MICHAEL ELLIS HOFFER
Medical Practice in San Diego, CA

6649621, Nov 18, 2003

Jan 23, 2001

09/766625

Richard D. Kopke - San Diego CA
Donald Henderson - Clarence NY
Michael E. Hoffer - San Diego CA

The United States of America as represented by the Secretary of the Navy - Washington DC

A61K 31517

5142661, 514369, 514562, 514547, 514956, 514517

The invention presents methods for preventing and treating sensorineural hearing loss and is directed to the restoration or protection of hair cells in individuals experiencing a non-presbycusis type sensorineural hearing loss or who are at risk for an acute hearing loss due to exposure to noise, toxins, or other stressors. More specifically, the present invention relates to the use of agents which augment inner ear antioxidant defenses (e. g. acetyl-L-carnitine, steroids, compounds that are transported into inner ear hair cells and then synthesized by said cells into glutahione) to prevent and/or reverse hearing loss induced by noise, toxins, or other stressors.

6177434, Jan 23, 2001

Jul 31, 1998

9/126707

Richard D. Kopke - San Diego CA
Donald Henderson - Clarence NY
Michael E. Hoffer - San Diego CA

The United States of America as represented by the Secretary of the Navy - Washington DC

A61K 3152, A61K 31425, A61K 31195, A01N 4390, A01N 4378

514266

The invention is accomplished by preventing and/or reversing inner ear damage due to noise or toxins. In part, this is accomplished by upregulating antioxidant enzyme activity by applying agents such as R-N6-Phenylisopropyl adenosine (R-PIA) to the round window membrane of the inner ear or systemically, and/or by also applying agents such as 1-2-oxothiazolidine-4-carboxylic acid (Procysteine) to the round window membrane. Also, the invention is accomplished by giving the compounds systemically. Selective auditory hair cell protection in the face of gentamicin exposure by concomitant delivery of an NMDA antagonist or glial derived neurotrophic factor (GDNF) with the gentamicin. These and additional agents are also accomplished by curtailing activated programmed cell death pathways and/or inducing/enhancing cell repair mechanisms in the inner ear. The agent (s) may be applied before, during or after the noise trauma or toxin exposure.