[Federal Register Volume 74, Number 77 (Thursday, April 23, 2009)]
[Notices]
[Pages 18581-18582]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: E9-9345]


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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, HHS.

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

[[Page 18582]]

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.

Identification of Subjects Likely To Benefit From Copper Treatment

    Description of Technology: Menkes disease is an infantile onset X-
linked recessive neurodegenerative disorder caused by deficiency or 
dysfunction of a copper-transporting ATPase, ATP7A. The clinical and 
pathologic features of this condition reflect decreased activities of 
enzymes that require copper as a cofactor, including dopamine-[beta]-
hydrolase, cytochrome c oxidase and lysyl oxidase. Recent studies 
indicate that ATP7A normally responds to N-methyl-D-aspartate receptor 
activation in the brain, and an impaired response probably contributes 
to the neuropathology of Menkes disease. Affected infants appear 
healthy at birth and develop normally for 6 to 8 weeks. Subsequently, 
hypotonia, seizures and failure to thrive occur and death by 3 years of 
age is typical. Occipital horn syndrome (OHS) is also caused by 
mutations in the copper transporting ATPase ATP7A, although its 
symptoms are milder than Menkes syndrome, including occipital horns and 
lax skin and joints.
    Treatment with daily copper injections may improve the outcome in 
Menkes disease if commenced within days after birth; however, newborn 
screening for this disorder is not available and early detection is 
difficult because clinical abnormalities in affected newborns are 
absent or subtle. Moreover, the usual biochemical markers (low serum 
copper and ceruloplasmin) are unreliable predictors in the neonatal 
period, since levels in healthy newborns are low and overlap with those 
in infants with Menkes disease. Although molecular diagnosis is 
available, its use is complicated by the diversity of mutation types 
and the large size of ATP7A (about 140kb). Thus, there is a need for 
improved methods for early detection of infants with Menkes disease or 
OHS in order to improve outcomes.
    This technology relates to methods of identifying individuals who 
may benefit from treatment with copper, particularly those having 
Menkes disease or Occipital Horn Syndrome.
    Inventor: Stephen G. Kaler (NICHD).
    Publication: SG Kaler, CS Holmes, DS Goldstein, JR Tang, SC Godwin, 
A Donsante, CJ Liew, S Sato, N Patronas. Neonatal diagnosis and 
treatment of Menkes disease. N Engl J Med. 2008 Feb 7;358(6):605-614.
    Patent Status: PCT Application No. PCT/US2008/078966 filed 06 Oct 
2008 (HHS Reference No. E-186-2008/0-PCT-01).
    Licensing Status: Available for licensing.
    Licensing Contact: Fatima Sayyid, M.H.P.M.; 301-435-4521; 
[email protected].
    Collaborative Research Opportunity: The National Institute of Child 
Health and Human Development, Division of Intramural Research, 
Molecular Medicine Program, Unit on Pediatric Genetics, is seeking 
statements of capability or interest from parties interested in 
collaborative research to further develop, evaluate, or commercialize 
population-based newborn screening for Menkes disease and related 
disorders of copper transport in order to identify subjects likely to 
benefit from copper injections and other treatments. Please contact 
Alan Hubbs, PhD at 301-594-4263 or [email protected] for more 
information.

Polyclonal Antibody Against Bloom's Syndrome Protein (BLM) for Research 
and Diagnostic Use

    Description of Technology: Investigators at the National Institutes 
of Health have generated a polyclonal antibody against Bloom's syndrome 
protein (BLM). The BLM protein is a DNA helicase enzyme and a key 
component of the DNA damage response signaling pathway. Several protein 
kinases including ATM, DNA-PK, and ATR can mediate the phosphorylation 
of BLM. The polyclonal antibody is generated by using a phosphorylated 
peptide belonging to the N-terminus of BLM. The antibody shows a rapid 
phosphorylation of BLM on threonine 99 (T99p-BLM) following DNA damage 
by anti-cancer agents and could serve as a therapeutic marker of drug 
action on DNA. The antibody is also useful for microscopic and 
biochemical analysis of DNA damage signaling.
    Applications:
     A therapeutic marker of drug action on DNA
     A diagnostic indicator of inherent genomic instability
    Inventors: Yves Pommier and V. Ashutosh Rao (NCI)
    Patent Status: HHS Reference No. E-053-2006/0--Research Tool. 
Patent protection is not being sought for this technology.
    Licensing Status: Threonine 99 specific polyclonal antibody against 
the BLM protein is available for licensing.
    Licensing Contact: Betty Tong, PhD; 301-594-6565; 
[email protected].

    Dated: April 16, 2009.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. E9-9345 Filed 4-22-09; 8:45 am]
BILLING CODE 4140-01-P