational Medicine in Pain Drug Development—Can NHP Models, Biomarkers for Proof of Mechanism and Patient Selection Improve Our Success Rate?

Hong Wan, Ph.D., Director, Translational Medicine, Pfizer, Inc.

Translational medicine strategies are needed in pre-clinical discovery and clinical development to "buy down" the risk and select the "winners". Examples and case studies will be provided to illustrate: the use of experimental human models and NHP animal models to bridge the gap between preclinical discovery and clinical development; the use of biomarkers to demonstrate proof of mechanism; and the use of biomarkers to provide insights into the pathological mechanisms in the pain condition and patient stratification.

11:25 Discovery of PF-04457845, a Highly Selective Urea FAAH Inhibitor that Reduces Inflammatory Pain

Douglas S. Johnson, Ph.D., Senior Principal Scientist, Medicinal Chemistry, Pfizer Global Research & Development

Fatty acid amide hydrolase (FAAH) is an integral membrane enzyme that degrades the fatty acid amide family of signaling lipids, including the endocannabinoid anandamide. Genetic or pharmacological inactivation of FAAH leads to analgesic and anti-inflammatory phenotypes in rodents without showing the undesirable side effects observed with direct cannabinoid receptor agonists, indicating that FAAH may represent an attractive therapeutic target for the treatment of inflammatory pain. This talk will describe the discovery and characterization of a series of FAAH piperidine urea inhibitors including our clinical candidate PF-04457845.

11:55 Luncheon Presentations (Sponsorship Opportunities Available) or Lunch on Your Own


ION CHANNELS AND PAIN


1:25 pm Chairperson's Remarks

Richard Lewis, Ph.D., CSO, Research & Development, Xenome Ltd.

KEYNOTE ADDRESS

Learning from Men on Fire: Sodium Channels and Human Pain

Stephen WaxmanStephen G. Waxman, M.D., Ph.D., Bridget Marie Flaherty Professor of Neurology, Neurobiology, and Pharmacology; Director, Center for Neuroscience & Regeneration/Rehabilitation Research, Yale University School of Medicine

This lecture will review the status of sodium channels as therapeutic targets for chronic pain. The presence of multiple sodium channel isoforms within primary sensory neurons and dysregulated channel expression after nerve injury, with emphasis on the most tractable molecular targets, will be discussed, together with recent translational studies that have demonstrated, in humans, the roles of sodium channels in chronic pain, e.g. in hereditary erythromelalgia (the “man on fire” syndrome), paroxysmal extreme pain disorder, and channelopathy-associated insensitivity to pain.

2:05 Selective Pharmacological Blockade of Sodium Nav1.8 Channels Relieves Experimental Inflammatory and Neuropathic Pain

Michael F. Jarvis, Ph.D., Vowiler Research Fellow, Associate Director, Neuroscience, Global Pharmaceutical Research & Development , Abbott

Activation of tetrodotoxin-resistant (TTX-R) sodium channels contributes to action potential electrogenesis in neurons. Antisense oligonucleotide studies directed against Nav1.8 sodium channels have shown that this channel contributes to experimental inflammatory and neuropathic pain. Recently developed selective blockers of Nav1.8 channels effectively inhibit the generation of sensory nerve spontaneous and electrically-evoked action potentials in vitro and block mechanically evoked firing of wide dynamic range neurons in the rat spinal dorsal horn in spinal nerve ligated (SNL) rats, in vivo. In experimental pain models, Nav1.8 blockers dose-dependently reduce mechanical allodynia in neuropathic and inflammatory pain conditions. These data demonstrate a predominant role for Nav1.8 sodium channel activation in chronic pain states.

2:35 Computational Genetics: Pain and Beyond

Gary PeltzGary Peltz, M.D., Ph.D., Professor, Anesthesia, Stanford University

Our understanding of genetic factors effecting human disease susceptibility and drug treatment response is advanced by analysis of murine genetic models. A novel computational method was developed to reduce the time and cost required for mouse genetic analysis. This method rapidly identifies a causative genetic factor by correlating a pattern of observable physiological or pathological differences among selected strains of mice with the pattern of genetic variation. It was used to identify the genetic basis for strain-specific differences in response to pain medications, and identified novel methods for treatment of narcotic drug withdrawal and for amelioration of post-incisional pain.

3:05 Evaluation of the Antinociceptive Potential of Neu-P12, a New Drug Candidate, in Rodent Pain Models

Nava Zisapel, Ph.D., Professor, Neurobiology, Faculty of Life Sciences, Tel Aviv University

Neu-P12 is a new non-COX inhibiting drug candidate in development for pain.  We used three rodent models of pain to investigate the antinociceptive potential of this compound.  Neu-P12 demonstrates significant does-dependent antinociceptive effects in a number of rodent pain models of neurogenic, inflammatory and neuropathic pain.

3:35 Grand Opening Refreshment Break in the Exhibit Hall

 

PLENARY KEYNOTE PANEL

4:15 Shifting Sands of Pharmaceutical Discovery

Panelists:

Cris Waller Chris L. Waller, Ph.D., Senior Director, HealthCare Informatics, Medical Business Technology, Pfizer, Inc.







Gary PeltzGary Peltz, M.D., Ph.D., Professor, Anesthesia, Stanford University







Marvin Bayne Marvin Bayne, Ph.D., Vice President, Head, Discovery Technologies, Merck & Co.







Thomas BocanThomas Bocan, Ph.D., Senior Director, Head, Pre-clinical BioImaging Center, Pfizer Global R&D,, Pfizer, Inc.







Peggy Guzzie-PeckPeggy Guzzie-Peck, Ph.D., DABT, Vice President, Head, Toxicology, Pathology & LAM, Johnson & Johnson, Pharma R&D






Key questions to be addressed:

  • How does academic research impact pharma drug discovery?
  • How does the creation of cross-pharma pre-competitive collaborations impact drug discovery, spanning chemistry, biology, and knowledge management?
  • Adoption of new technologies, such as, molecular Imaging: Can it help drug discovery and how quickly?
  • How effectively and efficiently can we collaborate to develop safer drugs?

5:45 Happy Hour in the Exhibit Hall

6:45 End of Day


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SPONSORSHIPS & EXHIBITS

The exhibit hall has sold out the past four years, so please contact us early to reserve your place. To customize your sponsorship or exhibit package for 2015, contact:

Joseph Vacca
Associate Director, Business Development
781-972-5431
jvacca@healthtech.com 

 

 

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