National Institutes of Health, HHS.
This is notice, in accordance with 35 U.S.C. 209 and 37 CFR part 404, that the National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Department of Health and Human Services, is contemplating the grant of a start-up exclusive license to Cogentis Therapeutics, Inc. which is located in Maryland, to practice the inventions embodied in the following patents: U.S. Patent 8,597,660, issued December 3, 2013 (HHS reference E-144-2010/0-US-02).
The patent rights in these inventions have been assigned to the United States of America. The prospective start-up exclusive license territory may be worldwide and the field of use may be limited to Frontotemporal dementia, Alzheimer's disease excluding intranasal delivery, Neuronal injury (stroke, traumatic brain injury (TBI) and epilepsy), and Progressive Supranuclear Palsy.
Only written comments and/or applications for a license which are received by NINDS Technology Transfer on or before October 11, 2016 will be considered.
Requests for copies of the patent application, inquiries, comments, and other materials relating to the contemplated start-up exclusive license Start Printed Page 65663should be directed to: Susan Ano, Ph.D., NINDS Technology Transfer, 31 Center Drive, Suite 8A52, MS2540, Bethesda, MD 20892; Telephone: (301) 435-5515; Email: email@example.com.
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This invention discloses treating neurodegenerative diseases by administering cyclin dependent kinase 5 (Cdk5) inhibitory peptides derived from P35, the activator of Cdk5. Abnormally hyperactive Cdk5 has been shown to be associated with a variety of neurodegenerative disorders. This invention describes isolated peptide fragments, pharmaceutical compositions and methods for use of such for treating subjects with a neurodegenerative disease, such as Alzheimer's disease (AD), Amyotrophic Lateral Sclerosis (ALS) and Parkinson's disease (PD). An inhibitory fragment, TFP5, disclosed in this invention, has been shown to ameliorate symptoms of AD in disease animal models without any evidence of toxicity. In particular, TFP5 treatment of rat cortical neurons reduced hyperactivation of Cdk5 upon neuronal stress and insults. Following intraperitoneal (ip) injection, TFP5 was capable of crossing the blood-brain barrier and localizing within the brain where it was found to rescue memory deficits and pathology in a double transgenic mouse (APP/PS1) AD model.
The prospective start-up exclusive license may be granted unless within fifteen (15) days from the date of this published notice, the NIH receives written evidence and argument that establishes that the grant of the license would not be consistent with the requirements of 35 U.S.C. 209 and 37 CFR part 404.
Complete applications for a license in the field of use filed in response to this notice will be treated as objections to the grant of the contemplated start-up exclusive license. Comments and objections submitted to this notice will not be made available for public inspection and, to the extent permitted by law, will not be released under the Freedom of Information Act, 5 U.S.C. 552.
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Dated: September 19, 2016.
Technology Development Coordinator, NINDS Technology Transfer, National Institutes of Health.
[FR Doc. 2016-22897 Filed 9-22-16; 8:45 am]
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