[Federal Register Volume 68, Number 24 (Wednesday, February 5, 2003)]
[Notices]
[Pages 5900-5901]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 03-2626]


-----------------------------------------------------------------------

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 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.

Fibroblast Growth Factor 3 (FGFR3) Receptor Knockin Mice

    Dr. Chuxia Deng (NIDDK), DHHS Reference No. E-060-2003/0--Research 
Tool.
    Licensing Contact: Marlene Shinn-Astor; 301/435-4426; 
[email protected].
    Missense mutations in Fibroblast Growth Factor Receptor 3 (FGFR3) 
result in several human skeletal dysplasias, including the most common 
form of dwarfism, achondroplasia.
    The NIH announces the generation of FGFR3 knockin mice, which have 
a Gly369Cys mutation, inserted into the mouse genome. Phenotypic 
analysis of the mice reveals that the FGF/FGFR3 signals affect both 
chondrogenesis and osteogenesis by regulating Stat proteins and cell-
cycle inhibitors, and the activities of chondrocytes, osteoclasts, and 
osteoblasts during endochondral ossification. These mice provide a new 
animal model to study functions of FGF/FGFR3 signals in achondroplasia 
patients, which could lead to new drug discovery and therapeutic 
treatments.

Compositions and Methods for Inhibiting Group B Streptococcal-Induced 
Pulmonary Hypertension in Neonates

    Rodney L. Levine et al. (NHLBI), DHHS Reference No. E-259-2002/0 
filed Oct. 15, 2002.
    Licensing Contact: Susan Ano; 301/435-5515; [email protected].
    Group B streptococcus (GBS), the most common cause of sepsis and 
meningitis in human newborns, often results in respiratory distress. 
The underlying cause of this distress is pulmonary hypertension, 
historically believed to be induced by increased production of 
thromboxane A2 as stimulated by GBS. The technology described here 
reveals that the phospholipids cardiolipin and phosphotidylglycerol are 
causative agents of GBS-induced pulmonary hypertension. Furthermore, 
the technology describes administration of these phospholipids or 
immunogenic fragments thereof in an appropriate fashion to elicit an 
immune response, including administration as conjugates to hapten to 
enhance the binding selectivity of the resulting antibodies. 
Additionally, administration of antibodies to these phospholipids for 
the same purpose is related. The phospholipids or immunogenic fragments 
can also be administered in a dose-dependent manner to increase blood 
pressure in pulmonary arteries. Kits for administration of these 
phospholipids and/or anti-phospholipid antibodies are also described. 
The standard treatment for GBS infection is the penicillin class of 
antibiotics, which increases the synthesis and excretion of the two 
phospholipids revealed in this technology to cause pulmonary 
hypertension. Thus, the current technology offers a potential 
improvement over existing treatments. In the course of the research 
that led to the above discovery, a method of separating recombinantly 
expressed membrane-bound proteins and membrane-associated endotoxin in 
gram-negative prokaryote expression systems was also developed.

p-Toluemesulfonhydrazide Derivatization for Separation and Measurement 
of Endogenous Estrogen Metabolites by High-Pressure Liquid 
Chromatography-Electrospray-Mass Spectrometry

    Dr. Xia Xu (NCI), U.S. Provisional Patent Application 60/372,848 
filed Apr. 15, 2002.
    Licensing Contact: Brenda Hefti; 301/435-4632; [email protected].
    The current invention relates to a method for measuring endogenous 
estrogen levels, and this technology may be generalizable to all 
endogenous ketolic steroids, including estrogens, androgens, and 
phytoestrogens.
    Specifically, the current invention is a derivatization technique 
that forms estrogen-p-toluenesulfonhydrazones, which can be separated 
and then measured using high-pressure liquid chromatography-
electrospray-mass spectrometry (HPLC-ESI-MS). This method offers a 
number of improvements over current methods. It is more sensitive, it 
is faster, it is more accurate, and it requires a smaller sample size.

FXR/BAR Knockout Mouse Model

    Frank Gonzalez (NCI), DHHS Reference No. E-323-2001/0--Research 
Tool.
    Licensing Contact: Marlene Shinn-Astor; 301/435-4426; 
[email protected].
    Cholesterol lowering drugs are being prescribed more and more as a 
way to combat high cholesterol levels associated as a precursor to 
heart disease. The NIH announces a new knockout mouse model that lacks 
the nuclear receptor FXR/BAR (bile acid receptor). The receptor 
controls the synthesis and transport of bile salts, which are 
degradation products of cholesterol. These mice could, therefore, be 
used to test new targets for cholesterol lowering drugs that use a new 
mechanism which is distinct from the current statin drugs that control 
HMG CoA reductase.

Telomerase Immortalized Hepatocyte Cell Lines

    Xin W. Wang and Curtis Harris (NCI), DHHS Reference No. E-251-2000/
0-US-01 filed Dec. 14, 2000.
    Licensing Contact: Catherine Joyce; 301/435-5031; 
[email protected].

[[Page 5901]]

    This technology relates to the development of new immortalized 
human liver cell lines that may be used for experimental, 
toxicological, physiological and gene therapeutic purposes. The cell 
lines were immortalized using a human telomerase reverse transcriptase 
(hTERT) gene via a retroviral vector and were derived from human 
hepatocytes.
    A PCT patent application corresponding to this technology (PCT/
US01/47755) was published on June 20, 2002 with publication number WO 
02/48319.
    The above-mentioned invention is available for licensing on a non-
exclusive basis.

    Dated: January 28, 2003.
Jack Spiegel,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 03-2626 Filed 2-4-03; 8:45 am]
BILLING CODE 4140-01-P