63160 Federal Register / Vol. 69, No. 209 / Friday, October 29, 2004 / Notices 

(b) the accuracy of the agency’s estimate 

of the burden of the proposed collection 

of information; (c) ways to enhance the 

quality, utility, and clarity of the 

information to be collected; and (d) 

ways to minimize the burden of the 

collection of information on 

respondents, including through the use 

of automated collection techniques or 

other forms of information technology.

FOR FURTHER INFORMATION CONTACT:

Send comments to Carrie N. Klabunde, 

Ph.D., Epidemiologist, National Cancer 

Institute, EPN 4005, 6130 Executive 

Boulevard, Bethesda, Maryland 20892–

7344. Telephone: (301) 402–3362; Fax: 

(301) 435–3710 E-mail: ck97b@nih.gov.

Comments Due Date: Comments 

regarding this information collection are 

best assured of having their full effect if 

received within 60-days of the date of 

this publication.

Dated: October 18, 2004

Rachelle Ragland-Green, 

NCI Project Clearance Liaison, National 

Institutes of Health.

[FR Doc. 04–24165 Filed 10–28–04; 8:45 am] 

BILLING CODE 4140–01–M

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Government-Owned Inventions; 

Availability for Licensing

AGENCY: National Institutes of Health, 

Public Health Service, DHHS.

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 (4G11) 

Against Insulin-Like Growth Factor I 

Receptor 

Peter Nissley, Peta-Gay Jackson-Booth, 

Cheryl Terry, Brett Lackey, Martyna 

Lopaczynska (NCI) 

DHHS Reference No. E–342–2004/0–

US–01 

Licensing Contact: John Stansberry; 

(301) 435–5236; 

stansbej@mail.nih.gov.

The insulin-like growth factor I 

receptor (IGF–IR) is emerging as a 

molecular target for cancer treatment. 

Prospective studies in humans provide 

evidence for a relationship between 

circulating levels of both IGF–I and IGF 

binding protein 3 (IGFBP–3) and the 

risk for the development of cancers of 

the prostate, breast, lung, and colon. 

Many human cancers express or overexpress components of the IGF signaling 

pathway, in particular IGF–II and the 

IGF–I receptor. This technology 

describes a mouse monoclonal antibody 

that binds the insulin-like growth factor 

I receptor. The IGF–IR monoclonal 

antibody 4G11 blocks binding of IGF–I 

to its receptor and promotes down 

regulation of the receptor in MCF–7 

breast cancer cells, MG–63 

osteosarcoma cells and a panel of colon 

cancer cells. Additionally, 4G11 

stimulated down-regulation of the IGF–

I receptors in MCF–7 cells results in 

inhibition of Akt and MAPK activation 

by IGF–I. This monoclonal antibody has 

utility as a laboratory reagent for 

immunoprecipitations, and as an 

inhibitor of the IGF–I signaling 

pathway. A humanized form of 

monoclonal antibody 4G11 would 

potentially have utility as a therapeutic 

to treat a variety of cancers in which 

IGF–IR signaling has been shown to be 

important. This research is partially 

described in Horm Metab Res 2003; 35: 

850–856.

Beta-Glucuronidase Cleavable Prodrugs 

of O6-Alkylguanine-DNA 

Alkyltransferase Inactivators 

Robert C. Moschel et al. (NCI) 

U.S. Provisional Application filed 08 

Sep 2004 (DHHS Reference No. E–

307–2004/0–US–01) 

Licensing Contact: George Pipia; (301) 

435–5560; pipiag@mail.nih.gov.

The present invention relates to 

prodrugs of inactivators of O6-

alkylguanine-DNA alkyltransferase. The 

prodrugs are cleaved by the betaglucuronidase enzyme found in tumor 

cells or co-administered to the patient, 

and the drugs are targeted for use in 

cancer treatment in combination with 

antineoplastic alkylating agent such as 

1,3-bis(2-chloroethyl)-1-nitrosouria or 

temozolomide. 

Transcytosis of Adeno-Associated 

Viruses 

John A. Chiorini and Giovanni Di 

Pasquale (NIDCR) 

U.S. Provisional Application filed 08 

Sep 2004 (DHHS Reference No. E–

298–2004/0–US–01) 

Licensing Contact: Jesse Kindra; (301) 

435–5559; kindraj@mail.nih.gov.

