[Federal Register Volume 71, Number 97 (Friday, May 19, 2006)]
[Notices]
[Pages 29164-29165]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: E6-7627]


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DEPARTMENT OF HEALTH AND HUMAN SERVICES

National Institutes of Health


Government-Owned Inventions; Availability for Licensing

AGENCY: National Institutes of Health, Public Health Service, HHS.

ACTION: Notice.

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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.

Viral Entry or Replication Inhibition Using siRNA, Small Molecules, or 
Other Tec Tyrosine Kinase Inhibitors

Julie Readinger and Pamela L. Schwartzberg (NHGRI).
U.S. Provisional Application filed 29 Mar 2006 (HHS Reference No. E-
151-2006/0-US-01).
Licensing Contact: Susan Ano; 301/435-5515; [email protected].

    The Tec family of tyrosine kinases, consisting of five family 
members Tec, Btk, Itk, Rlk, and BMX, are key regulators of signaling 
pathways of T lymphocytes. Many existing antiviral therapies rely on 
inhibition of viral replication, which leads to emergence or selection 
of resistant viruses. The current technology provides an alternative 
target for the prevention or treatment of viral infection through 
administration of a Tec tyrosine kinase inhibitor. Such inhibitors can 
be siRNA, small chemical compounds, antisense or antibody. The current 
technology describes the inhibition of Itk (also

[[Page 29165]]

known as Emt and Tsk) and the resulting decrease in HIV infectivity, 
replication, and transcription for exemplary purposes. Importantly, 
inhibition of Itk expression does not affect the expression of HIV 
receptors CCR5, CXCR4, or CD4. The current technology could be used in 
combination with therapeutics that target multiple stages of the virus 
life cycle.
    This research is described, in part, in the following:
    1. D Dombroski, R Houghtling, CM Labno, J Burkhardt, and PL 
Schwartzberg, ``Kinase-independent functions for Itk in the regulation 
of Vav and the actin cytoskeleton,'' J. Immunol. 174: 1385-1392, 2005.
    2. A Takesono, R Horai, M Mandai, D Dombroski, and PL Schwartzberg, 
``Requirement for Tec family kinases in chemokine-induced migration and 
activation of Cdc42 and Rac,'' Curr. Biol. 10:917-22, 2004.
    3. E Schaeffer, G Yap, CM Lewis, M Czar, DW McVicar, AW Cheever, A 
Sher, and PL Schwartzberg, ``Mutation of Tec family kinases alters T 
helper cell differentiation,'' Nature Immunol. 2:1183-8, 2001.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors: The NHGRI, Genetic Disease Research Branch/Cell Signalling 
Section, is seeking statements of capability or interest from parties 
interested in collaborative research to further develop, evaluate, or 
commercialize the use of Tec family kinase inhibitors as a therapeutic 
target for HIV and other viral infections. Please contact Claire 
Driscoll, Director, NHGRI Technology Transfer Office, at 301/402-2537 
or [email protected] for more information.

Peptide Inhibitors of HIV-1 Integrase Useful for the Treatment of 
Retroviral Infection and HIV

Peter P. Roller et al. (NCI)
U.S. Provisional Application No. 60/534,378 filed 06 Jan 2004 (HHS 
Reference No. E-039-2004/0-US-01).
U.S. Provisional Application No. 60/547,067 filed 25 Feb 2004 (HHS 
Reference No. E-039-2004/1--US-01).
U.S. Provisional Application No. 60/599,856 filed 10 Aug 2004 (HHS 
Reference No. E-039-2004/2-US-01).
PCT Application No. PCT/US2004/42726 filed 21 Dec 2004 (HHS Reference 
No. E-039-2004/3-PCT-01), which published as WO 2005/068492 on 29 Dec 
2005.
Licensing Contact: Sally Hu, Ph.D., M.B.A.; 301/435-5606; 
[email protected].

    The invention describes the discovery of short peptides, derived 
from the natural peptide named indolicidin that have an ability to 
inhibit HIV-1 integrase and exhibit antiviral activity. In particular, 
this invention shows that synthesized derivatives of the indolicidin 
peptides named RIN-25 exhibit a significant higher anti-viral and anti-
integrase activity when compared to the parent compound named RIN-42. 
HIV-1 integrase has a good potential of being the next therapeutic 
target since HIV-1 integrase is essential for viral replication and 
there is no cellular equivalent. Thus, subject invention may be used in 
the development of therapeutics for the treatment of retroviral 
infections, such as AIDS, or other retroviral-related diseases (i.e., 
cancer, immune disorders). In addition, the novel peptides described in 
this invention may also have particular value when used in combination 
treatments with other antiviral therapies directed at other viral 
targets, such as protease and reverse transcriptase.

Identification of Candidate Ligands which Modulate Antigen Presenting 
Cells

Polly Matzinger, John P. Ridge (NIAID).
U.S. Patent No. 6,680,176 issued 20 Jan 2004 (HHS Reference No. E-055-
1999/0-US-01).
Licensing Contact: Cristina Thalhammer-Reyero; 301/435-4507; 
[email protected].

    Available for licensing and commercial development are novel 
biotechnological tools, prophylactics, therapeutics, and methods for 
modulating the activation state of an antigen presenting cell (APC) and 
thereby modulating the activation of a killer T cell. The activation of 
a killer T cell can occur in a two cell complex and two sequential 
steps: (a) In the first step, an APC stimulates a T helper T cell, 
which in turn stimulates or ``superactivates'' the APC to differentiate 
to a state where it can independently stimulate a killer T cell; (b) In 
the second step, the APC encounters the killer T cell and stimulates it 
so that killer T cell priming is achieved in a helper independent 
fashion. The first step can be bypassed altogether by viral infection 
or an interaction with certain molecules at the cell surface of APCs, 
such as CD40. More specifically, the invention consists of a method of 
identifying a ligand as a candidate for incorporation into a 
pharmaceutical composition, such as a therapeutic or prophylactic 
product, that modulates antigen presenting cell activity, comprising 
contacting an APC with a candidate ligand which interacts with the APC, 
analyzing the activation state of the APC; and selecting ligands that 
activate a killer T cell in the absence of a helper T cells as the 
candidates for incorporation into the pharmaceutical. Also claimed are 
related methods where the ligand interacts with CD40 or where the APC 
is a dendritic cell. The embodiments have several applications in the 
field of immunology, and enable to manufacture novel pharmaceuticals 
and vaccine components for the treatment and prevention of cancer, 
systemic infection, and autoimmune responses.
    The technology is further described in JP Ridge, F Di Rosa, and P 
Matzinger, ``A conditioned dendritic cell can be a temporal bridge 
between a CD4+ T-helper and a T-killer cell,'' Nature 1998 Jun 4; 
393(6684):474-8.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

    Dated: May 11, 2006.
David R. Sadowski,
Acting Director, Division of Technology Development and Transfer, 
Office of Technology Transfer, National Institutes of Health.
[FR Doc. E6-7627 Filed 5-18-06; 8:45 am]
BILLING CODE 4140-01-P