[Federal Register Volume 70, Number 211 (Wednesday, November 2, 2005)]
[Notices]
[Pages 66446-66448]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 05-21832]


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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.

Method To Disrupt Protein-Protein Interactions and Its Use To Identify 
Compounds Able To Inhibit HIV-1 Rev Protein Multimerization

George Pavlakis and Leonid Suvoroz (NCI).
HHS Reference No. E-303-2005/0--Research Tool.
Licensing Contact: Sally Hu; 301/435-5606; <a href="/cdn-cgi/l/email-protection#dbb3aea89bb6bab2b7f5b5b2b3f5bcb4ad"><span class="__cf_email__" data-cfemail="9ef6ebeddef3fff7f2b0f0f7f6b0f9f1e8">[email protected]</span></a>.

    The invention provides a FRET-based assay for the study of Rev-Rev 
interaction in vitro, based on YFP and CFP expression constructs for 
Rev. Using this assay, Rev-derived small peptides that can inhibit Rev-
Rev interactions and disrupt dimerization were discovered. This assay 
can be used as an in vitro assay for studying protein-protein 
interactions in general, and for the discovery of inhibitors or 
agonists of such interactions as potential drugs against HIV 
infections, as well as for the

[[Page 66447]]

discovery of Rev dimerization inhibitors. Thus this assay can be useful 
for drug screening.
    NIH will not seek patent protection for this invention, and it will 
be available for licensing through a Biological Materials License (BML) 
or though a Material Transfer Agreement (MTA).
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Furin Inhibitors and Alpha-Defensin for Preventing Papilloma Virus 
Infection

Patricia Day, Rebecca Richards, John Schiller, Douglas Lowy, 
Christopher Buck (NCI).
U.S. Provisional Application No. 60/692,846 filed 21 Jun 2005 (HHS 
Reference No. E-104-2005/1-US-01).
Licensing Contact: Michael Shmilovich; 301/435-5019; 
<a href="/cdn-cgi/l/email-protection#04776c696d686b72694469656d682a6a6d6c2a636b72"><span class="__cf_email__" data-cfemail="fd8e95909491928b90bd909c9491d3939495d39a928b">[email protected]</span></a>.

    Available for licensing and commercial development are intellectual 
properties that claim compositions and methods for preventing papilloma 
virus (PV) infection in humans using furin inhibitors or alpha-
defensins. PV viruses include a minor capsid protein L2 which requires 
a functional intracellular furin (a cell-encoded proprotein convertase 
present in endosomes) for escape from the endosomal spaces into the 
cytoplasm and viral infection. Accordingly, a disruption of viral 
infection by the inhibition of furin with molecules such as decanoyl-
RVKR-CMK is potentially useful as a broad spectrum anti-HPV 
prophylactic.
    Alpha-defensins, which are naturally secreted by the cervix, are 
reported to have potent and non-type specific anti-HPV properties. They 
can be administered as a topic microbicide to prevent infection by many 
HPV genotypes, including types not covered by the vaccines currently in 
Phase III clinical trials.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Identification of a Fusion/Entry Receptor for Human Herpesvirus-8

Edward A. Berger, Johnan Kaleeba (NIAID).
U.S. Provisional Application No. 60/681,098 filed 13 May 2005 (HHS 
Reference No. E-051-2005/0-US-01).
Licensing Contact: Robert M. Joynes; 301/594-6565; 
<a href="/cdn-cgi/l/email-protection#a2c8cddbccc7d1d0e2cfc3cbce8ccccbca8cc5cdd4"><span class="__cf_email__" data-cfemail="73191c0a1d160001331e121a1f5d1d1a1b5d141c05">[email protected]</span></a>.