The invention relates to a method for 

delivering nucleic acids to a variety of 

cells including those of the gut, kidney, 

lung and central nervous system. The 

underlying cells of such organs are 

covered by a barrier of endothelial or 

epithelial cells which can limit the 

transfer of nucleic acids, or other 

potentially therapeutic agents, to the 

underlying target cells. To overcome 

this limitation, the method employs 

certain members of the parvovirus 

family to transcytose the barrier cells. 

During transcytosis, the virus passes 

through these barrier cells and can 

infect cells of the underlying layer. 

Therefore, this method could facilitate 

the transfer of nucleic acids to cells that 

currently available viral vectors are 

unable to reach. 

The method could be applied to the 

treatment of neurodegenerative diseases 

such as Parkinson’s, Alzheimer’s, 

Huntington’s, lysosomal storage 

diseases, the dominant spinal cerebellar 

ataxias, and Krabbe’s disease without 

the need for stereotactic injection. The 

method could potentially also be used 

in the treatment of genetic muscle 

disorders such as muscular dystrophy. 

Several of the viruses described in the 

invention are serologically distinct and 

could be used in patients who have 

developed an immune response to other 

vectors. 

Multimeric Protein Toxins to Target 

Cells Having Multiple Identifying 

Characteristics 

Stephen Leppla (NIAID), Shi-hui Liu 

(NIAID), and Thomas Bugge (NIDCR) 

U.S. Provisional Application No. 60/

543,417 filed 09 Feb 2004 (DHHS 

Reference No. E–059–2004/0–US–01) 

Licensing Contact: Brenda Hefti; (301) 

435–4632; heftib@mail.nih.gov.

This technology relates to multimeric 

bacterial protein toxins which can be 

used to specifically target cells. 

Specifically, this is a modified 

recombinant anthrax toxin protective 

antigen (PrAg) that has been modified in 

several ways. First, the PrAg can be 

activated both by a metalloproteinase 

(MMP) and by urokinase plasminogen 

activator (uPA). Second, the native PrAg 

Federal Register / Vol. 69, No. 209 / Friday, October 29, 2004 / Notices 63161

lethal factor (LF) binding site has been 

modified so that only a modified PrAg 

comprising two different monomers can 

bind anthrax LF. When administered 

with an effector component, the 

recombinant anthrax toxins are toxic 

only to cells expressing both a MMP and 

uPA on their surface. This technology is 

therefore useful for selective methods of 

treating cancers, because many cancer 

cells express multiple cell-surface 

proteases. 

Novel Human Cancer Antigen, NY 

ESO–1/CAG–3, and Gene Encoding 

Same 

Rong-fu Wang (EM), Steven A. 

Rosenberg (NCI) 

U.S. Provisional Application No. 60/

061,428 filed 08 Oct 1997 (DHHS 

Reference No. E–265–1997/0–US–01); 

PCT Application No. PCT/US98/

19609 filed 21 Sep 1998, which 

published as WO 99/18206 on 15 Apr 

1999 (DHHS Reference No. E–265–

1997/0–PCT–02); U.S. Patent 

Application No. 09/529,206 filed 21 

Sep 1998 (DHHS Reference No. E–

265–1997/0–US–04) 

Licensing Contact: Jesse Kindra; (301) 

435–5559; kindraj@mail.nih.gov.

The current invention embodies the 

identification, isolation and cloning of a 

gene encoding a novel tumor antigen, 

NY ESO–1/CAG–3, as well as cancer 

peptides thereof and antigenic cancer 

epitopes contained within the cancer 

peptides. This novel antigen is 

recognized by cytotoxic T lymphocyte 

clones derived from the TIL586 (tumor 

infiltrating lymphocyte) cell line in an 

HLA restricted manner.

The inventors believe that cancer 

peptides which are encoded by the NY 

ESO–1/CAG–3 gene represent potential 

cancer vaccines, protecting an 

individual from development of cancer 

by inhibiting the growth of cells or 

tumors which express the NY ESO–1/

CAG–3 antigen. Also embodied in the 

invention are pharmaceutical 

compositions comprising the NY ESO–

1/CAG–3 antigen, peptide, or an 

antigenic cancer epitope thereof in 

combination with one or more 

immunostimulatory molecules. These 

compositions represent potential 

anticancer therapeutics, stimulating NY 

ESO–1/CAG–3-specific T cells to elicit 

an anti-cancer immunogenic response 

and thereby eliminating or reducing the 

cancer. While these vaccines and 

pharmaceutical compositions may be 

developed for use against a variety of 

cancers, data obtained to date indicate 

that they may be of particular value for 

use against melanoma. 

