[Federal Register Volume 75, Number 231 (Thursday, December 2, 2010)]
[Notices]
[Pages 75179-75182]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2010-30278]


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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 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.

Mouse Monoclonal Antibody for CEACAM

    Abstract: The following biological material is a hybridoma cell 
line generated from mice lymphocytes immunized with human mammary 
carcinomas and fused to a myeloma cell line. The resulting mouse 
monoclonal antibody (MAb, clone B1.1) is directed against 
carcinoembryonic antigen (CEA). CEA are glyco-proteins whose expression 
levels are increased on the surface of metastatic cancer cells. 
Therefore, antibodies generated from the hybridoma clone B1.1 can be 
used to detect cancer cells. MAb B1.1 binds to the surface of human 
breast and melanoma cell lines and cells associated with colon 
carcinomas and adenomas. The antibody has been tested to work 
effectively in several techniques such as Immunofluorescence, Western 
Blot, Fluorescent Activated Cell Sorting (FACS), and 
Immunohistochemistry (IHC).

Commercial Applications

    <bullet> Developing cancer biomarker.
    <bullet> Developing cell sorting assays (e.g. FACS).
    <bullet> Immunofluorescence, Western Blotting, and 
Immunohistochemistry for CEA.
    <bullet> Developing prognostic assays for cancer.
    Competitive Advantages: Tested to bind CEA and can be used in 
different Immunological Techniques such as Immunofluorescence, Western 
Blot, Fluorescent Activated Cell Sorting (FACS), and 
Immunohistochemistry (IHC).
    Materials Available: 1 vial of Hybridoma cell line (B1.1).
    Inventors: Jeffrey Schlom and David Colcher (NCI).

Related Publications

    1. D. Colcher et al. (1983) [PubMed: 6365268].
    2. D. Stramignoni et al. (1983) [PubMed: 6852972].
    Patent Status: ``The Generation of Monoclonal Antibody (MAb) B1.1 
and Its Reactivity to Human Tumors,'' HHS Reference No. E-272-2010/0--
Research Material. Patent protection is not being pursued for this 
technology.
    Licensing Status: Available for licensing under a Biological 
Materials License Agreement.
    Licensing Contact: Sabarni Chatterjee, Ph.D.; 301-435-5587; 
<a href="/cdn-cgi/l/email-protection#b2d1dad3c6c6d7c0d8d7d7c1d3f2dfd3dbde9cdcdbda9cd5ddc4"><span class="__cf_email__" data-cfemail="80e3e8e1f4f4e5f2eae5e5f3e1c0ede1e9ecaeeee9e8aee7eff6">[email protected]</span></a>.

Novel Compounds That Specifically Kill Multi-Drug Resistant Cancer 
Cells

    Description of Technology: One of the major hindrances to 
successful cancer chemotherapy is the development of multi-drug 
resistance (MDR) in cancer cells. MDR is frequently caused by the 
increased expression or activity of ABC transporter proteins in 
response to the toxic agents used in chemotherapy. The increased 
expression or activity of the ABC transporter proteins causes the toxic 
agents to be removed from cells before they can act to kill the cell. 
As a result, research has generally been directed to overcoming MDR by 
inhibiting the activity of ABC transporters, thus causing the 
chemotherapeutic agents to remain in the cell long enough to exert 
their effects. However, compounds that inhibit ABC transporter activity 
often elicit strong and undesirable side-effects due to the inhibition 
of ABC transporter function in normal cells, thereby restricting their 
usefulness as therapeutics.

[[Page 75180]]

