Federal Register / Vol. 75, No. 231 / Thursday, December 2, 2010 / Notices 75179 

allow it to be utilized to treat a broader 

population of patients. 

• Versatile antigen recognition— 

These TCRs are CD8 and CD4 

independent meaning that cells 

expressing these TCRs are capable of 

eliciting an immune response in the 

absence of CD8 or CD4 molecule 

expression on the T cell. When utilized 

for immunotherapy, this versatility 

allows engineered T cells expressing 

this TCR to recognize and eliminate 

tumors expressing SSX–2 regardless of 

how the antigen is presented to the T 

cell. 

Development Status: This technology 

is in a preclinical stage of development. 

Inventors: Richard A. Morgan et al. 

(NCI). 

Publications 

1. N Chinnasamy, et al. Development 

of HLA–A2 Restricted TCR Against 

Cancer Testis Antigen SSX–2 for 

Adoptive Immunotherapy of Cancer. 

Abstracts for the 25th Annual Meeting 

of the International Society for 

Biological Therapy of Cancer, J 

Immunother. 2010 Oct;33(8):860, DOI 

10.1097/CJI.0b013e3181f1e08d. 

2. D Valmori, et al. Expression of 

synovial sarcoma X (SSX) antigens in 

epithelial ovarian cancer and 

identification of SSX–4 epitopes 

recognized by CD4+ T cells. Clin Cancer 

Res. 2006 Jan 15;12(2):398–404. 

[PubMed: 16428478] 

3. G Bricard, et al. Naturally acquired 

MAGE–A10- and SSX–2-specific CD8+ 

T cell responses in patients with 

hepatocellular carcinoma. J Immunol. 

2005 Feb 1;174(3):1709–1716. [PubMed: 

15661935] 

Patent Status: U.S. Provisional 

Application No. 61/384,931 filed 21 

Sept 2010 (HHS Reference No. E–269– 

2010/0–US–01). 

Related Technologies: T cell receptor 

technologies developed against other 

CTAs: E–304–2006/0 and E–312–2007/1 

(anti-NY–ESO–1) and E–236–2010/0 

(anti-MAGE–A3). 

Licensing Status: Available for 

licensing. 

Licensing Contact: Samuel E. Bish, 

Ph.D.; 301–435–5282; 

bishse@mail.nih.gov. 

Collaborative Research Opportunity: 

The National Cancer Institute, Surgery 

Branch, is seeking statements of 

capability or interest from parties 

interested in collaborative research to 

further develop, evaluate, or 

commercialize the use of T cell receptor 

gene therapy for the treatment of cancer. 

Please contact John Hewes, Ph.D. at 

301–435–3121 or hewesj@mail.nih.gov 

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. 2010–30279 Filed 12–1–10; 8:45 am] 

BILLING CODE 4140–01–P 

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. 

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 

• Developing cancer biomarker. 

• Developing cell sorting assays (e.g. 

FACS). 

• Immunofluorescence, Western 

Blotting, and Immunohistochemistry for 

CEA. 

• 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; 

chatterjeesa@mail.nih.gov. 

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. 

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75180 Federal Register / Vol. 75, No. 231 / Thursday, December 2, 2010 / Notices 

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 ‘‘MDRselective 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 sideeffects that have prevented the use of 

inhibitors of ABC transporters as 

therapeutics should not affect the 

therapeutic application of the MDRselective compounds. 

The inventors have now generated 

third generation MDR-selective 

compounds with further improved 

solubility, selectivity and killing activity 

toward MDR cells. The new MDRselective 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: 

• Treatment of cancers associated 

with MDR, either alone or in 

combination with other therapeutics. 

• Development of a pharmacophore 

for improved MDR-selective 

compounds. 

Advantages: 

• MDR-selective compounds 

capitalize on one of the most common 

drawbacks to cancer therapies (MDR) by 

using it as an advantage for treating 

cancer. 

