[Federal Register Volume 70, Number 154 (Thursday, August 11, 2005)]
[Notices]
[Pages 46877-46879]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 05-15939]


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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.

[[Page 46878]]

Chimeric Lentiviral Vectors

Suresh K. Arya (NCI).
HHS Reference No. E-191-2005/0--Research Tool.
Licensing Contact: Susan Ano; 301/435-5515; [email protected].

    Lentiviral vectors have extensive application in the areas of gene 
therapy, functional genomics, and target validation, among others. 
Available for licensing as biological materials are chimeric HIV-1 and 
HIV-2 lentiviral transfer and packaging vectors. When using lentiviral 
vectors, it is important that the vectors incorporate as many safety 
features as possible to avoid the generation of recombinants or 
replication competent viruses. In other available vector systems 
derived from HIV-1 or HIV-2, viral genetic elements needed for vector 
production have been split into three parts to address safety concerns. 
In the chimeric vectors available herein, the safety is further 
enhanced by taking advantage of the sequence divergence of HIV-1 and 
HIV-2 coupled with functionally complementary nature of the genetic 
elements. The chimeric packaging vectors primarily involve swapping of 
the gag-pol or tat-rev genes, while the transfer vectors involve 
swapping of the leader-gag sequences. These vectors are potential 
candidates for use in gene therapy, for cell therapy with genetically 
modifying stem cells ex vivo, for use of siRNA or RNA interference for 
therapeutics, for creation of transgenic animals, and for pathway 
analysis and target validation by introducing novel genes.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Scytovirin Domain 1 (SD1) Related Polypeptide

Barry R. O'Keefe et al. (NCI)
U.S. Provisional Application No. 60/684,353 filed 25 May 2005 (HHS 
Reference No. E-180-2005/0-US-01).
Licensing Contact: Sally Hu; 301/435-5606; e-mail: [email protected].

    The invention provides composition claims for a scytovirin domain 1 
(SD1) antiviral polypeptide, nucleic acids encoding the polypeptide, 
related fusion proteins and conjugates, isolated cells, vectors, and 
antibodies that bind to the polypeptide. The polypeptide of this 
invention has the ability to bind to viral proteins, such as gp41 and 
gp120 of HIV, and exhibit anti-viral activity against type C and D 
retroviruses such as HIV-1 and HIV-2, Ebola, SARS, Influenza viruses 
and others. The invention also provides for methods of use to inhibit 
viral infections therapeutically and prophylactically as well as 
methods of inhibiting virus in biological samples or inanimate objects. 
Thus, further development of the invention may yield novel therapies 
and methods in the prevention of HIV and other retroviruses, and 
treatment of chronic infection in patients with resistance to current 
therapies.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Recombinant MVA Viruses Expressing Clade A/G and Clade B Modified HIV 
Env, Gag and Pol Genes Useful for HIV Vaccine Development

Bernard Moss and Linda S. Wyatt (NIAID)
U.S. Provisional Application No. 60/604,918 filed 27 Aug 2004 (HHS 
Reference No. E-337-2004/0-US-01).
Licensing Contact: Susan Ano; 301/435-5515; [email protected].

    The current technology relates to the construction, 
characterization and immunogenicity of modified vaccinia Ankara (MVA) 
recombinant viruses. The MVA double recombinant viruses express 
modified/truncated HIV-1 Env and mutated HIV Gag Pol under the control 
of vaccinia virus early/late promoters. This technology describes the 
MVA double recombinant viruses made by homologous recombination of 
single MVA recombinants, one expressing Env and one expressing Gag Pol. 
These single MVA recombinants are made using a transiently expressed 
GFP marker that is deleted in the final viruses. Two recombinant MVA 
viruses (MVA 65A/G and MVA 62B) made by this technology have been shown 
to produce HIV virus-like-particles that are immunogenic in mice. In 
addition, these two recombinant MVA viruses demonstrate stability 
through repeated passage of the LVD Seed Stock. This invention provides 
safe and stable immunogenic clade A/G and clade B vectors that may be 
tested as an AIDS vaccine candidate. Therefore, it is a promising 
technology to develop prophylactic and therapeutic AIDS vaccines for 
U.S. and for West Africa, particularly when used in combination with a 
DNA vaccine.

Chondroitin Sulphate A Binding Domains: Potential Vaccine for Malaria

Louis H. Miller (NIAID), et al.
U.S. Provisional Application No. 60/615,300 filed 30 Sep 2004 (DHHS 
Reference No. E-221-2004/0-US-01).
Licensing Contact: Robert M. Joynes; 301/594-6565; 
[email protected].