    This invention relates to stable, nonhuman cell lines and 
transgenic mammals having cells that coexpress human xCT as valuable 
tools for the continuing research of Kaposi's Sarcoma Herpes Virus 
(KSHV) infection and the development of more effective anti-KSHV 
therapeutics. Kaposi's sarcoma (KS) is the most common malignancy in 
AIDS patients and manifests as highly proliferative vascular lesions 
that appear on body extremities. KSHV is invariably present in all 
known clinical forms of KS and sero-conversion to KSHV antigens is 
considered a risk factor for development of the lesions. KSHV is 
believed to enter target cells by direct fusion of virion membrane with 
the target cell plasma membrane. The susceptibility of KSHV infection 
depends on the cell surface expression of the human xCT molecule. xCT 
plays a role in the membrane fusion step of KSHV infection. The 
identification of xCT as a receptor for KSHV may pave the way for 
deciphering the mechanism of KSHV pathogenesis.
    This discovery has led to various potential commercial applications 
for this invention including the following:
    <bullet> Cell lines expressing recombinant xCT for analysis of KSHV 
entry/infection
    <bullet> Construction of xCT transgenic small animals for testing 
of KSHV inhibitors
    <bullet> Use of peptides or fragments derived from extracellular 
regions of xCT as KSHV inhibitors
    <bullet> Use of specific antibodies (including human versions) 
against xCT as KSHV inhibitors
    <bullet> Use of small molecules targeted to xCT as KSHV inhibitors
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Potent HIV-1 Entry Inhibitors and Immunogens

Dimiter S. Dimitrov et al. (NCI).
U.S. Patent Application No. 10/506,651 filed 05 Mar 2002; Publication 
Number US-2005-0106160 (HHS Reference No. E-039-2002/0-US-02).
Licensing Contact: Susan Ano; 301/435-5515; <a href="/cdn-cgi/l/email-protection#6e0f00011d2e030f07024000070640090118"><span class="__cf_email__" data-cfemail="680906071b280509010446060100460f071e">[email protected]</span></a>.

    This technology relates to tethered antigenic constructs where 
flexible linkers join gp120 and the ectodomain of gp41. The HIV-1 
envelope Glycoprotein (Env) undergoes conformational changes while 
driving entry. The inventors developed these constructs to mimic some 
of the intermediate Env conformations. Tethered Envs with long (15 to 
26 amino acid) linkers were stable and potently inhibited fusion 
mediated by R5, X4 and R5X4 Envs, most likely by exposure of gp41 
structures that bind DP178 and cluster II mAbs. The fusion proteins 
with long linkers exhibited enhanced exposure of DP178 and cluster II 
mAbs binding gp41 structures that are critical for entry. These 
findings suggest the existence of conserved structures that are 
critical for HIV-1 entry, and could be used as novel immunogens for 
elicitation of broadly neutralizing antibodies and as antigens for 
selection of potent neutralizing antibodies by phage display.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

A Novel Post-Transcriptional Regulatory Element (PRE) and Its Use in 
Expression Cassettes and Recombinant Viruses

George N. Pavlakis et al. (NCI).
U.S. Patent Number 6,919,442, issued July 19, 2005; EP Patent 
Application Serial Number 99924362.9 (HHS Reference Number E-143-1998/
0).
Licensing Contact: Susan Ano; 301/435-5515; <a href="/cdn-cgi/l/email-protection#81e0efeef2c1ece0e8edafefe8e9afe6eef7"><span class="__cf_email__" data-cfemail="53323d3c20133e323a3f7d3d3a3b7d343c25">[email protected]</span></a>.

    This invention concerns a novel post-transcriptional regulatory 
element (PRE) that can function as a RNA nucleo-cytoplasmic transport 
element (NCTE) and its inclusion in expression cassettes and 
recombinant viruses, including in recombinant attenuated HIV strains. 
HIV regulates its expression by controlling the nuclear transport of 
unspliced mRNA encoding structural proteins utilizing the Rev/RRE 
system. RRE (Rev Responsible Element) is an HIV encoded NCTE, which is 
part of every HIV RNA encoding the structural genes (gag/pol and env). 
Rev is an HIV encoded protein that binds to RRE. This interaction is 
essential for the nucleo-cytoplasmic transport of the RRE-containing 
viral mRNAs and the expression of Gag/Pol and Env proteins in 
transport. The invention discusses an attenuated HIV produced by 
disabling rev/RRE by point mutations and inserting in its place the 
novel PRE of the invention. The resultant HIV is attenuated between 50 
and 200 fold compared to wild-type HIV. In addition to HIV, the novel 
PRE element can increase expression from many mRNAs not efficiently 
transported on their own.
    In addition to licensing, the technology is available for further 
development through collaborative

[[Page 66448]]

research opportunities with the inventors.

    Dated: October 25, 2005.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 05-21832 Filed 11-1-05; 8:45 am]
BILLING CODE 4140-01-P


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