GLAUCOMA

Glaucoma is one of the leading causes of vision loss worldwide according to the Howard Hughes Medical Institute. Glaucoma is prevalent not only in the United States but throughout the world with several million individuals affected worldwide. The disease is typically associated with aging, and its frequency increases in patients over the age of 60. Glaucoma is the second-leading cause of blindness in Caucasians and the leading cause of blindness in people of African descent in the United States.



Glaucoma is often associated with an increase in the pressure within the front portion, or anterior chamber, of the eye. This increased intraocular pressure compresses the optic nerve, ultimately leading to atrophy of the nerve and compromise of the visual fields. Intraocular pressure is determined by the balance between the inflow of fluid into and the outflow of fluid from the anterior chamber.

A variety of ion channels are expressed in tissues that are involved in maintaining fluid balance in key regions of the eye. These channels may play a role in maintaining the balance of inflow and outflow from the anterior chamber and, therefore, may participate in regulating intraocular pressure. Therefore, selective modulation of particular ion channels in inflow and outflow pathways of the anterior chamber may reduce intraocular pressure.

We have profiled the distribution of all human ion channels known to us in the pathways involved in fluid inflow and outflow of the anterior chamber of the human eye. We have found that both pathways express an extensive and distinctly different array of ion channels. Based upon our knowledge of the physiology and likely roles of these channels, we have selected particular ion channels as potential drug targets because we believe that they have potential therapeutic utility in the treatment of glaucoma. We have identified compounds that modulate an ion channel target and that lower intraocular pressure in an animal model of glaucoma. Due to their unique mechanisms of action, these compounds may prove effective either when used alone or in combination with existing drugs, thus potentially offering additional therapeutic options for treatment-resistant patients.

In order to focus our research efforts, we have decided to no longer actively pursue our glaucoma program. The assets from this program remain available to us should we seek to expand our research efforts into this area in the future.

Icagen may also selectively consider potential corporate partnership opportunities in its glaucoma program.