[Federal Register Volume 69, Number 204 (Friday, October 22, 2004)]
[Notices]
[Pages 62059-62060]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 04-23650]


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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, DHHS.

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.

Inhibitors of HIV Ribonuclease H Antiviral Properties

Drs. John Beutler, Stuart LeGrice, Scott Budihas, Antony Wamiru, 
Roberta Gardella, and Jennifer Wilson (all of NCI); Dr. Michael Parniak 
(EM)
U.S. Provisional Application filed 30 Aug 2004 (DHHS Reference No. E-
256-2004/0-US-01)

Licensing Contact: Sally Hu; 301/435-5606; <a href="/cdn-cgi/l/email-protection#f8908d8bb895999194d6969190d69f978e"><span class="__cf_email__" data-cfemail="365e4345765b575f5a18585f5e18515940">[email protected]</span></a>.

    The invention describes a class of compounds that inhibit HIV RNase 
H and the methods of using these compounds for the treatment of HIV 
infections. More specifically, these compounds are vinylogous urea 
derivative containing substituted thiophene core structures and these 
compounds were part of the 100,000 member library of compounds 
purchased by NCI from ChemBridge. The selectivity of the antiviral 
activity was demonstrated in their selective inhibition of HIV-1 and 
HIV-2 Rnase H enzymes 1 in the CEM cell line of CD4+ lymphoblast cells. 
Five members of this class of compounds were able to block the 
cytopathic effect of the virus at concentrations that did not inhibit 
cell growth. Thus, these compounds may be used in the development of 
therapeutics for the treatment of retroviral infections, such as AIDS. 
In addition, these compounds 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 integrase.

Protozoan Derived Antagonist of CCR5

Drs. Alan Sher, Julio Aliberti, Jose Ribeiro, and John Andersen (all of 
NIAID); Dr. Hana Golding (FDA)
U.S. Provisional Application No. 60/586,884 filed 08 Jul 2004 (DHHS 
Reference No. E-272-2004/0-US-01)
Licensing Contact: Sally Hu; 301/435-5606; <a href="/cdn-cgi/l/email-protection#87eff2f4c7eae6eeeba9e9eeefa9e0e8f1"><span class="__cf_email__" data-cfemail="d7bfa2a497bab6bebbf9b9bebff9b0b8a1">[email protected]</span></a>.

    The invention describes the anti-HIV properties of cyclophilin-18, 
a protein expressed by the protozoan parasite Toxoplasma gondii. The 
protein was found to bind to the chemokine receptor CCR5 which is also 
a co-receptor for the HIV virus. Both the native and recombinant 
molecules display inhibitory activity in HIV-1 fusion (syncitia 
formation) and infectivity assays with human T cells and macrophages. 
Thus, Toxoplasma gondii cyclophilin-18 or modified versions of the 
molecule may be used in the development of treatment for AIDS. In 
particular, the protein described in this invention may have particular 
value when used as a microbicide for blocking initial HIV infection. 
More details of this invention can be found in Golding et al., 
``Inhibition of HIV-1 Infection by a CCR5 Binding Cyclophilin from 
Toxoplasma gondii'', Blood 1 Nov 2003 102(9): 3280-3286.

Treatment of Human Viral Infections (Resveratrol)

Drs. Steven Zeichner and Vyjayanthi Krishnan (NCI)
U.S. Provisional Application No. 60/588,013 filed 13 Jul 2004 (DHHS 
Reference No. E-279-2004/0-US-01)
Licensing Contact: Sally Hu; 301/435-5606; <a href="/cdn-cgi/l/email-protection#dbb3aea89bb6bab2b7f5b5b2b3f5bcb4ad"><span class="__cf_email__" data-cfemail="e9819c9aa984888085c7878081c78e869f">[email protected]</span></a>.

    This application describes the methods for treating or preventing 
an HIV infection by the administration of an Egr 1 activator called 
Resveratrol (3, 5, 4''-trihydroxystilbene) and its derivatives. It has 
been known that HIV, once it infects a cell, integrates into the 
cellular genome and can (1) rapidly undergo lytic infection, or (2) lay 
dormant for a period of time (latent infection). The existence of 
latent infected cells poses a great challenge to HIV therapy because 
(1) there are no good existing means that can separate the latent 
infected cells from the uninfected cells; (2) even when antiretroviral 
drugs are able to completely suppress detectable HIV replication, these 
latent infected cells will remain and HIV can subsequently complete the 
viral replication cycle to produce more virus. Since Resveratrol and 
its derivatives can activate lytic replication from latent infected 
cells via its effects on Erk1/2 signaling, Resveratrol and its 
derivatives may lead to therapies in which Resveratrol and/or its 
derivatives is given together with highly active antiretroviral therapy 
in an

[[Page 62060]]

effort to decrease or eliminate the reservoir of latent infected cells 
with hope of perhaps eventually curing a patient of HIV infection.

