Arthur H. Neufeld, Ph.D.
Dr. Neufeld is an ophthalmic researcher who is currently the Bernard Becker Research Professor of Ophthalmology in the Department of Ophthalmology and Visual Science at Washington University School of Medicine in St. Louis, Missouri.
Dr. Neufeld has been a major contributor to the field of ophthalmic pharmacology, particularly in the area of glaucoma. He has studied the pharmacological regulation of aqueous humor dynamics, pharmacological neuroprotection of the optic nerve in glaucoma, pharmacological inhibition of prostaglandins in ocular tissues during inflammation, and wound healing of the corneal epithelium and endothelium. At Yale University Medical School, Dr. Neufeld published numerous papers demonstrating that cyclic AMP is the second messenger by which epinephrine lowers IOP. In addition, his laboratory first demonstrated that a non-steroidal anti-inflammatory drug could block the breakdown of the blood-aqueous barrier caused by prostaglandins.
At the Eye Research Institute and the Department of Ophthalmology of Harvard University in Boston, Dr. Neufeld expanded his laboratory and research interests into corneal epithelial and endothelial cell biology as well as continuing his work on pharmacological regulation of IOP.
In 1989, Dr. Neufeld left academia to found and to join an entrepreneurial startup, Telor Ophthalmic Pharmaceuticals, Inc., as Chief Scientific Officer. Over the next six years, Dr. Neufeld led a team of scientists to file four INDs with the FDA in order to conduct clinical trials on several lead compounds to treat glaucoma, postoperative increased IOP, corneal pain, intraoperative miosis and presbyopia.
In 1995, Dr. Neufeld rejoined academia at his current position to pursue his newly formulated interest in developing a pharmacological agent to directly protect the optic nerve in glaucoma patients. His work has demonstrated that excessive nitric oxide is damaging to the optic nerve in glaucoma and that in an animal model of glaucoma inhibiting the synthesis of nitric oxide prevents the loss of retinal ganglion cells due to elevated intraocular pressure.