Federal Register / Vol. 74, No. 68 / Friday, April 10, 2009 / Notices 16405 

Hyperthyroidism, or an overactive 

thyroid gland, affects about 1% of 

people in the United States and is often 

caused by autoimmune over-stimulation 

of the thyroid gland (Graves’ disease), or 

by thyroid tumors. Drugs currently used 

for treatment of hyperthyroidism inhibit 

synthesis of thyroid hormones; the TSH 

receptor antagonist compounds 

encompassed by this technology have 

the advantage of directly inhibiting 

activity of the TSH receptor, rather than 

inhibiting thyroid hormone synthesis. 

Applications: 

• Diagnostic tools for evaluation and 

treatment of thyroid cancer. 

• Therapeutics for thyroid cancer, 

hyperthyroidism, and hypothyroidism. 

Market: Approximately 1 in 13 

Americans suffers from a thyroid 

disorder, and 10 million have a thyroidrelated condition that requires ongoing 

immunodiagnostic monitoring. 

Development Status: Early stage. 

Inventors: Marvin C. Gershengorn et 

al. (NIDDK) 

Publications: 

1. S Moore, H Jaeschke, G Kleinau, S 

Neumann, S Costanzi, JK Jiang, J 

Childress, BM Raaka, A Colson, R 

Paschke, G Krause, CJ Thomas, MC 

Gershengorn. Evaluation of smallmolecule modulators of the luteinizing 

hormone/choriogonadotropin and 

thyroid stimulating hormone receptors: 

structure-activity relationships and 

selective binding patterns. J Med Chem. 

2006 Jun 29;49(13):3888–3896. 

2. S Neumann, G Kleinau, S Costanzi, 

S Moore, BM Raaka, CJ Thomas, G 

Krause, MC Gershengorn. A low 

molecular weight antagonist for the 

human thyrotropin receptor with 

therapeutic potential for 

hyperthyroidism. Endocrinology 2008 

Dec;149(12):5945–5950. 

3. Unpublished data are also available 

for review under a CDA. 

Patent Status: 

HHS Reference Nos. E–223–2006/0 

and E–223–2006/1 — 

• International Patent Application 

No. PCT/US2007/011951 filed 17 May 

2007, which published as WO 2007/ 

136776 on 29 Nov 2007. 

• National Phase entered in Australia, 

Canada, Europe, Japan, and the United 

States. 

HHS Reference No. E–284–2008/0 — 

• International Patent Application 

No. PCT/US2008/011958 filed 20 Oct 

2008. 

Licensing Status: Available for 

licensing. 

Licensing Contact: Tara L. Kirby, PhD; 

301–435–4426; tarak@mail.nih.gov. 

Collaborative Research Opportunity: 

The NIDDK, Clinical Endocrinology 

Branch is seeking statements of 

capability or interest from parties 

interested in collaborative research to 

further develop, evaluate, or 

commercialize small molecule TSH 

receptor modulators. Please contact 

Patricia Mello Lake; 301–451–3636; 

lakep@mail.nih.gov for more 

information. 

April 3, 2009. 

Richard U. Rodriguez, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. E9–8208 Filed 4–9–09; 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. 

Selective Killing of Cancer Cells by 

Inhibition of Geminin 

Description of Technology: The 

current strategy for developing cancer 

therapeutics is to identify unique 

differences between cancer cells and 

normal cells that can serve as specific 

targets for chemotherapeutic drugs, 

thereby allowing elimination of cancer 

cells with minimal toxicity to normal 

tissues. Geminin, an inhibitor of DNA 

replication, is typically undetectable in 

normal cells while rapidly proliferating 

cancer cells express geminin and hence 

could be targeted for cancer treatment. 

The NIH researchers have discovered 

that inhibition of geminin expression 

induced DNA re-replication in most of 

the tested cancer cell lines, but not in 

matched non-cancer cell lines from the 

same tissues. DNA re-replication occurs 

when DNA synthesis is initiated 

multiple times from the same 

replication origin during one cycle of 

cell division resulting in DNA damage 

which halts cell proliferation and 

induces apoptosis in a wide variety of 

cancer cells. The researchers also 

analyzed the effect of suppression of 

geminin expression on apoptosis and 

cell survival in cancer and non-cancer 

cell lines. They found that the geminin 

siRNA induced apoptosis in a colon 

carcinoma cell line, but not in a normal 

skin fibroblast cell line. Furthermore, 

suppression of geminin expression 

markedly reduced cell survival of 

several cancer cell lines, but not noncancer cell lines. Therefore, suppressing 

the level of geminin expression can be 

potentially used to selectively kill 

cancer cells. 