Treatment of Human Viral Infections (Proteosome Inhibitors)

Drs. Steven Zeichner and Vyjayanthi Krishnan (NCI)
U.S. Provisional Application No. 60/587,810 filed 13 Jul 2004 (DHHS 
Reference No. E-280-2004/0-US-01)
Licensing Contact: Sally Hu; 301/435-5606; <a href="/cdn-cgi/l/email-protection#85edf0f6c5e8e4ece9abebecedabe2eaf3"><span class="__cf_email__" data-cfemail="563e2325163b373f3a78383f3e78313920">[email protected]</span></a>.

    This application describes the methods for treating or preventing 
an HIV infection by the administration of proteosome inhibitors and 
their derivatives. It has been known that HIV, once it infects a cell, 
integrates into the cellular genome and can (1) rapidly undergo lytic 
infection, or (2) lay dormant for a period of time (latent infection). 
The existence of latent infected cells poses a great challenge to HIV 
therapy because (1) there are no good existing means that can separate 
the latent infected cells from the uninfected cells; (2) even when 
antiretroviral drugs are able to completely suppress detectable HIV 
replication, these latent infected cells will remain and HIV can 
subsequently complete the viral replication cycle to produce more 
virus. Since proteosome inhibitors can activate lytic replication from 
latent infected cells, proteosome inhibitors may lead to therapies in 
which proteosome inhibitors are given together with highly active 
antiretroviral therapy in an effort to decrease or eliminate the 
reservoir of latent infected cells with hope of perhaps eventually 
curing a patient of HIV infection.

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; <a href="/cdn-cgi/l/email-protection#cba3beb88ba6aaa2a7e5a5a2a3e5aca4bd"><span class="__cf_email__" data-cfemail="59312c2a193438303577373031773e362f">[email protected]</span></a>.

    This application describes the methods for treating or preventing 
an HIV infection by the administration of abl-kinase inhibitor called 
imatinib and its derivatives. It has been known that HIV, once it 
infects a cell, integrates into the cellular genome and can (1) rapidly 
undergo lytic infection, or (2) lay dormant for a period of time 
(latent infection). The existence of latent infected cells poses a 
great challenge to HIV therapy because (1) there are no good existing 
means that can separate the latent infected cells from the uninfected 
cells; (2) even when antiretroviral drugs are able to completely 
suppress detectable HIV replication, these latent infected cells will 
remain and HIV can subsequently complete the viral replication cycle to 
produce more virus. Since imatinib and its derivatives can activate 
lytic replication from latent infected cells by activating NF-kB, 
imatinib and its derivatives may lead to therapies in which imatinib 
and/or its derivatives is given together with highly active 
antiretroviral therapy in an effort to decrease or eliminate the 
reservoir of latent infected cells with hope of perhaps eventually 
curing a patient of HIV infection.

Treatment of Human Viral Infections (Farnesyl Transferase Inhibitors)

Drs. Steven Zeichner and Vyjayanthi Krishnan (NCI)
U.S. Provisional Application No. 60/587,771 filed 13 Jul 2004 (DHHS 
Reference No. E-282-2004/0-US-01)
Licensing Contact: Sally Hu; 301/435-5606; <a href="/cdn-cgi/l/email-protection#7c14090f3c111d151052121514521b130a"><span class="__cf_email__" data-cfemail="11796462517c70787d3f7f78793f767e67">[email protected]</span></a>.

    This application describes the methods for treating or preventing 
an HIV infection by the administration of farnesyl transferase 
inhibitors such as FTI277, L-744832, BMS214662, R115777 and SCH66336. 
It has been known that HIV, once it infects a cell, integrates into the 
cellular genome and can (1) rapidly undergo lytic infection, or (2) lay 
dormant for a period of time (latent infection). The existence of 
latent infected cells poses a great challenge to HIV therapy because 
(1) there are no good existing means that can separate the latent 
infected cells from the uninfected cells; (2) even when antiretroviral 
drugs are able to completely suppress detectable HIV replication, these 
latent infected cells will remain and HIV can subsequently complete the 
viral replication cycle to produce more virus. Since farnesyl 
transferase inhibitors can activate lytic replication from latent 
infected cells by modulating membrane-bound Ras-Rho levels, farnesyl 
transferase inhibitors may lead to therapies in which farnesyl 
transferase inhibitor is given together with highly active 
antiretroviral therapy in an effort to decrease or eliminate the 
reservoir of latent infected cells with hope of perhaps eventually 
curing a patient of HIV infection.

    Dated: October 15, 2004.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 04-23650 Filed 10-21-04; 8:45 am]
BILLING CODE 4140-01-P


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