Government-Owned Inventions; Availability for Licensing, 56473-56475 [05-19172]

Download as PDF 56473 Federal Register / Vol. 70, No. 186 / Tuesday, September 27, 2005 / Notices DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health National Institutes of Health/National Institute of Environmental Health Sciences; Submission for OMB Review; Comment Request; Active Living by Design Program Evaluation SUMMARY: Under the provisions of Section 3507(a)(1)(D) of the Paperwork Reduction Act of 1995, the National Institute of Environmental Health Sciences (NIEHS), the National Institute of Health (NIH) has submitted to the Office of Management and Budget (OMB) a request to review and approve the information collection listed below. This proposed information collection was previously published in the Federal Register on February 14, 2005 (Volume 70, Number 29, Pages 7508–7509, and allowed 60–days for public comment. No public comments were received. The purpose of this notice is to allow an additional 30 days for public comment. The National Institutes of Health may not conduct or sponsor, and the respondent is not required to respond to the collection of information unless it displays a currently valid OMB control number. Proposed Collection: Title: Active Living by Design Program Evaluation. Type of Information Collection Request: NEW. Need and Use of Information Collection: The purpose of this study is to provide NIEHS with an overall evaluation of the Active Living by Design (ALbD) program to determine the extent to which program strategies to increase physical activity influence change, as measured by increased physical activity and reduction of Body Mass Index (BMI), in residents of participating communities. The objective of this study is to determine the degree to which the changes in the built environment, communication strategies and policy as a result of ALbD’s program has impacted physical activity and BMI in residents within the twenty-five (25) participating communities relative to a set of ten (10) control communities. Two types of data collection will occur throughout the study. A telephone survey, which relies on self-reports, and Number of respondents Type of respondents a clinical survey, which will collect physical activity data using measures of physical activity such as, accelerometers; measures of BMI and an interview on respondents’ perceptions of their neighborhood. The findings of this study will provide valuable information concerning (1) The Impact ALbD strategies have on increasing physical activity and bringing about positive changes in health associated with exercise, such as weight loss; and (2) possible reduction of health risks and diseases related to physical inactivity through implementation of ALbd strategies. Frequency of Response: Three times over a period of five (5) years, during three rounds of data collection. Affected Public: Individuals or households. Type of Respondents: Respondents includes adults and children ages 13 through 17 years and their parents. The clinical procedures require respondents under 18 years of age to be accompanied by their parent/ guardian, therefore the burden has been doubled for these respondents. The annual reporting burden is respected in the following table: Frequency of response Average time per response Annual hour burden Respondents to Telephone Survey ................................................................. Respondents to Clinical Study—Adults ........................................................... Respondents to Clinical Study—Children/Parent ............................................ 2,450 1,855 595 1 1 1 .334 .9185 1.837 818.3 1,703.8 1,093.0 Total .......................................................................................................... ........................ ........................ ........................ 3,615.1 There are no Capital Costs to report. There are no Operating or Maintenance Costs to report. Request For Comments: Written comments and/or suggestions from the public and affected agencies should address one or more of the following points: (1) Evaluate whether the proposed collection of information is necessary for the proper performance of the function of the agency, including whether the information will have practical utility; (2) evaluate the accuracy of the agency’s estimate of the burden of the proposed collection of information, including the validity of the methodology and assumptions used; (3) enhance the quality, utility, and clarity of the information to be collected; and (4) minimize the burden of the collection of information on those who are to respond, including the use of appropriated automated, electronic, mechanical, or other technological collection techniques or other forms of information technology. Direct Comments To OMB: Written comments and/or suggestions regarding VerDate Aug<31>2005 14:52 Sep 26, 2005 Jkt 205001 the item(s) contained in this notice, especially regarding the estimated public burden and associated response time, should be directed to the: Office of Management and Budget, Office of Regulatory Affairs, New Executive Office Building, Room 10235, Washington, DC 20503, Attention: Desk Officer for NIH. To request more information on the proposed project or to obtain a copy of the data collection plans and instruments, contact: Shobha Srinivasan, Ph.D., Division of Extramural Research and Training, National Institute of Environmental Health Sciences, P.O. Box 12233, MD EC–21, 111 T.W. Alexander Drive, RTP, NC 27709. Phone: (919) 541–2506. Fax: (919) 316–4606. E-mail: ss688k@nih.gov. Comments Due Date: Comments regarding this information collection are best assured of having their full effect if received within 30-days of the date of this publication. PO 00000 Frm 00034 