NEW HAVEN, CT, May 2, 2011 - Yale School of Medicine has entered into a collaboration with Icagen, Inc. and Pfizer to explore the potential efficacy of investigational compounds as novel treatments for pain. These compounds, which were identified from an existing collaboration between Icagen and Pfizer may be useful in treating pain in people with a rare genetic disorder called inherited erythromelalgia (IEM), or the "man on fire syndrome." Individuals afflicted with the syndrome experience a debilitating, life-long burning pain.
The collaboration with the laboratory of Stephen G. Waxman, M.D., Ph.D. and Sulayman D. Dib-Hajj, Ph.D. in the Department of Neurology, Yale School of Medicine, will study the effects of selectively blocking Nav1.7 (SCN9A) sodium channels with molecules previously identified by Pfizer and Icagen. Nav1.7 is responsible for producing impulses in pain-sensing neurons. The Waxman team, working at the Veterans Affairs Healthcare System in West Haven, CT, has previously shown that mutations of Nav1.7 channels occur in patients suffering from IEM. These genetic mutations increase activity in these neurons, leading to the pain associated with IEM. Working together, investigators at Yale, Pfizer and Icagen will seek to determine whether compounds identified by Icagen and Pfizer block IEM Nav 1.7 channels in vitro, which may in turn provide a rationale for future clinical studies in IEM patients and other pain disorders.
Dr. Waxman noted, "We are committed to finding new, more effective treatments for pain in inherited erythromelalgia and related disorders. Sodium channels are the molecular generators within nerve cells, which produce electrical impulses. In patients with IEM, these mutations make Nav1.7 overactive. By blocking these over-active channels, we believe that we potentially can more effectively treat pain in inherited erythromelalgia. My colleagues and I at Yale are excited about working with Icagen and Pfizer in this area of research and in studying the effect of compounds which are potent and selective blockers of Nav1.7. It is our hope that this joint effort will lead to effective treatments for IEM patients."
P. Kay Wagoner, Ph.D., CEO of Icagen added, "We are very pleased that Drs. Waxman and Dib-Hajj have agreed to work with us and our partner Pfizer in the study of Nav1.7 channels from IEM patients. They are among the world's leading researchers in the role of sodium channels in pain. The studies we are jointly undertaking should help us better understand how modulating Nav1.7 channels in IEM patients may reduce the extreme pain they experience. This information may additionally assist our broader efforts to find novel sodium channel treatments for patients with various pain conditions."
Ruth McKernan, Ph.D., Chief Scientific Officer of Pfizer's new Pain and Sensory Disorders Research Unit, Neusentis, based in Cambridge, UK, noted, "There is a significant body of evidence to suggest that sodium channels, particularly Nav1.7, play an important role in pain disorders. By combining the scientific and clinical expertise of Dr. Waxman's lab with that of Pfizer and Icagen, we look forward to potentially developing medicines in this area of high medical need."