    Investigators at the NIH previously identified novel compounds with 
the ability to kill multi-drug resistant cancer cells while leaving 
normal cells relatively unharmed. These ``MDR-selective compounds'' 
were not inhibitors of ABC transporters because they killed multi-drug 
resistant cells without affecting the activity of ABC transporters. 
Furthermore, their activity was dependent directly on the level of 
expression of ABC transporters, thus increasing their selectivity for 
diseased cells. As a result, the undesirable side-effects that have 
prevented the use of inhibitors of ABC transporters as therapeutics 
should not affect the therapeutic application of the MDR-selective 
compounds.
    The inventors have now generated third generation MDR-selective 
compounds with further improved solubility, selectivity and killing 
activity toward MDR cells. The new MDR-selective compounds selectively 
kill MDR cancer cells, and their efficacy correlates directly with the 
level of ABC transporter expression. This suggests that the third 
generation MDR-selective compounds represent a powerful strategy for 
treating MDR cancers.
    Applications:
    <bullet> Treatment of cancers associated with MDR, either alone or 
in combination with other therapeutics.
    <bullet> Development of a pharmacophore for improved MDR-selective 
compounds.
    Advantages:
    <bullet> MDR-selective compounds capitalize on one of the most 
common drawbacks to cancer therapies (MDR) by using it as an advantage 
for treating cancer.
    <bullet> The compositions do not inhibit the activity of ABC 
transporters, thereby reducing the chance of undesired side-effects 
during treatment.
    <bullet> The effects of MDR-selective compounds correlate with the 
level of ABC transporter expression, allowing healthy cells to better 
survive treatments.
    <bullet> Increased specificity and solubility of the new MDR-
inverse compounds allows greater access to MDR cells, thereby 
increasing therapeutic effectiveness.
    Development Status: Preclinical stage of development, in vitro 
data.
    Inventors: Hall (NCI) et al.
    U.S. Patent Status: U.S. Provisional Application 61/375,672 (E-249-
2010/0-US-01).
    For more information, see:
    <bullet> Hall, MD et al. (2009) ``Synthesis, activity, and 
pharmacophore development for isatin-beta-thiosemicarbazones with 
selective activity toward multidrug-resistant cells'' J Med Chem. 
52(10):3191-204.
    <bullet> PCT Publication WO 2009/102433 (PCT Patent Application 
PCT/US2009/000861).
    Licensing Status: Available for licensing.
    Licensing Contact: David A. Lambertson, Ph.D.; 301-435-4632; 
<a href="/cdn-cgi/l/email-protection#85e9e4e8e7e0f7f1f6eaebe1c5e8e4ece9abebecedabe2eaf3"><span class="__cf_email__" data-cfemail="076b666a6562757374686963476a666e6b29696e6f29606871">[email protected]</span></a>.
    Collaborative Research Opportunity: The Center for Cancer Research, 
Laboratory of Cell Biology, is seeking statements of capability or 
interest from parties interested in collaborative research to further 
develop, evaluate, or commercialize this technology. Please contact 
John Hewes, Ph.D. at 301-435-3121 or <a href="/cdn-cgi/l/email-protection#18707d6f7d6b72587579717436767170367f776e"><span class="__cf_email__" data-cfemail="48202d3f2d3b22082529212466262120662f273e">[email protected]</span></a> for more 
information.

Isocitrate Dehydrogenase 1 (IDH1) R132 Mutation Human Melanoma 
Metastasis Cell Line

