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.

Metal Chelators and Target-Moiety Complexes for Imaging

Martin W. Brechbiel and Thomas Clifford (NCI).

U.S. Provisional Application filed 23 Aug 2004 (DHHS Reference No. E-317-2004).

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

Available for licensing and commercial development are bifunctional metal chelators, metal chelator-targeting moiety complexes, metal chelator-targeting moiety-metal conjugates, kits, and methods of preparing them. These chelators are useful in diagnosing and/or treatment of cancer and thrombosis. The metal chelators may be used in conventional and solid-phase synthetic methods to form targeting moieties (e.g., peptides, and Starburst polyamidoamine dendrimers (PAMAM), capable of conjugating diagnostic and/or therapeutic metals. The formulae for two such chelators is shown below:

Anti-HIV Peptide Secreting Bacteria: Therapeutics and Methods of Use

Dean Hamer (NCI).

U.S. Provisional Application No. 60/604,051 filed 25 Aug 2004 (DHHS Reference No. E-233-2004/0-US-01).

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

Available for licensing and commercial development are genetically engineered commensal bacteria compositions that secrete HIV infectivity interfering peptides with the aid of co-expressed translocation mediators such as HylB, HylD or tolC gene products. The bacteria can be, for example, Escherichia coli and are preferably those that colonize the gastrointestinal or genitourinary tracts. The secreted anti-HIV peptide can be a functional inhibitory fragment from the C-terminus of HIV, SHIV or SIV, or an inhibitory peptide derived from the N-terminus receptor-binding domain of SIV gp41, HIV-1 gp41, or HIV-2 gp41. The secreted anti-HIV peptide can also be a peptide from the allosteric domain of gp120, an extracellular loop of CCR5, an anti-CD4 immunoglobulin, a mimetic of CD4, an alpha-defensin or theta-defensin, a CD38 fragment homologous to the V3 loop of gp120, polphemusin II (a CXCR4 antagonist), a RANTES peptide that binds to CCR5 or an HIV surface binding peptide such as cyanovirin.

Method of Assessing Ischemia in a Patient

Steven Warach, Lawrence Latour (NINDS).

U.S. Provisional Application No. 60/381,611 filed 17 Mar 2002 (DHHS Reference No. E-082-2002/0-US-01); PCT Application No. PCT/US03/15368 filed 16 May 2003 (DHHS Reference No. E-082-2002/0-PCT-02).

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

Hyperintense acute reperfusion marker (HARM) is well correlated with reperfusion and is a precursor to or concomitant with reperfusion injury. The inventors have developed a novel technique of assessing injuries associated with ischemia, stroke, or reperfusion injury in a patient by administering a contract agent to the patient, acquiring a fluid-attenuated inversion-recovery (FLAIR) image, and observing the presence or absence of HARM on the acquired image. The technique can also be used to determine the effectiveness of a therapeutic protocol for the treatment or prevention of reperfusion injury in a patient that has previously suffered an ischemic event.

This research has been described, in part, in Latour et al., “Early Blood-Brain Barrier Disruption in Human Focal Brain Ischemia,” Ann. Neurol. 2004 56:568-477.