Applications: Therapeutic for treating 

breast, colon and rectal, kidney (renal 

cell), lung, brain, and bone cancers. 

Advantages: Targeted therapeutic; No 

requirement for use of other cell cycle 

inhibitors 

Market: Cancer continues to be a 

burden to the public health of 

Americans. After heart disease, cancer is 

the most common cause of death in the 

United States. For 2008, it was 

estimated that about 565,650 Americans 

were expected to die of cancer. The 

incidence of cancer has been dropping 

over the years but it is estimated that 

over 1.4 million Americans would be 

diagnosed with cancer in 2008. 

Therefore, there is a continued need for 

the development of new therapies to 

effectively treat this disease. 

Inventors: Wenge Zhu and Melvin L. 

DePamphilis (NICHD) 

Publications: Paper accepted for 

publication in Cancer Research. 

Patent Status: U.S. Provisional 

Application No. 61/106,465 filed 17 Oct 

2008 (HHS Reference No. E–324–2008/ 

0–US–01) 

Licensing Status: Available for 

licensing. 

Licensing Contact: Betty Tong, PhD; 

301–594–6565; tongb@mail.nih.gov. 

Transgenic Mice in Which the Gene for 

MCP–1 Is Deleted 

Description of Technology: Dr. 

Yoshimura has developed a transgenic 

mouse which does not express the 

chemokine MCP–1 due to a deletion of 

the gene for MCP–1. MCP–1 is a CC 

chemokine which is responsible for 

recruiting monocytes into sites of 

16406 Federal Register / Vol. 74, No. 68 / Friday, April 10, 2009 / Notices 

inflammation and cancer. Using a 

thioglycollate challenge as a measure of 

the impact of the deletion of MCP–1, 

MCP–1 deficient mice exhibit a 60% 

reduction in the number of monocytes/ 

macrophages at 96 hours compared to 

wild type mice. Unlike previously 

generated MCP–1 deficient mice in 

which the expression of the neighboring 

gene for MCP–3 is down-regulated (our 

own data), the expression of MCP–3 is 

up-regulated in this mouse model. 

Applications: This mouse may be 

useful as an in vivo model for 

evaluating the role of MCP–1 and MCP– 

3 in cancer or other diseases associated 

with inflammation due to the 

accumulation of monocytes. 

Inventor: Teizo Yoshimura (NCI) 

Patent Status: HHS Reference No. E– 

241–2005/0—Research Tool. Patent 

protection is not being pursued for this 

technology. 

Licensing Status: Available for 

licensing under a Biological Materials 

License Agreement. 

Licensing Contact: Betty Tong, PhD; 

301–594–6565; tongb@mail.nih.gov. 

Collaborative Research Opportunity: 

The National Cancer Institute, Center for 

Cancer Research, Laboratory of 

Molecular Immunoregulation, Cancer 

and Inflammation Program, is seeking 

statements of capability or interest from 

parties interested in collaborative 

research to further develop, evaluate, or 

commercialize agents useful to treat 

patients with inflammation or cancer. 

Please contact John D. Hewes, PhD at 

301–435–3121 or hewesj@mail.nih.gov 

for more information. 

DU145 Camptothecin (CPT)-Resistant 

Cell Line 

Description of Technology: Drug 

resistance is a major limitation of 

chemotherapy. Understanding how drug 

resistance develops may lead to more 

effective treatments. This invention 

describes the DU145 Camptothecin 

(CPT)-resistant prostate cancer cell line 

that can be used to study mechanisms 

of drug resistance. 

Inventor: Yves G. Pommier (NCI) 

Related Publication: Y Urasaki et al. 

Characterization of a novel 

topoisomerase I mutation from a 

camptothecin-resistant human prostate 

cancer cell line. Cancer Res. 2001 Mar 

1;61(5):1964–1969. 

Patent Status: HHS Reference No. E– 

159–2005/0—Research Tool. Patent 

protection is not being pursued for this 

technology. 

Licensing Status: Available for 

licensing under a Biological Materials 

License Agreement. 

Licensing Contact: Betty Tong, PhD; 

301–594–6565; tongb@mail.nih.gov. 

