Skip to Content


Government-Owned Inventions; Availability for Licensing

Document Details

Information about this document as published in the Federal Register.

Published Document

This document has been published in the Federal Register. Use the PDF linked in the document sidebar for the official electronic format.

Start Preamble


National Institutes of Health, Public Health Service, DHHS.




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.


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.

Farnesyltransferase Inhibitors for Treatment of Laminopathies, Cellular Aging and Atherosclerosis

Francis Collins (NHGRI) et al.

U.S. Provisional Application No. 60/648,307 filed 28 Jan 2005 (DHHS Reference No. E-055-2005/0-US-01).

Licensing Contact: Fatima Sayyid; 301/435-4521;

Hutchinson-Gilford Progeria Syndrome (HGPS) is a very rare progressive childhood disorder characterized by premature aging (progeria). Recently, the gene responsible for HGPS was identified (Eriksson M, Brown WT, Gordon LB, Glynn MW, Singer J, Scott L, et al. Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome. Nature 2003; 423(6937): 293-8), and HGPS joined a group of syndromes—the laminopathies—all of which are caused by various mutations in the lamin A/C gene (LMNA). Lamin A is one of the family of proteins that is modified post-translationally by the addition of a farnesyl group. In progeria, the abnormal protein (progerin) can still be farnesylated, however, a subsequent cleavage is blocked.

The present invention describes a possible treatment of laminopathies, cellular aging and aging-related conditions such as HGPS through the use of farnesyltransferase inhibitors (FTIs) and other related compounds. This treatment should lead to a decrease in the accumulation of abnormal proteins such as progerin in case of HGPS patients and therefore reduce or eliminate many of the devastating clinical symptoms of the underlying biological defect of nuclear membrane instability (Goldman R, Shumaker DK, Erdos MR, Eriksson M, Goldman AE, Gordon LB, Gruenbaum Y, Khuon S, Mendez M, Varga R, Collins FS. Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome. Proc Natl Acad Sci U S A 2004; 8963-8968.).

In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors.

Cell Culture System for Efficient Expression of Self-Replicating Norwalk Virus

Kyeong-Ok Chang, Stanislav Sosnovtsev, Gael M. Belliot, Kim Y. Green (NIAID).

U.S. Provisional Application filed 08 Apr 2005 (DHHS Reference No. E-043-2005/0-US-01).

Licensing Contact: Michael Shmilovich; 301/435-5019;

Available for licensing and commercial development is a cell culture system for the efficient expression of self-replicating Norwalk virus (NV) RNA (NV replicons). This invention provides compositions and methods for preparing a cell-based system for molecular studies of NV replication and the development of antiviral drugs. A method related to effectively clearing NV replicons, by subjecting cells infected with NV replicon to IFN-alpha is included that demonstrates the applicability of this invention to drug development. A method of effectively clearing NV replicons, by subjecting cells expressing the NV replicon to nucleotide analogues is also provided. These methods provide molecular tools for the identification and development of treatments for NV and may also extend to other members Start Printed Page 33184of the Calicivirus(es) (e.g., Norovirus, Sapovirus, Lagovirus and Vesivirus).

Therapeutic Delivery of Nitric Oxide From Novel Diazeniumdiolated Derivatives of Acrylonitrile-based Polymers

Joseph Hrabie, Michael Citro, Frank DeRosa, and Larry Keefer (NCI).

U.S. Provisional Application No. 60/613,257 filed 27 Sep 2004 (DHHS Reference No. E-188-2004/0-US-01).

Licensing Contact: Norbert Pontzer; 301/435-5502;

Nucleophile/nitric oxide adduct ions (materials containing the X-N2 O2-functional group; known as diazeniumdiolates or NONOates) spontaneously dissociate at physiological pH to release nitric oxide (NO) with reproducible half-lives ranging from 2 seconds to 20 hours. The bulk of the known and patented NIH compositions and methods using diazeniumdiolates are derived from amine nucleophiles (i.e., where X-is R1 R2 N-). These inventors more recently developed simple and efficient chemical methods to produce diazeniumdiolates by bonding the N2 O2-functional group directly to carbon atoms. Using these methods, the NIH inventors have now produced and tested polymers in which the NO releasing group is attached directly to the carbon backbone of polyacrylonitrile containing polymers.

Available for licensing are compounds, compositions, medical devices, and methods of treatment using acrylonitrile-based polymers that release NO for a week or longer. Polyacrylonitrile itself, co-polymers, admixtures, and products such as cloth and hollow fiber hemofilters have been treated and shown to release NO over time. These polyacrylonitrile-based products could be useful in conjunction with medical devices where the many therapeutic actions of NO would be beneficial. Treatments using stents,

extracorporeal blood tubing, shunts, wound dressings and many other devices could be greatly improved by NO actions including but not limited to prevention of clotting, promotion of tissue vascularization, and reduction of excessive tissue proliferation.

In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors.

A New Antiviral Pathway that is Responsible for Viral Clearance: Modulation of ADAR1 Activities Enhance Antiviral Therapies and Virus Infection of Tissue Culture Systems

Deborah R. Taylor et al. (FDA).

U.S. Provisional Application No. 60/605,238 filed 27 Aug 2004 (DHHS Reference No. E-121-2004/0-US-01).