    Description of Technology: Isocitrate dehydrogenase 1 (IDH1) plays 
an important role in glucose metabolism in the cytoplasm, converting 
isocitrate to [alpha]-ketoglutarate while reducing nicotinamide adenine 
dinucleotide phosphate (NADP+ to NADPH). However, when IDH1 harbors a 
R132 mutation it results in the accumulation of 2-hydroxyglutarate and 
has a corresponding association with cancer. This mutation in IDH1 has 
previously been identified in approximately 80% of progressive gliomas 
and 10% acute myeloid leukemias (AML). In contrast, this mutation is 
very rare in other cancers. Therefore, additional research on the IDH1 
R132 mutation could be useful for diagnostic, prognostic, and 
therapeutic purposes.
    The researchers at the NIH have developed a human melanoma cell 
line designated 2633, which harbors the IDH1 R132C mutation. The 
inventors used low passage cell lines derived from a panel of confirmed 
metastatic melanoma tumor resections, paired with apheresis-collected 
peripheral blood mononuclear cells to identify IDH1 mutations. 
Sequencing of IDH1 in this panel allowed them to discover a melanoma 
cell line with the IDH1 R132C mutation. Until now no such cell line has 
been found and this has hindered the understanding of the effects 
mutated IDH1 has on cancer progression as well as the development of 
drugs that would be specific for cells that harbor this mutation. Use 
of this cell line will allow researchers to decipher the biology of 
this gene as well as aid in the development of specific inhibitors of 
its mutated form.
    Applications:
    <bullet> In vitro and in vivo cell model for the IDH1 R132C 
mutation in melanoma. This would be an extremely useful research tool 
for investigating the underlying biology of IDH1 phenotypes, including 
effects on growth, motility, invasion, and metabolite production.
    <bullet> Research tool for testing the activity of inhibitors to 
IDH1, where such inhibitors could be used as a therapeutic drug to 
treat particular cancers including potentially glioma, AML and 
melanoma.
    <bullet> Research tool to generate cell lines where the R132C 
mutation is knocked out or the wild type gene is knocked in using an 
adeno-associated virus. These resulting cells can be used to understand 
the underlying biology of IDH1 phenotypes or to identify candidate 
small molecule and other therapeutic drugs.
    Advantages:
    <bullet> Cell line is derived from a melanoma patient: This cell 
line likely retains many features of primary melanoma samples. For 
example novel melanoma antigens identified from this cell would be 
expected to correlate with antigens expressed on human melanoma tumors. 
Studies performed using this cell line could be used to elucidate to 
the biological basis of the initiation and progression of melanoma in 
humans as well as aid in the identification and/or testing of IDH1 
R132-targeted inhibitors.
    <bullet> Expresses the R132 IDH1 mutation in melanoma: IDH1 R132 
mutations frequently occur in advanced gliomas, however this is the 
first identification of an IDH1 mutation in melanoma. Therefore, the 
2633 cell line represents a tool that can be utilized to study the 
impact of this IDH1 gene and the R132C mutation on melanoma and other 
cancers.
    Inventors: Yardena Samuels (NHGRI) and Steven Rosenberg (NCI).
    Publication: Lopez GY, Reitman ZJ, Solomon D, Waldman T, Bigner DD, 
McLendon RE, Rosenberg SA, Samuels Y, Yan H. IDH1(R132) mutation 
identified in one human melanoma metastasis, but not correlated with 
metastases to the brain. Biochem Biophys Res Commun. 2010 Jul 
30;398(3):585-587. [PubMed: 20603105]
    Patent Status: HHS Reference No. E-232-2010/0--Research Tool. 
Patent protection is not being pursued for this technology.
    Licensing Status: Available for licensing.
    Licensing Contact: Whitney Hastings; 301-451-7337; 
<a href="/cdn-cgi/l/email-protection#147c7567607d7a73635479757d783a7a7d7c3a737b62"><span class="__cf_email__" data-cfemail="3951584a4d50575e4e795458505517575051175e564f">[email protected]</span></a>.
    Collaborative Research Opportunity: The National Human Genome 
Research Institute's Cancer Genetics Branch is seeking statements of 
capability or

[[Page 75181]]

interest from parties interested in collaborative research to further 
develop, evaluate and/or commercialize this newly identified melanoma-
associated gene as a diagnostic marker as well as utilize the IDH1 R132 
cell line to identify and test IDH1 inhibitors as possible therapeutic 
drug candidates to treat melanoma and other cancers. Please contact Dr. 
Yardena Samuels at <a href="/cdn-cgi/l/email-protection#2d5e4c405848415e546d404c444103434445034a425b"><span class="__cf_email__" data-cfemail="c4b7a5a9b1a1a8b7bd84a9a5ada8eaaaadaceaa3abb2">[email protected]</span></a> for more information.

ERBB4 Mutations Mutation Identified in Human Melanoma Metastasis Cell 
Lines (2690, 2379, 2197, 2183, 2535, 2645, 1770, 2359, 2238, 2319, 
2190)

