[Federal Register: November 30, 1998 (Volume 63, Number 229)] [Notices] [Page 65798-65799] From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr30no98-95] ----------------------------------------------------------------------- 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. ----------------------------------------------------------------------- SUMMARY: The inventions listed below are owned by agencies 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 contacting Dennis H. Penn, Pharm.D., Technology Licensing Specialist, Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, Maryland 20852-3804; telephone: 301/496-7056 ext. 211; fax: 301/402-0220. A signed Confidential Disclosure Agreement will be required to receive copies of the patent applications. A Mitochondrial-Specific ATP-Binding Transporter Gene (ABC7) Is An Iron Transporter In An Interhited Ataxia-Anemia Syndrome MC Dean, R Allikmets, AA Hutchinson (NCI) DHHS Reference No. E-181-98/0 filed Oct 23, 1998 The gene responsible for the rare genetic disease, X-linked siderblastic anemia and ataxia (XLSA/A) has been identified and linked to a mutation of the ATP-Binding transporter gene (ABC7). Two sequence changes which correspond to amino acid changes at positions 50 and 396 were detected. This gene may prove useful as a diagnostic for XLSA/A carriers or as a means to rule out XLSA/A from other siderblastic anemias. ABC7, an iron transporter, may prove to be a valuable tool for studying the function and regulation of muscle cells and the loss of motor function associated with many diseases with faculty iron metabolism, i.e. neuromuscular disease, cardiac disorders and neurological disorders. Compsitions And Uses of FIG-alpha Gene J Dean, L Liang, S soyal (NIDDK) Serial No. 60/069,037 filed Dec. 12, 1997 This application related to an isolated and purified polynucleotide encoding an isolated and purified polypeptide associated with the expression of zona pellucida genes. The mouse zona pellucida is composed of three glycoproteins, ZP1, ZP2 and ZP3, encoded by single- copy genes whose expression is temporarlly and spatially restricted to oocytes. All three proteins are required for the formation of the extracellular zona matrix and female mice with a single disrupted zona gene lack a zona and are infertile. An E-box (CANNTG), located approximately 200 bp upstream of the transcription start site of the ZP1, ZP2 and ZP3, forms a protein-DNA complex present in oocytes and, to a much lesser extent, in testes. The integrity of this E-box in ZP2 and ZP3 promoters is required for expression of luciferase reporter genes microinjected into growing oocytes. The presence of the ubiquitous transcription factor E12 in the complex was used to identify a novel basic helix-loop-helix protein FIG (Factor In the Germline alpha) whose expression was limited to oocytes within the ovary.) This invention relates to the molecular characterization of FIG, a novel germ cell specific bHLB transcription factor that binds as a heterodimer with E12 to the E-box in the promoter region of all three mouse zona pellucida genes and has the ability to transactivate reporter gene constructs in vitro. FIG is critical for folliculogenesis and has a role in the coordinate, oocyte- specific expression of the three zona pellucida genes, the products of which for an extracellular matrix required for fertilization and early development. This invention also relates to monoclonal and polyclonal antibodies, which recognize the FIG polypeptide. [[Page 65799]] Ureido Derivatives Of Poly-4-Amino-2-Carboxy-1-Methyl Pyrrole Compounds For Treatment Of inflammation OM Zac Howard (SAIC), JJ Oppenheim (NCI), WJ Murphy (SAIC), EA Sausville (NCI) Serial No. 60/067,526 filed Dec 4, 1997 Inflammatory reactions arising from a variety of medical conditions may have serious medical consequences when poorly controlled. Such inflammatory reactions contribute to a variety of disease states such as arthritis, asthma, non-bacterial medicated respiratory distress syndrome, reperfusion injury, and blunt force trauma. Accordingly, there is a need for new methods of diminished inflammation, especially acute inflammation. This invention describes a method of inhibiting inflammation, particularly non-TNF dependent inflammation, by administering pharmacologically active ureido derivatives of distamycin. Since TNF is only one of many inducers of chemokines, this invention provides a more inclusive method for treatment of many inflammatory conditions, including conditions in which TNF does not play a substantial deleterious role in the pathology of the condition. Therapeutic Chemokine Antagonists JJ Oppenheim, JM Wang, OY Chertov, LO Arthur, F Ruscetti (NCI) DHHS Reference No. E-170-96/0 filed Sep 06, 1996; PVT/US97/15594 filed Sep 05, 1997 This invention relates to a new class of chemoattractant antagonists, which are therapeutic candidates for treating disease conditions involving recruitment of inflammatory cells. These chemoattractant antagonists are comprised of a group consisting of gp120, gp41, domains and variants of gp41 and gp120. Chemoattractants include the subgroup of chemokines and are known to mediate chemotaxis and other pro-inflammatory phenomena. The chemoattractants are generally short peptides. The family of chemokines is subdivided into distinct subfamilies, C-X-C and C-C, based on the arrangements of the first two cysteines of the primary amino acid sequence. Members of the chemokine subfamily have remarkable similarities in their structural organization and biochemical properties. These homologies are consistent with the similarities observed in their biological effects, both in vitro and in vivo. These properties have prompted speculation that chemokines are mediators in autoimmune and allergic disorders. Dated: November 16, 1998. Jack Spiegel, Director, Division of Technology Development and Transfer, Office of Technology Transfer. [FR Doc. 98-31730 Filed 11-27-98; 8:45 am] BILLING CODE 4140-01-M