• The compositions do not inhibit the 

activity of ABC transporters, thereby 

reducing the chance of undesired sideeffects during treatment. 

• The effects of MDR-selective 

compounds correlate with the level of 

ABC transporter expression, allowing 

healthy cells to better survive 

treatments. 

• 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: 

• Hall, MD et al. (2009) ‘‘Synthesis, 

activity, and pharmacophore 

development for isatin-betathiosemicarbazones with selective 

activity toward multidrug-resistant 

cells’’ J Med Chem. 52(10):3191–204. 

• 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; 

lambertsond@mail.nih.gov. 

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 hewesj@mail.nih.gov 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 

a-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: 

• 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. 

• 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. 

• 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: 

• 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. 

• 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; hastingw@mail.nih.gov. 

Collaborative Research Opportunity: 

The National Human Genome Research 

Institute’s Cancer Genetics Branch is 

seeking statements of capability or 

WReier-Aviles on DSKGBLS3C1PROD with NOTICES

Federal Register / Vol. 75, No. 231 / Thursday, December 2, 2010 / Notices 75181 

interest from parties interested in 

collaborative research to further 

develop, evaluate and/or commercialize 

this newly identified melanomaassociated 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 

samuelsy@mail.nih.gov 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: 

• In vitro and in vivo cell model for 

understanding the biology of ERBB4, 

including growth, motility, invasion, 

and metabolite production. 

• High throughput drug screening to 

test for ERBB4 inhibitors that could be 

used to treat particular cancers, such as 

melanoma. 

• Diagnostic array for the detection of 

ERBB4 mutations. 

• 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: 

• 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. 

• 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; hastingw@mail.nih.gov. 

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 

samuelsy@mail.nih.gov for more 

information. 

Synthetic Analogs of RGD and NGR 

Cyclic Peptides 

Description of Technology: Cell 

surface biomolecules such as integrins 

(avb3, avb5, avb8, a6b4), 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 avb3 and avb5

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 

avb3 and avb5 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 avb3 and avb5

integrins. 

Advantages: 

• 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. 

• The RGD and NGR cyclic peptides 

are amenable to large scale synthesis, 

chemical modification and are nonimmunogenic, while the linear RGD 

peptide counterparts are prone to 

protease degradation making them 

much less stable and limiting their use 

in in vivo applications. 

• 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 

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75182 Federal Register / Vol. 75, No. 231 / Thursday, December 2, 2010 / Notices 

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; hastingw@mail.nih.gov. 

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: 

• Development of therapies against 

tumors that are resistant to bortezomib. 

• Use in therapies in combination 

with proteasome inhibitors. 

• Development of 

immunosuppressive therapies that 

target the ubiquitin proteasome system. 

• Studies of the mechanism of protein 

degradation and other biological 

processes that involve the p97 ATPase. 

• Bioprobes to detect endoplasmic 

reticulum (ER) structures in live cells. 

Advantages: 

• Potent anti-tumor activity. 

• Simpler chemical structure makes 

synthesis easier and more cost-effective 

than previous ERAD inhibitors. 

• Retain activity against bortezomibresistant cells and can synergize with 

bortezomib. 

• Fluorescent. 

• 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; 

vathyams@mail.nih.gov. 

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 Dupre ́ 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: 

• U.S. Provisional Application No. 

61/203,377 filed 22 Dec 2008 (HHS 

Reference No. E–154–2009/0–US–01). 

• 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; 

mccuepat@mail.nih.gov. 

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 

hewesj@mail.nih.gov 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 

DEPARTMENT OF HOMELAND 

SECURITY 

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Services 

Agency Information Collection 

Activities: Form I–914, Extension of a 

Currently Approved Information 

Collection; Comment Request 

ACTION: 30-Day Notice of Information 

Collection under Review: Form I–914 

and Supplements A and B, Application 

for T Nonimmigrant Status; Application 

for Immediate Family Member of T–1 

Recipient; and Declaration of Law 

Enforcement Officer for Victim of 

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