    Description of Technology: Protein tyrosine kinases (PTKs) have 
been associated with a wide variety of cancers, including melanoma. 
Using high-throughput gene sequencing, the NIH has analyzed PTKs in 
melanoma and identified several novel somatic alterations, including 
alterations in ERBB4 (also called HER4). These mutations were found to 
increase the sensitivity of cells in which they reside to small 
molecule inhibitors, such as lapatinib.
    Available for licensing are several melanoma cell lines that harbor 
ERBB4 mutations. These cell lines provide methods of identifying 
specific inhibitors to ERBB4 that could be used to treat patients with 
ERBB4 mutations as well as methods to further understand the role of 
ERBB4 mutations in melanoma. Given the recent success of small molecule 
protein kinase inhibitors and specifically inhibitors to epidermal 
growth factor receptor (EGFR) (such as gefinitib and erlotinib), these 
reagents could be used to further the development of specific 
inhibitors to ERBB4 and improve existing melanoma treatments for 
patients with these mutations.
    Applications:
    <bullet> In vitro and in vivo cell model for understanding the 
biology of ERBB4, including growth, motility, invasion, and metabolite 
production.
    <bullet> High throughput drug screening to test for ERBB4 
inhibitors that could be used to treat particular cancers, such as 
melanoma.
    <bullet> Diagnostic array for the detection of ERBB4 mutations.
    <bullet> Research tool to generate cell lines where the ERBB4 
mutation is knocked out or the wild type gene is knocked in using an 
adeno-associated virus. These resulting cells can be used to understand 
the underlying biology of ERBB4 phenotypes or to identify candidate 
small molecule and other therapeutic drugs.
    Advantages:
    <bullet> Cell lines are derived from melanoma patients: These cell 
lines are likely to retain many features of primary melanoma samples. 
For example novel melanoma antigens identified from this cell line 
would be expected to correlate with antigens expressed on human 
melanoma tumors. Studies performed using these cell lines could be used 
to elucidate the biological basis of initiation and progression of 
melanoma in humans as well as aid in the identification and/or testing 
of ERBB4 inhibitors.
    <bullet> Expresses the ERBB4 mutation in melanoma: ERBB4 is a 
highly mutated gene in melanoma, suggesting its important functional 
role in the disease. Therefore, these cell lines represent a tool that 
can be utilized to study the impact of the ERBB4 gene and the 
associated mutations on melanoma, and possible other cancers since 
mutations in ERBB family members such as EGRF and ERBB2 are prevalent 
in lung cancer, glioblastoma and gastric cancer.
    Inventors: Yardena Samuels (NHGRI), Steven Rosenberg (NCI), and 
Todd Prickett (NHGRI).
    Publication: Prickett TD, Agrawal NS, Wei X, Yates KE, Lin JC, 
Wunderlich JR, Cronin JC, Cruz P, Rosenberg SA, Samuels Y. Analysis of 
the tyrosine kinome in melanoma reveals recurrent mutations in ERBB4. 
Nature Genet. 2009 October; 41(10):1127-1132. [PubMed: 19718025]
    Patent Status: HHS Reference No. E-229-2010/0--Research Tool. 
Patent protection is not being pursued for this technology.
    Licensing Status: Available for licensing.
    Licensing Contact: Whitney Hastings; 301-451-7337; 
<a href="/cdn-cgi/l/email-protection#f69e9785829f989181b69b979f9ad8989f9ed8919980"><span class="__cf_email__" data-cfemail="6008011314090e0717200d01090c4e0e09084e070f16">[email protected]</span></a>.
    Collaborative Research Opportunity: The National Human Genome 
Research Institute's Cancer Genetics Branch is seeking statements of 
capability or interest from parties interested in collaborative 
research to further develop, evaluate and/or commercialize these newly 
characterized ERBB4 mutant cell lines as well as to identify and test 
ERBB4 inhibitors as possible therapeutic drug candidates to treat 
melanoma and other cancers. Please contact Dr. Yardena Samuels at 
<a href="/cdn-cgi/l/email-protection#6e1d0f031b0b021d172e030f07024000070640090118"><span class="__cf_email__" data-cfemail="2a594b475f4f4659536a474b434604444342044d455c">[email protected]</span></a> for more information.

