Federal Register / Vol. 75, No. 231 / Thursday, December 2, 2010 / Notices 75177 

of the Food and Drug Administration 

(FDA). The meeting will be open to the 

public. 

Name of Committee: Gastrointestinal 

Drugs Advisory Committee. 

General Function of the Committee: 

To provide advice and 

recommendations to the Agency on 

FDA’s regulatory issues. 

Date and Time: The meeting will be 

held on January 12, 2011, from 8 a.m to 

5 p.m. 

Location: FDA White Oak Campus, 

10903 New Hampshire Ave., Silver 

Spring, MD 20993–0002, Bldg. 31, the 

Great Room, White Oak Conference 

Center (rm. 1503). Information regarding 

special accommodations due to a 

disability, visitor parking and 

transportation may be accessed at: 

http://www.fda.gov/ 

AdvisoryCommittees/default.htm; under 

the heading ‘‘Resources for You,’’ click 

on ‘‘White Oak Conference Center 

Parking and Transportation Information 

for FDA Advisory Committee Meetings.’’ 

Please note that visitors to the White 

Oak Campus must have a valid driver’s 

license or other picture ID, and must 

enter through Building 1. 

Contact Person: Kristine T. Khuc, 

Center for Drug Evaluation and 

Research, Food and Drug 

Administration, 10903 New Hampshire 

Ave., Bldg. 31, rm. 2417, Silver Spring, 

MD 20993–0002, 301–796–9001, FAX: 

301–847–8533, e-mail: 

kristine.khuc@fda.hhs.gov, or FDA 

Advisory Committee Information Line, 

1–800–741–8138 (301–443–0572 in the 

Washington, DC area), code 

3014512538. Please call the Information 

Line for up-to-date information on this 

meeting. A notice in the Federal 

Register about last minute modifications 

that impact a previously announced 

advisory committee meeting cannot 

always be published quickly enough to 

provide timely notice. Therefore, you 

should always check the Agency’s Web 

site and call the appropriate advisory 

committee hot line/phone line to learn 

about possible modifications before 

coming to the meeting. 

Agenda: On January 12, 2011, the 

committee will discuss the safety and 

efficacy of new drug application (NDA) 

022–486, for Solpura (liprotamase) 

Capsules, by Alnara Pharmaceuticals, 

for the proposed indication (use) in the 

treatment of exocrine pancreatic 

insufficiency due to cystic fibrosis, 

chronic pancreatitis, pancreatectomy 

(surgical removal of all or part of the 

pancreas), or other conditions that may 

impair or limit function of the pancreas. 

The pancreas is an organ involved, in 

part, in the digestion of food through the 

use of specialized proteins called 

enzymes. Exocrine pancreatic 

insufficiency is a decreased ability to 

digest food due to deficient enzyme 

production by the pancreas. 

FDA intends to make background 

material available to the public no later 

than 2 business days before the meeting. 

If FDA is unable to post the background 

material on its Web site prior to the 

meeting, the background material will 

be made publicly available at the 

location of the advisory committee 

meeting, and the background material 

will be posted on FDA’s Web site after 

the meeting. Background material is 

available at http://www.fda.gov/ 

AdvisoryCommittees/Calendar/ 

default.htm. Scroll down to the 

appropriate advisory committee link. 

Procedure: Interested persons may 

present data, information, or views, 

orally or in writing, on issues pending 

before the committee. Written 

submissions may be made to the contact 

person on or before December 28, 2010. 

Oral presentations from the public will 

be scheduled between approximately 1 

p.m. to 2 p.m. Those individuals 

interested in making formal oral 

presentations should notify the contact 

person and submit a brief statement of 

the general nature of the evidence or 

arguments they wish to present, the 

names and addresses of proposed 

participants, and an indication of the 

approximate time requested to make 

their presentation on or before 

December 17, 2010. Time allotted for 

each presentation may be limited. If the 

number of registrants requesting to 

speak is greater than can be reasonably 

accommodated during the scheduled 

open public hearing session, FDA may 

conduct a lottery to determine the 

speakers for the scheduled open public 

hearing session. The contact person will 

notify interested persons regarding their 

request to speak by December 20, 2010. 

Persons attending FDA’s advisory 

committee meetings are advised that the 

Agency is not responsible for providing 

access to electrical outlets. 