Licensing Contact: Robert M. Joynes; 301/594-6565;

This technology relates to the finding that the antiviral activity of interferon (IFN) is mediated by the activation of an enzyme RNA adenosine deaminase (ADAR1). This enzyme acts by deaminating adenosine residues in dsRNA molecules of the virus into inosine residues. This, in turn, may lead to mutations, genomic instability and ultimately to complete degradation and elimination of the virus. The subject patent application focuses on Hepatitis C virus (HCV), but may be broadly applied to the other viruses.

Based on the above-described finding, the technology offers two important utilities in the medical field:

1. Antiviral therapeutics: Because ADAR is so potent as an inhibitor of the growth of HCV, an agonist of this pathway or specifically of ADAR should enhance the clearance of the virus from the cells. Methods to identify such ADAR agonists are described in the subject patent applications.

2. HCV cell line for drug and vaccine research: The finding described in the subject patent application may lead to an efficient cell line for growing HCV. Currently, there is not a good system to grow this virus. The addition of ADAR inhibitors (such as RNAi or chemicals that target the catalytic domain of ADAR) to the system will result in a system that can efficiently grow the virus. Such a cell line is important for vaccine development against HCV as well as the development of anti-viral therapeutics.

In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors.

Compositions Comprising T Cell Receptors and Methods of Use Thereof

Richard Morgan (NCI) and Steven Rosenberg (NCI).

PCT Application No. PCT/US2004/029608 filed 13 Sep 2004 (DHHS Reference No. E-106-2004/0-PCT-01).

Licensing Contact: Michelle A. Booden; 301/451-7337;

Historically, adoptive immunotherapy has shown promise in treating cancer. Traditionally, these adoptive techniques developed to date have relied on isolating and expanding T-cells reactive to a specific tumor associated antigen. However, the approach has been limited by number of isolatable T cells specific to a tumor-associated antigen in a cancer patient's immune system and a very time consuming procedure to isolate and expand the appropriate T-cells.

This invention describes the composition and use of nucleic acid sequences that encode polypeptides capable of forming a T cell receptor (TCR) in a genetically engineered cell. Specifically, these nucleic acid sequences will encode TCR's specific to tumor associated antigens (TAA), gp100, NY-ESO-1, and MART-1. T Cells engineered with these tumor associated antigen specific TCRs show specific immune responses against TAA expressing cancer cells. This observation has a profound effect on the potential efficiency of new adoptive therapies targeted towards cancer.

An adoptive therapy method has been developed using the TAA specific TCR nucleic acids to engineer isolated, non-specific T-cells. This method could eliminate the need to isolate and expand T-cells that may or may not be present in a cancer patient. Clinical trials are currently underway to prove the efficacy of this new adoptive therapy in malignant melanoma.

Details of this invention are published in:

1. Morgan RA, Dudley ME, Yu YY, Zheng Z, Robbins PF, Theoret MR, Wunderlich JR, Hughes MS, Restifo NP, Rosenberg SA. High efficiency TCR gene transfer into primary human lymphocytes affords avid recognition of melanoma tumor antigen glycoprotein 100 and does not alter the recognition of autologous melanoma antigens. J Immunol. 2003 Sep 15;171(6):3287-95.

2. Zhao Y, Zheng Z, Robbins PF, Khong HT, Rosenberg SA, Morgan RA. Primary human lymphocytes transduced with NY-ESO-1 antigen-specific TCR genes recognize and kill diverse human tumor cell lines. J Immunol. 2005 Apr 1;174(7):4415-23.

3. Hughes MS, Yu YY, Dudley ME, Zheng Z, Robbins PF, Li Y, Wunderlich J, Hawley RG, Moayeri M, Rosenberg SA, Morgan RA. Transfer of a TCR Gene Derived from a Patient with a Marked Antitumor Response Conveys Highly Active T-Cell Effector Functions. Hum Gene Ther. 2005 Apr;16(4):457-72.

In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors.

Retrovirus-Like Particles and Retroviral Vaccines

David E. Ott (NCI).

PCT Application filed 27 Oct 2003 (DHHS Reference No. E-236-2003/0-PCT-01).Start Printed Page 33185

Licensing Contact: Susan Ano; 301/435-5515;

This technology describes retrovirus-like particles and their production from retroviral constructs in which the gene encoding all but seven amino acids of the nucleocapsid (NC) protein was deleted. This deletion functionally eliminates packaging of the genomic RNA, thus resulting in non-infectious retrovirus-like particles. These particles can be used in vaccines or immunogenic compositions. Specific examples using HIV-1 constructs are given. Furthermore, efficient formation of these particles requires inhibition of the protease enzymatic activity, either by mutation to the protease gene in the construct or by protease inhibitor thereby ensuring the production of non-infectious retrovirus-like particles. This technology is further described in Ott et al., Journal of Virology, 2003, 77(5), 5547.

Start Signature

Dated: May 26, 2005.

Steven M. Ferguson,

Director, Division of Technology Development and Transfer, Office of Technology Transfer,National Institutes of Health.

End Signature End Preamble

[FR Doc. 05-11221 Filed 6-6-05; 8:45 am]