Synthetic Analogs of RGD and NGR Cyclic Peptides

    Description of Technology: Cell surface biomolecules such as 
integrins ([alpha]<INF>v</INF>[beta]3, [alpha]<INF>v</INF>[beta]5, 
[alpha]<INF>v</INF>[beta]8, [alpha]<INF>6</INF>[beta]4), folate 
receptors, and CD13 are highly expressed in cancer cells and are 
involved in angiogenesis, invasion and metastasis. Consequently, this 
has made these cellular biomolecules attractive targets for delivery of 
drugs that can bind to them selectively. The peptide motifs RGD (Arg-
Gly-Asp) and NGR (Asn-Gly-Arg), in particular, are recognized by 
integrins [alpha]<INF>v</INF>[beta]<INF>3</INF> and 
[alpha]<INF>v</INF>[beta]<INF>5</INF> and CD13 with high affinity. 
Further, short peptide sequences of RGD and NGR are commercially useful 
because they are amenable to large scale synthesis, chemical 
modification and are non-immunogenic. Therefore, there is a need for 
cyclic compounds having the NGR peptide motif to target CD13 or having 
the RGD peptide motif to target [alpha]<INF>v</INF>[beta]<INF>3</INF> 
and [alpha]<INF>v</INF>[beta]<INF>5</INF> integrins.
    Accordingly, the researchers at the NIH have developed cyclic NGR 
and RGD pentapeptide analogs efficiently synthesized on resin via click 
chemistry. These cyclic peptides are potentially useful in targeted 
delivery of drugs, antibodies, or nanoparticles to the site of 
angiogenic blood vessels and tumors. By allowing for targeted drug 
delivery, these peptides can minimize general cytotoxicity and improve 
bioavailability. The cyclic peptides described are novel, synthetic 
analogs of RGD and NGR cyclic peptides. Therefore, their inherent 
cyclic structure and the cyclization strategy will make these compounds 
stable from hydrolytic degradation, thereby prolonging their half life 
in circulation.
    Applications: Targeted drug delivery and medical imaging of cancer 
tissues expressing CD13 or [alpha]<INF>v</INF>[beta]<INF>3</INF> and 
[alpha]<INF>v</INF>[beta]<INF>5</INF> integrins.
    Advantages:
    <bullet> These cyclic peptides contain a triazole unit that would 
be less likely to be attacked by hydrolytic enzymes and esterases, thus 
making them ideal candidates for in vivo targeted delivery and imaging.
    <bullet> The RGD and NGR cyclic peptides are amenable to large 
scale synthesis, chemical modification and are non-immunogenic, while 
the linear RGD peptide counterparts are prone to protease degradation 
making them much less stable and limiting their use in in vivo 
applications.
    <bullet> Both linear and disulfide-bridged cyclic peptides 
containing the NGR motif have been used to deliver various anti-tumor 
compounds and viral particles to tumor vessels, with the cyclic 
versions showing more than a 10 fold higher binding affinity than their 
linear counterparts.
    Development Status: Pre-clinical proof of principle.
    Inventors: Belhu B. Metaferia and Javed Khan (NCI).
    Publications: B Metaferia et al. Synthesis of novel cyclic NGR/RGD

[[Page 75182]]

peptide analogs via on resin click chemistry. In preparation.
    Patent Status: U.S. Provisional Application No. 61/347,038 filed 21 
May 2010 (HHS Reference No. E-130-2010/0-US-01).
    Licensing Status: Available for licensing.
    Licensing Contact: Whitney Hastings; 301-451-7337; 
<a href="/cdn-cgi/l/email-protection#5c343d2f2835323b2b1c313d353072323534723b332a"><span class="__cf_email__" data-cfemail="a3cbc2d0d7cacdc4d4e3cec2cacf8dcdcacb8dc4ccd5">[email protected]</span></a>.

Novel Therapeutic Compounds for Treatment of Cancer and Immune 
Disorders

    Description of Invention: The global market for cancer therapeutics 
is over $40 billion and is anticipated to continue to rise in the 
future. There remains a significant unmet need for therapeutics for 
cancers that affect blood, bone marrow, and lymph nodes and the immune 
system, such as leukemia, multiple myeloma, and lymphoma. The 
proteasome inhibitor bortezomib, which may prevent degradation of pro-
apoptotic factors permitting activation of programmed cell death in 
neoplastic cells dependent upon suppression of pro-apoptotic pathways, 
has been a successful mode of treatment for such cancers. However, some 
patient's cancers have been found to be resistant to the drug.
    Researchers at the National Institutes of Health have developed 
novel hydrazone and diacyl hydrazine compounds that are inhibitors of 
the endoplasmic reticulum-associated protein degradation (ERAD) 
pathway. These compounds preferentially target the proteasome assistant 
ATPase p97/VCP at a site independent of nucleotide binding. The 
researchers have shown that these ERAD inhibitors can induce cancer 
cell death and can also synergize with bortezomib in cytotoxic 
activity. In addition to treating diseases or disorders in which 
inhibition of the ERAD pathway is an effective therapy, these novel 
compounds may also be useful in the study of protein degradation.
    Advantages:
    <bullet> Development of therapies against tumors that are resistant 
to bortezomib.
    <bullet> Use in therapies in combination with proteasome 
inhibitors.
    <bullet> Development of immunosuppressive therapies that target the 
ubiquitin proteasome system.
    <bullet> Studies of the mechanism of protein degradation and other 
biological processes that involve the p97 ATPase.
    <bullet> Bioprobes to detect endoplasmic reticulum (ER) structures 
in live cells.
    Advantages:
    <bullet> Potent anti-tumor activity.
    <bullet> Simpler chemical structure makes synthesis easier and more 
cost-effective than previous ERAD inhibitors.
    <bullet> Retain activity against bortezomib-resistant cells and can 
synergize with bortezomib.
    <bullet> Fluorescent.
    <bullet> High affinity for the ER.
    Development Status: Pre-clinical.
    Inventors: Adrian Wiestner (NHLBI), William Trenkle (NIDDK), Yihong 
Ye (NIDDK) et al.
    Relevant Publications:

1. Qiuyan Wang et al. ERAD inhibitors integrate ER stress with an 
epigenetic mechanism to activate BH3-only protein NOXA in cancer cells. 
Proc Natl Acad Sci USA 2009 Feb 17;106(7):2200-2205. [PubMed: 19164757]
2. Qiuyan Wang et al. The ERAD inhibitor Eeyarestatin I is a 
bifunctional compound with a membrane-binding domain and a p97/VCP 
inhibitory group. PloS ONE 2010, in press.