FDA welcomes the attendance of the 

public at its advisory committee 

meetings and will make every effort to 

accommodate persons with physical 

disabilities or special needs. If you 

require special accommodations due to 

a disability, please contact Kristine T. 

Khuc at least 7 days in advance of the 

meeting. 

FDA is committed to the orderly 

conduct of its advisory committee 

meetings. Please visit our Web site at 

http://www.fda.gov/ 

AdvisoryCommittees/ 

AboutAdvisoryCommittees/ 

ucm111462.htm for procedures on 

public conduct during advisory 

committee meetings. 

Notice of this meeting is given under 

the Federal Advisory Committee Act (5 

U.S.C. app. 2). 

Dated: November 26, 2010. 

Leslie Kux, 

Acting Assistant Commissioner for Policy. 

[FR Doc. 2010–30274 Filed 12–1–10; 8:45 am] 

BILLING CODE 4160–01–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. 

Novel Compositions and Methods To 

Treat Glioblastoma and Other Cancers 

Description of Technology: There 

remains a significant unmet need for 

therapeutics to treating glioblastoma 

multiforme, a very aggressive type of 

brain tumor. Glioblastoma is difficult to 

treat with conventional surgery, 

chemical, and radiation therapies. With 

approximately 18,000 new glioblastoma 

cases in the U.S. each year, and a 

comparable market in Europe, the global 

market for such products forecast to be 

over $300 million. In light of the high 

unmet need in malignant astrocytoma 

and little in the way of pipeline 

competition, this indication represents a 

potential easy route to market for new 

drugs. 

WReier-Aviles on DSKGBLS3C1PROD with NOTICES

75178 Federal Register / Vol. 75, No. 231 / Thursday, December 2, 2010 / Notices 

Researchers at the National Cancer 

Institute (NCI) have identified two novel 

molecular targets, annexin 1 (Anx A1) 

and its receptor formyl peptide receptor 

1 (FPR1), for new anti-glioblastoma 

therapies. Anx A1 and FPR1 mediate 

growth, invasion, production of 

angiogenic factors, tumor formation, and 

are abnormally expressed by more 

highly malignant glioblastomas. 

Depletion of Anx A1 in glioblastoma 

cells resulted in their reduced capacity 

to form tumors; additional depletion of 

FPR1 further reduced this capacity. 

Further, the NCI researchers have found 

a correlation between Anx A1 

expression and the degree of 

malignancy of human gliomas. 

Novel anti-glioblastoma therapies 

encompassed by this invention include 

neutralizing antibodies against Anx A1 

and FPR1, small compound agonists of 

Anx A1 and FPR1, small interference 

RNAs (siRNAs) that deplete Anx A1 and 

FPR1 from glioblastoma cells, as well as 

delivery methods to effectively 

administer the Anx A1 and FPR1 

targeting drugs into brain tissues. 

Applications 

• Treatment of glioblastoma 

multiforme and other brain tumors. 

• Treatments for inhibiting neoplastic 

cell growth. 

• Treatments for inhibiting tumor 

progression and metastasis. 

• Treatments for inhibiting 

angiogenesis in a tumor. 

Advantages 

• High specificity. 

• Does not require radiation. 

• A correlation between expression of 

the molecular target and the degree of 

tumor malignancy is known. 

• Wide-range/flexibility of potential 

therapies and approaches. 

Development Status: Pre-clinical. 

Inventors: Ji Ming Wang et al. (NCI). 

Relevant Publication: Y Zhou, et al. 

Formylpeptide receptor FPR and the 

rapid growth of malignant human 

gliomas. J Natl Cancer Inst. 2005 Jun 

1;97(11):823–835. [PubMed: 15928303] 

Patent Status: U.S. Provisional 

Application No. 61/388,983, filed 01 

Oct 2010 (HHS Reference No. E–297– 

2010/0–US–01). 

Licensing Status: Available for 

licensing. 

Licensing Contact: Patrick P. McCue, 

Ph.D.; 301–435–5560; 

mccuepat@mail.nih.gov. 

Collaborative Research Opportunity: 

The Center for Cancer Research, 

Laboratory of Molecular 

Immunoregulation, 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. 