Methods for diagnosing cancer via the 

detection of NY ESO–1/CAG–3 are also 

embodied in the invention. 

Method for Inhibiting Angiogenesis 

Elise C. Kohn, Lance A Liotta, and 

Riccardo Alessandro (NCI) 

U.S. Patent No. 5,744,492 issued 28 Apr 

1998 (expires 28 Apr 2015) (DHHS 

Reference No. E–220–1993/1–US–01) 

Licensing Contact: John Stansberry; 

(301) 435–5236; 

stansbej@mail.nih.gov and 

Combinatorial Therapy for Protein 

Signaling Diseases 

Arpita Mehta (NCI), Lance Liotta (NCI), 

Emmanuel Petricoin (FDA) 

U.S. Provisional Application No. 60/

453,629 filed 10 Mar 2003 (DHHS 

Reference No. E–039–2003/0–US–01) 

Licensing Contact: Michael Shmilovich; 

(301) 435–5019; 

shmilovm@mail.nih.gov.

Angiogenesis is a composite of 

regulated proliferation and regulated 

invasion occurring in a variety of 

normal and pathologic conditions. In 

this invention, the claimed compound 

and its related analogs are useful for 

inhibiting angiogenesis in a host and 

offer a novel approach to the treatment 

of cancer, diabetic retinopathy, 

hemangiomata, vasculidities, macular 

degeneration and other disease associate 

with angiogenesis. Additionally, the 

compound has shown efficacy at lower 

doses when co-administered with other 

anti-angiogenesis agents. 

Refer to issued patent 5,744,492 

(April 28, 1998), and journal articles: 

PNAS (1995) 92(5):1307–11, and In Vivo

(1996) 10(2):153–60.

Dated: October 22, 2004. 

Steven M. Ferguson, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health.

[FR Doc. 04–24166 Filed 10–28–04; 8:45 am] 

BILLING CODE 4140–01–P

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Notice of Meeting; Interagency Autism 

Coordinating Committee 

The National Institutes of Health 

(NIH) hereby announces a meeting of 

the Interagency Autism Coordinating 

Committee (IACC) to be held on 

November 19, 2004, on the NIH campus 

in Bethesda, Maryland. 

The Children’s Health Act of 2000 

(Pub. L. 106–310), Title I, Section 104, 

mandated the establishment of an IACC 

to coordinate autism research and other 

efforts within the Department of Health 

and Human Services. In April 2001, 

Secretary Tommy Thompson delegated 

the authority to establish the IACC to 

the NIH. The National Institute of 

Mental Health (NIMH) at the NIH has 

been designated the lead for this 

activity. 

The IACC meeting will be open to the 

public, with attendance limited to space 

available. Individuals who plan to 

attend and need special assistance, such 

as sign language interpretation or other 

reasonable accommodations, should 

notify the contact person listed below in 

advance of the meeting.

Name of Committee: Interagency Autism 

Coordinating Committee. 

Date: November 19, 2004. 

Time: 9 a.m.–4:30 p.m. 

Agenda: Discussion of autism activities 

across Federal agencies. 

Place: National Institutes of Health, 31 

Center Drive, Building 31, Conference Room 

10 (6th floor), Bethesda, Maryland 20892. 

Contact Person: Ann Wagner, Ph.D., 

Division of Services and Intervention 

Research, National Institute of Mental Health, 

NIH, 6001 Executive Boulevard, Room 7142, 

MSC 9633, Bethesda, Maryland 20892. Email: awagner@mail.nih.gov. Phone: 301–

443–4283.

Any member of the public interested 

in presenting oral comments to the 

Committee may notify the contact 

person listed on this notice at least 5 

days in advance of the meeting. 

Interested individuals and 

representatives of organizations may 

submit a letter of intent, a brief 

description of the organization 

represented, and a short description of 

the oral presentation. Presentations may 

be limited to 5 minutes; both printed 

and electronic copies are requested for 

the record. In addition, any interested 

person may file written comments with 

the Committee by forwarding his/her 

statement to the contact person listed on 

this notice. The statement should 

include the name, address, telephone 

number, and, when applicable, the 

business or professional affiliation of 

the interested person. 

Information about the meeting and 

online registration forms are also 

available on-line on the NIMH home 

page at http://www.nimh.nih.gov/

autismiacc/index.cfm.

Dated: October 20, 2004. 

Raynard S. Kington, 

Deputy Director, National Institutes of Health.

[FR Doc. 04–24168 Filed 10–28–04; 8:45 am] 

BILLING CODE 4140–01–P