    Patent Status: U.S. Provisional Application No. 61/266,760 filed 04 
Dec 2009 (HHS Reference No. E-291-2009/0-US-01).
    Licensing Status: Available for licensing.
    Licensing Contact: Surekha Vathyam, Ph.D.; 301-435-4076; 
<a href="/cdn-cgi/l/email-protection#84f2e5f0ecfde5e9f7c4e9e5ede8aaeaedecaae3ebf2"><span class="__cf_email__" data-cfemail="bec8dfcad6c7dfd3cdfed3dfd7d290d0d7d690d9d1c8">[email protected]</span></a>.

Targeted Anti-Cancer Compounds for Treating Chromosomal Instability 
Syndromes

    Description of Invention: At $47 billion, cancer is one of the 
largest, fastest growing markets in the pharmaceutical industry. There 
remains a significant unmet need for new therapeutics that target 
cancer cells while sparing normal cells. Cancer cells show higher 
levels of DNA damage than normal cells, and therefore rely more heavily 
than normal cells on DNA repair mechanisms for survival. There is a 
particular need for cancer therapies for cancer-prone chromosomal 
instability syndromes such as Ataxia Telangiectasia, Nijmegen Breakage, 
Bloom, and Fanconi's anemia, which result from dysfunctional DNA repair 
systems.
    Researchers at Columbia University and the National Cancer 
Institute (NCI) have developed compositions and methods of useful in 
the treatment of cancer and in the sensitization of cancer cells to 
cancer therapy. The compositions target the MRE11-RAD50-NBS1 (MRN) 
complex, a DNA repair complex essential for sensing and responding to 
DNA damage.
    Given the dependency of cancer cells on DNA repair systems, they 
are susceptible to compositions that inhibit DNA damage repair. Thus, 
cancers that already have one or more defects in DNA repair systems, 
such as those from patients with chromosomal instability syndromes, are 
effectively treated with the present compositions.
    Applications: Development of treatments for cancer.
    Development Status: Pre-clinical.
    Inventors: Levy Kopelovich (NCI) et al.
    Relevant Publication: A Dupr[eacute] et al. A forward chemical 
genetic screen reveals an inhibitor of the Mre11-Rad50-Nbs1 complex. 
Nat Chem Biol. 2008;4(2):119-125. [PubMed: 18176557]
    Patent Status:
    <bullet> U.S. Provisional Application No. 61/203,377 filed 22 Dec 
2008 (HHS Reference No. E-154-2009/0-US-01).
    <bullet> International Application No. PCT/US09/69171 filed 22 Dec 
2009, which published as WO 2010/075372 on 01 Jul 2010 (HHS Reference 
No. E-154-2009/0-PCT-02).
    Licensing Status: Available for licensing.
    Licensing Contact: Patrick P. McCue, Ph.D.; 301-435-5560; 
<a href="/cdn-cgi/l/email-protection#b0ddd3d3c5d5c0d1c4f0ddd1d9dc9eded9d89ed7dfc6"><span class="__cf_email__" data-cfemail="4e232d2d3b2b3e2f3a0e232f27226020272660292138">[email protected]</span></a>.
    Collaborative Research Opportunity: The National Cancer Institute, 
Division of Cancer Prevention, Chemopreventive Agent Development 
Research Group, is seeking statements of capability or interest from 
parties interested in collaborative research to further develop, 
evaluate, or commercialize agents for the prevention and treatment of 
cancer. Please contact John Hewes, Ph.D. at 301-435-3121 or 
<a href="/cdn-cgi/l/email-protection#7018150715031a301d11191c5e1e19185e171f06"><span class="__cf_email__" data-cfemail="046c617361776e4469656d682a6a6d6c2a636b72">[email protected]</span></a> for more information.

    Dated: November 24, 2010.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 2010-30278 Filed 12-1-10; 8:45 am]
BILLING CODE 4140-01-P


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