Synovial Sarcoma X Breakpoint-2 

(SSX–2) Specific Human T Cell 

Receptors for Treating a Wide-Range of 

Cancers 

Description of Technology: Many 

current approaches for treating cancer 

also generate harsh side effects in 

patients. In addition, a sizable patient 

population does not respond to 

generalized chemotherapy and radiation 

treatments for cancer. There is an urgent 

need to develop new therapeutic 

strategies aimed at reducing side-effects 

and increasing specific anti-tumor 

activity in individual patients. Adoptive 

immunotherapy is a promising new 

approach to cancer treatment that 

engineers an individual’s innate and 

adaptive immune system to fight against 

specific diseases, including cancer. As 

research and development continues in 

this area, scientists continue to improve 

cell transfer therapies by targeting an 

increasing collection of tumor antigens 

with more effective immune cell 

cultures. 

T cell receptors (TCRs) are proteins 

that recognize antigens in the context of 

infected or transformed cells and 

activate T cells to mediate an immune 

response and destroy abnormal cells. 

TCRs consist of two domains, one 

variable domain that recognizes the 

antigen and one constant region that 

helps the TCR anchor to the membrane 

and transmit recognition signals by 

interacting with other proteins. When a 

TCR is stimulated by an antigen, such 

as a tumor antigen, some signaling 

pathways activated in the cell lead to 

the production of cytokines, which 

mediate the immune response. 

Scientists at the National Institutes of 

Health (NIH) have developed T cells 

genetically engineered to recognize 

synovial sarcoma X breakpoint-2 (SSX– 

2) peptide antigens. SSX proteins, 

including SSX–2, are expressed 

primarily by tumor cells from a variety 

of cancers, including pancreatic cancer 

where very few treatment options exist. 

Other than germ cells of the testis, 

normal cells do not express SSX 

proteins and, thus, should not be 

targeted by therapies directed against 

these proteins. Therefore, SSX proteins 

represent a promising target for cancer 

immunotherapy. There are ten (10) 

known members of the SSX protein 

family designated SSX–1 through SSX– 

10. The T cell receptors (TCRs) 

developed by these NIH scientists have 

specificity for SSX–2 and deliver a 

robust immune response when they 

encounter SSX–2 expressing cells. 

However, these TCRs also recognize five 

(5) other SSX family members, 

including SSX–3, SSX–4, SSX–5, SSX– 

9, and/or SSX–10, and deliver a 

productive, intermediate immune 

response in the context of target cells 

expressing these antigens. This versatile 

antigen coverage could allow these SSXspecific TCRs to be utilized in the 

treatment of multiple types of cancer in 

a wide array of cancer patients. Infusing 

cancer patients with SSX–2 specific T 

cells via adoptive immunotherapy could 

prove to be a powerful approach for 

selectively attacking tumors without 

generating toxicity against 

noncancerous cells. 

Applications 

• Immunotherapeutics to treat and/or 

prevent the recurrence of a variety of 

human cancers, including pancreatic 

cancer and melanoma, by adoptively 

transferring the gene-modified T cells 

into patients whose tumors express a 

SSX family member protein recognized 

by this TCR. 

• A drug component of a combination 

immunotherapy regimen aimed at 

targeting specific tumor-associated 

antigens, including SSX–2, SSX–3, 

SSX–4, SSX–5, SSX–9, and/or SSX–10 

expressed by cancer cells within 

individual patients. 

• A research tool to investigate 

signaling pathways in SSX–2 expressing 

cancer cells. 

• An in vitro diagnostic tool to screen 

for cells expressing an SSX antigen from 

a recognized member of the SSX protein 

family. 

Advantages 

• Selective toxicity for tumor cells— 

SSX–2 and other SSX proteins are only 

expressed on testis germ cells and tumor 

cells. Thus, infused cells expressing an 

anti-SSX–2 TCR should target SSXexpressing tumor cells with little or no 

toxicity to normal cells. Immunotherapy 

with these cells is not anticipated to 

elicit harsh side effects to patients. 

• Ability to recognize multiple SSX 

antigens—Since these SSX–2 directed 

TCRs can also recognize five (5) 

additional SSX family members (SSX–3, 

4, 5, 9, and 10), cells expressing these 

TCRs are expected to be able to fight a 

larger range of tumor types. If in the 

course of attacking SSX–2 expressing 

tumor cells in a patient these cells also 

encounter tumor cells expressing other 

recognized SSX antigens, then these 

cells would still be capable of 

eliminating the non-SSX–2 expressing 

cell. The ability of these TCRs to 

recognize multiple SSX antigens may 

WReier-Aviles on DSKGBLS3C1PROD with NOTICES

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. 

WReier-Aviles on DSKGBLS3C1PROD with NOTICES