National Institutes of Health, Public Health Service, HHS.
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.
Use of Replicators in Gene Therapy
Mirit Aladjem, Cindy Tseng, Haiqing Fu and Lixin Wang (NCI).
U.S. Provisional Application No. 60/715,113 filed 07 Sep 2005 (HHS Reference No. E-309-2005/0-US-01).
Licensing Contact: Susan Carson, D. Phil.; 301/435-5020; firstname.lastname@example.org.
There remains a need for a gene therapy vector capable of delivering a stably maintained, appropriately-regulated therapeutic transgene without adverse side effects. Lack of expression of a therapeutic transgene is still a major obstacle for gene therapy and the extent of transcriptional silencing of gene therapy vectors depends on their chromosomal location and on the presence of nearby heterochromatin. Most active genes replicate early during S phase, while transcriptional silencing correlates with late replication. The location of DNA replication initiation events on chromatin is affected by DNA sequences termed replicators, which interact with distal sequences to establish an epigenetic permissive state that directs the replication machinery to the replicator at a specific time during S phase. NIH researchers at the National Cancer Institute have now shown that inclusion of functional replicators in transgenes are able to prevent gene silencing, suggesting that replicator sequences have an important role in stabilizing gene expression patterns. The ideal gene delivery vector system would include functional elements that permit stable maintenance and long-term regulated transgene expression and the inclusion of replicators may be key Start Printed Page 10981in the prevention of gene silencing and replication delay.
Claims are directed to specific constructs and methods of using replicators and transgene constructs to inhibit, delay or prevent gene silencing and are available for licensing. The addition of these sequences to non-replicating or self-replicating gene delivery systems may be key in the development of effective gene delivery vectors.
Related portfolios available for licensing include: (1) the Mammalian Artificial Chromosome Portfolio [HHS Ref. No. E-128-2005/0-US-01, U.S. Provisional Patent Application No. 60/669,589 filed 08 Apr 2005 and HHS Ref. No. E-253-2000/0-US-03, U.S. Patent Application Publication No. U.S. 2004/0245317 filed 08 Apr 2002) and (2) the TAR Cloning Portfolio (HHS Ref. No. E-121-1996/0-US-06 and HHS Ref. No. E-158-2001/0-US-02, U.S. Patent Application Publication No. U.S. 2004/0248289 filed 04 Oct 2002].
In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors.
TNF-alpha Converting Enzyme Inhibitory Agents and Stimulatory Agents
Stewart J. Levine et al. (NHLBI).
U.S. Provisional Application No. 60/505,394 filed 24 Sep 2003 (HHS Reference No. E-208-2003/0-US-01); PCT Application No. PCT/US2004/031608 filed 24 Sep 2004, which published as WO 2005/030798 on 07 Apr 2005 (HHS Reference No. E-208-2003/0-PCT-02).
Licensing Contact: Marlene Astor; 301/435-4426; email@example.com.
The action of Tumor Necrosis Factor alpha (TNF-alpha) has been implicated in such diseases as arthritis, sepsis, ulcerative colitis, multiple sclerosis, Crohn's disease, septic shock, graft rejection, cachexia, insulin resistance, post-ischemic reperfusion injury, tumor metastasis, tissue ulceration, abnormal wound healing, periodontal disease, bone disease, proteinuria, aneurismal aortic disease, degenerative cartilage loss, demyelinating diseases of the nervous system, and HIV infection. TNF-alpha converting enzyme (TACE) or ADAM 17 (A Disintegrin And Metalloprotease) is a member of a family of zinc metalloproteases, and is an important regulator of inflammation, immune regulation, and cellular proliferation as a consequence of its ability to catalyze the activation of TNF-alpha from a membrane bound to a soluble form.
The NIH announces the identification of a protein, corresponding to the amino-terminus of the TACE prodomain, that possesses a TACE inhibitory activity that is independent of a cysteine-switch mechanism. This TACE inhibitory protein could be used as a new therapeutic agent against chronic inflammatory diseases that are mediated by TNF-alpha.Start Signature
Dated: January 21, 2006.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health.
[FR Doc. E6-3013 Filed 3-2-06; 8:45 am]
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