Creation and Characterization of 

Carcinogen-Altered Mouse Epidermal 

Cell Lines 

Description of Technology: The 

invention relates to the creation of three 

(3) cell lines that may be used as models 

of putative initiated cancer cells. The 

cell lines can be used in basic research 

assays and low/high throughput 

screening assays. 

Cell line 308 evolved from a calciumresistant focus from adult mouse 

epidermis that was exposed to the 

carcinogen, 7,12- 

dimethylbenz[a]anthracene (DMBA). 

Cell lines F and D were derived by 

treating primary newborn mouse 

epidermal cells in culture with Nmethyl-Nı ́-nitro-N-nitrosoguanidine 

(MNNG) and DMBA, respectively. These 

three (3) noncancerous cell lines 

derived from differentiation-resistant, 

carcinogen-induced foci may be 

considered to be putative initiated cells. 

Inventor: Stuart H. Yuspa (NCI) 

Related Publications: 

1. SH Yuspa and DL Morgan. Mouse 

skin cells resistant to terminal 

differentiation associated with initiation 

of carcinogenesis. Nature 1981 Sep 

3;293(5287):72–74. 

2. H Hennings et al. Response of 

carcinogen-altered mouse epidermal 

cells to phorbol ester tumor promoters 

and calcium. J Invest Dermatol. 1987 

Jan;88(1):60–65. 

Patent Status: HHS Reference No. E– 

154–2004/0—Research Tool. Patent 

protection is not being pursued for this 

technology. 

Licensing Status: Available for 

licensing under a Biological Materials 

License Agreement. 

Licensing Contact: Betty Tong, PhD; 

301–594–6565; tongb@mail.nih.gov. 

A Mouse Model for Conditional Gene 

Deletion of c-Met Receptor 

Description of Technology: c-Met 

oncogene has been implicated in a 

variety of human cancers as well as 

degenerative diseases. Signaling via the 

c-Met receptor is essential for survival 

as evidenced by the embryonal death of 

mice in which the c-Met has been 

deleted. Further analysis of the role of 

the signaling pathway supported by cMet receptor in the adult organism is 

hindered by its embryonic lethality. The 

establishment of a mouse model for the 

conditional c-Met gene deletion will 

provide a unique opportunity to explore 

the function of c-Met in the adult mouse 

by selectively deleting the receptor gene 

in various tissues. Such a mouse model 

is established at the National Institutes 

of Health and available for licensing. 

Applications: 

• Animal model to study the 

physiological role of the c-Met receptor. 

• Animal model for testing potential 

drug targeted to the c-Met signal 

transduction pathway. 

Inventor: Snorri S. Thorgeirsson (NCI) 

Patent Status: HHS Reference No. E– 

048–2003/0—Research Tool. Patent 

protection is not being pursued for this 

technology. 

Licensing Status: c-Met receptor 

conditional KO mice are available for 

licensing. 

Licensing Contact: Betty Tong, PhD; 

301–594–6565; tongb@mail.nih.gov. 

Dated: April 6, 2009. 

Richard U. Rodriguez, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. E9–8212 Filed 4–9–09; 8:45 am] 

BILLING CODE 4140–01–P 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Center for Scientific Review; Amended 

Notice of Meeting 

Notice is hereby given of a change in 

the meeting of the Center for Scientific 

Review Special Emphasis Panel, March 

26, 2009, 12 p.m. to March 27, 2009, 3 

p.m., National Institutes of Health, 6701 

Rockledge Drive, Bethesda, MD 20892 

which was published in the Federal 

Register on March 12, 2009, 74 FR 

10748. 

The meeting will be held April 16, 

2009, 3 p.m. to April 17, 2009, 6 p.m. 

The meeting location remains the same. 

The meeting is closed to the public. 

Dated: April 2, 2009. 

Jennifer Spaeth, 

Director, Office of Federal Advisory 

Committee Policy. 

[FR Doc. E9–8018 Filed 4–9–09; 8:45 am] 

BILLING CODE 4140–01–M 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Center for Scientific Review; Amended 

Notice of Meeting 

Notice is hereby given of a change in 

the meeting of the Center for Scientific 

Review Special Emphasis Panel, April 

20, 2009, 9 a.m. to April 21, 2009, 3 

p.m., National Institutes of Health, 6701 

Rockledge Drive, Bethesda, MD 20892 

which was published in the Federal 

Register on March 31, 2009, 74 FR 

14570–14571.