Government-Owned Inventions; Availability for Licensing

AGENCY:

National Institutes of Health, Public Health Service, DHHS.

ACTION:

Notice.

SUMMARY:

The inventions listed below are owned by an agency 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.

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.

Methods and Compositions for Protecting Cells From Ultrasound-Mediated Cytolysis

Joe Z. Sostaric (NCI), Norio Miyoshi (EM), Peter Riesz (NCI).

U.S. Provisional Application No. 60/620,258 filed 19 Oct 2004 (DHHS Reference No. E-311-2004/0-US-01).

Licensing Contact: Michael Shmilovich; 301/435-5019; shmilovm@mail.nih.gov.

Available for licensing and commercial development are methods for protecting cells from ultrasound-mediated cytolysis. Therapeutic uses of ultrasound (e.g., sonoporation, thrombolysis, HIFU, sonophoresis, acoustic hemostasis) may induce changes in tissue state, including apoptosis and cytolysis, through thermal effects (e.g., hyperthermia), mechanical effects (e.g., acoustic cavitation or through radiation force, acoustic streaming and other ultrasound induced forces), and chemical effects (via sonochemistry or by the activation of solutes by sonoluminescence). Furthermore, ultrasound exposure conditions in biological processes, e.g. ultrasound bioreactors, are limited by the need to decrease cytolysis of microbes or animal and plant cells. Accordingly, the protecting molecules used to carry out the methods of the invention possess the ability to protect cells against ultrasound mediated cytolysis, without hindering ultrasound induced physical effects that could be utilized to create beneficial effects. The protecting solutes are surface active and possess at least one “carbohydrate unit” as described. The solutes include, but are not limited to: alkyl-β-D-thioglucopyranoside, alkyl-β-D-thiomaltopyranoside, alkyl-β-D-galactopyranoside, alkyl-β-D-thiogalactopyranoside, or alkyl-β-D-maltrioside, hexyl-β-D-glucopyranoside, heptyl-β-D-glucopyranoside, octyl-β-D-glucopyranoside, nonyl-β-D-glucopyranoside, hexyl-β-D-maltopyranoside, n-octyl-β-D-maltopyranoside, n-octyl-β-D-thioglucopyranoside, 2-propyl-1-pentyl-β-D-maltopyranoside, methyl-6-O-(N-heptylcarbamoyl)-α-D-glucopyranoside, 3-cyclohexyl-1-propyl-β-D-glucoside, 6-O-methyl-n-heptylcarboxyl-α-D-glucopyranoside.

In addition to licensing, the technology is available for further development through collaborative research with the inventors via a Cooperative Research and Development Agreement (CRADA).

Treatment of Human Viral Infections (Imatinib)

Drs. Steven Zeichner and Vyjayanthi Krishnan (NCI).

U.S. Provisional Application No. 60/588,015 filed 13 Jul 2004 (DHHS Reference No. E-281-2004/0-US-01).

Licensing Contact: Sally Hu; 301/435-5606; hus@mail.nih.gov.

This application describes the methods for treating or preventing a HIV infection by the administration of abl-kinase inhibitor called imatinib and its derivatives. Several available agents can inhibit HIV replication by targeting one or another viral protein, such as the viral reverse transcriptase, protease, envelope fusion process, or integrase, or by targeting the interaction of a viral component with a host cell component, for example the host cell viral receptor or co-receptor. However, HIV can readily become resistant to these drugs, and new therapeutic approaches for HIV infection are needed. The studies described in the application show that the expression of many host cell genes changes in response to HIV replication, and show that targeting one of these changes with imatinib can inhibit viral replication. Thus targeting the host cell, and making the host cell less hospitable to the virus can inhibit viral replication. The application thus describes a new agent that inhibits viral replication by acting on the host cell, which may offer new approaches to therapy for HIV infection. These approaches may be less likely to engender rapid resistance in the virus to the therapy.

This abstract replaces one published in the Federal Register on Friday, October 22, 2004 (69 FR 62060).