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###### Department of Health and Human Services

###### National Institutes of Health

# AGENCY:

National Institutes of Health, Public Health Service, DHHS.

# ACTION:

Notice.

# SUMMARY:

The inventions listed below are owned by agencies of the U.S. Government and are available for licensing in the U.S. in accordance with 35 U.S.C. 207 to achieve expeditious commercialization of results of federally-funded research and development. Foreign patent applications are filed on selected inventions to extend market coverage for companies and may also be available for licensing.

      ( print page 65215)    

# ADDRESSES:

Licensing information and copies of the U.S. patent applications listed below may be obtained by writing to the indicated licensing contact at the Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, Maryland 20852-3804; telephone: 301/496-7057; fax: 301/402-0220. A signed Confidential Disclosure Agreement will be required to receive copies of the patent applications.

## Neurotrophic Components of the ADNF I Complex

Brenneman et al. (NICHD)

DHHS Reference No. E-209-01/0 filed 12 Sep 2001

*Licensing Contact:*                     Jonathan Dixon; 301/496-7056 ext. 270;                     *dixonj@od.nih.gov*

Neuronal cell death has been associated with a variety of diseases and conditions, including Alzheimer's, AIDS-related dementia, Huntington's disease, and Parkinson's disease to name a few. Neuronal cell death has also been associated with developmental retardation and learning impairments that have lifelong effects on individuals diagnosed with these conditions.

This invention discloses new Activity Dependent Neurotrophic Factor I (ADNF I) complex polypeptides. Previously, Activity Dependent Neurotrophic Factor (ADNF) polypeptides have been shown to prevent neuronal cell death. ADNF polypeptides are secreted by astroglial cells in the presence of vasoactive intestinal peptide (VIP). These new ADNF I complex polypeptides are effective for reducing neuronal cell death, for reducing oxidative stress, for reducing condition(s) associated with fetal alcohol syndrome in a subject, for enhancing learning and memory, both pre- and post-natally, and for other conditions.

With these additional ADNF I complex polypeptides it will be easier to target specific receptors in different cell types and to individually tailor drug treatment regimes to those afflicted with neurodegenerative disorders.

## Utilization of FPRL1 as a Functional Receptor by Serum Amyloid A (SAA)

Ji Ming Wang et al. (NCI)

DHHS Reference No. E-167-99/0 filed 22 Sep 1999 (PCT/US99/21770, WO 01/21188)

*Licensing Contact:*                     Marlene Shinn; 301/496-7056 ext. 285;                     *shinnm@od.nih.gov*

This technology identifies a means for modulating the interaction of Serum Amyloid A (SAA) with its functional receptor FPRL1. This modulation may have therapeutic applications in treating diseases such as infections, organ rejection, rheumatoid arthritis, atherosclerosis, neoplasms, and amyloidosis. The SAA, an acute phase protein, is normally present in serum but increases by 1,000 fold in systemic inflammatory conditions and is associated with leukocyte migration in these disease states. This technology identifies various means to modulate the association of SAA and FPRL1 in a SAA-FPRL1 complex or method of identifying agents that associate with the complex. It is available for immediate licensing and research collaborations via a Cooperative Research and Development Agreement (CRADA).

Dated: December 10, 2001.

Jack Spiegel,

Director, Division of Technology, Development and Transfer, Office of Technology Transfer, National Institutes of Health.

[FR Doc. 01-31048 Filed 12-17-01; 8:45 am]

BILLING CODE 4140-01-P