    The subject invention is related to a potential vaccine against 
malaria, and in particular to a vaccine that can prevent malaria 
infection in pregnant women. The invention relates to the 
identification of chondroitin sulphate A (CSA) binding domains in 
var2CSA homologs from different parasite strains. Malaria in pregnancy 
is a serious complication associated with the parasitized erythrocyte 
(PE) sequestration in the placenta. With successive pregnancies, 
pregnant women develop antibodies that recognize placental variants 
worldwide suggesting these isolates express conserved determinants. 
Plasmodium falciparum encodes multiple copies of an erythrocyte surface 
adhesion ligands called var genes. Recent work suggests that two 
different var genes (var1CSA and var2CSA) could have an important role 
in PE binding to chondroitin sulphate A (CSA), a primary placental 
adherence receptor. It has now been shown that var2CSA is transcribed 
in CSA-binding parasites and that the disruption of var2CSA results in 
the inability of the parasites to recover the CSA-binding phenotype. 
Furthermore, when expressed in Chinese hamster ovary (CHO) cells, three 
Duffy binding-like domains (DBL2-X, DBL3-X and DBL6-[egr]) from var2CSA 
revealed strong and specific binding to CSA. The identification of 
multiple binding domains in var2CSA is envisioned as forming the basis 
of a vaccine against malaria, especially in pregnancy.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Vaccines and Methods of Treating Drug-Resistant HIV-1 and Hepatitis B 
Viruses

Andrew Catanzaro (NCI), Jay A. Berzofsky (NCI), Robert Yarchoan (NCI), 
Takahiro Okazaki (NCI), James T. Snyder II (NCI), Samuel Broder.
U.S. Provisional Application No. 60/655,984 filed 22 Feb 2005 (DHHS 
Reference No. E-137-2003/1-US-01).
Licensing Contact: Robert M. Joynes; 301/594-6565; 
[email protected].

    This technology relates to methods for lowering a viral load of a 
virus where the virus causes a chronic viral infection and is resistant 
to an antiviral drug. The method comprises administering to a host a 
medicament comprising an antiviral drug to restrict the intracellular 
multiplication of the virus and that is capable of selecting for a 
predetermined

[[Page 46879]]

antiviral drug-resistant mutation in a viral protein. The medicament 
further comprises a synthetic peptide that comprises the predetermined 
antiviral drug-resistant mutation and at least six amino acid residues 
flanking that mutation that are identical to the amino acid sequence of 
the viral protein of the antiviral drug-resistant virus. The synthetic 
peptide induces a cytotoxic T lymphocyte (CTL) response specific for 
cells infected with the antiviral drug-resistant virus. The 
immunostimulating peptide may be further improved by epitope-
enhancement for inducing specific CTLs. The antiviral protection 
against drug-resistant virus shown by compositions of the present 
invention and mediated by human HLA-restricted CTL has not been 
previously achieved. Further, the compositions and methods of this 
technology are useful to target many viruses that can develop antiviral 
drug resistance, including HIV-1, HIV-2, hepatitis B virus, hepatitis C 
virus, and human herpesviruses.

Design of a Novel Peptide Inhibitor of HIV Fusion That Disrupts the 
Internal Trimeric Coiled-coil of gp41

Marius G. Clore, Carole A. Bewley, and John M. Louis (NIDDK).
U.S. Provisional Application No. 60/446,225 filed 11 Feb 2003 (HHS 
Reference No. E-236-2002/0-US-01);
PCT Application No. PCT/US04/03794 filed 10 Feb 2004, which published 
as WO 2004/072099 on 11 Aug 2004 (HHS Reference No. E-236-2002/0-PCT-
02).
Licensing Contact: Sally Hu; 301/435-5606; e-mail: [email protected].

    This invention provides a peptide derived from the sequence of the 
N-terminal helix (residues 546-581) of the gp41 ectodomain of HIV-1. 
The peptide, called N36Mut(e,g), contains nine substitutions 
and disrupts interactions with the C-terminal region of the gp41 
ectodomain. N36Mut(e,g) inhibits HIV-envelope mediated cell 
fusion about 50-fold more effectively than the native sequence 
(residues 546-581 of HIV-1 envelope) from which it was derived. Thus, 
N36Mut(e,g) and derivatives has potential as an anti-HIV 
therapeutic agent as a HIV fusion inhibitor.
    This research is described, in part, in CA Bewley et al., ``Design 
of a novel peptide inhibitor of HIV fusion that disrupts the internal 
trimeric coiled-coil of gp41,'' J. Biol. Chem. (2002 Apr 19) 
277(16):14238-14245; Epub on 21 Feb 2002 as doi:10.1074/jbc.M201453200.

    Dated: August 8, 2005.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 05-15939 Filed 8-10-05; 8:45 am]
BILLING CODE 4140-01-P