Fmt 4703 Sfmt 4703 Dated: September 15, 2005. Richard A. Freed, NIEHS, Associate Director for Management. [FR Doc. 05–19175 Filed 9–26–05; 8:45 am] BILLING CODE 4140–01–M DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health Government-Owned Inventions; Availability for Licensing National Institutes of Health, Public Health Service, HHS. ACTION: Notice. AGENCY: 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 E:\FR\FM\27SEN1.SGM 27SEN1 56474 Federal Register / Vol. 70, No. 186 / Tuesday, September 27, 2005 / Notices 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. Methods for Introducing Homologous Recombination in a Wide Variety of Bacteria Using Plasmids and Prophage Donald L. Court (NCI). U.S. Provisional Application No. 60/ 573,504 filed 21 May 2004 (HHS Reference No. E–207–2004/0–US–01; U.S. Provisional Application No. 60/ 653,259 filed 14 Feb 2005 (HHS Reference No. E–207–2004/1–US–01); U.S. Provisional Application No. 60/ 655,729 filed 22 Feb 2005 (HHS Reference No. E–207–2004/2–US–01); U.S. Patent Application filed 20 May 2005 (HHS Reference No. E–207– 2004/3–US–01). Licensing Contact: Norbert Pontzer; 301/ 435–5502; pontzern@mail.nih.gov. Homologous recombination is the process of exchanging DNA between two DNA molecules through regions of identical sequence. Homologous recombination provides an alternative to using restriction endonucleases and ligases for producing recombinant DNA. Although the background level of homologous recombination in native E. coli is very low even with long homology arms, it is possible to modify or clone nucleic acids using homologous recombination in specific genetically modified strains of E. coli. Whereas, a defective prophage used in these recombineering strains is optimally suited for expression of the lambda RED functions for homologous recombination it is hard for experimenters not familiar with E. coli genetics to move the defective prophage from strain to strain. Thus, methods of introducing the defective prophage and its recombineering functions into other strains of E. coli and other bacteria, including other gram negative bacteria, are also needed. This invention provides plasmids and methods of use that confer the recombineering function to a variety of cells, including strains like DH10B of E. coli, as well as other species like Salmonella, Pseudomonas, Cyanobacteria, and Yeresinia, among others. These plasmids can be isolated VerDate Aug<31>2005 14:52 Sep 26, 2005 Jkt 205001 in vitro and can be used to transform bacterial cells, such as gram negative bacteria. This research is described, in part, in: Thomason, L.C., Costantino, N., Sawitzke, JA., Datta, S., Bubunenko, M., Court, DL., Myers, R.S., Oppenheim, AB. 2005. Recombineering in Prokaryotes. In Phages: Their Role in Bacterial Pathogenesis and Biotechnology. pp. 383–399. (MK. Waldor, DI. Friedman, and SL. Adhya) ASM Press, Herndon, VA. Also provided are Lambda phages and methods of use for their introduction as prophages to provide recombineering functions into E. coli cells (Virology 319: 185–189, 2004). These phages include appropriate amber mutations in genes to prevent cell death and allow high expression of lambda RED recombination functions. The phage also carry a selectable drug marker used to make lysogens. The phages can be used to infect an E. coli cell that includes a suppressor of the amber mutations which allows the phage to reproduce, lyse the infected cell, and produce high titers of the phage. However, the phage will not be able to destroy cells that do not carry the suppressor mutations and in these cells the phage can lysogenise and be used as a defective prophage to generate recombination activity in those cells. Such cells lacking the suppressor are DH10B cells in which genomic libraries of BACs are cloned. Such random libraries can be lysogenized in mass (or individually) with these phages by selecting for the drug marker they carry. These lysogens can then be manipulated for homologous recombination in the same way as BAC containing derivatives off DY380 described elsewhere. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. homeostasis, and electrical excitability in neurons and smooth muscle. The NIH announces new treatment methods for asthma, bronchitis and cystic fibrosis. The treatments consist of either increasing or decreasing the activity of inositol 1,3,4,5,6 pentakisphosphate 1-phosphatase in a patient, thereby controlling Ins (3,4,5,6) P4-signaling which in turn affects the chloride channels, ultimately regulating salt, fluid and mucus secretion. This modulation of inositol 1,3,4,5,6 pentakisphosphate 1-phosphatase is accomplished by either pharmacological or genetic intervention. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. Cancer Therapy Using Vasoactive Intestinal Peptide Antagonists T. Moody (NCI), D. Brenneman (NICHD), et al. U.S. Patent No. 5,217,953 issued 08 Jun 1993 (HHS Reference No. E–009– 1991/0–US–01); U.S. Patent No. 5,565,424 issued 15 Oct 1996 (HHS Reference No. E–009–1991/1–US–01); U.S. Patent No. 6,630,124 issued 07 Oct 2003 (HHS Reference No. E–301– 1998/2–US–06); Worldwide IP coverage. Licensing Contact: Susan Carson; 301/ 435–5020; carsonsu@mail.nih.gov. The second leading cause of death in the United States is cancer and more than one million Americans are diagnosed with cancer each year, with this number likely to increase as the population ages. There remains a need for effective therapeutics with improved safety profiles, and promising results can be obtained through targeting receptors which are highly expressed on specific cancers. Vasoactive Intestinal Peptide (VIP) is a 28 amino-acid peptide hormone and one of several small neuropeptides that can function as Regulation of INS (3456) P4 Signalling autocrine growth factors. VIP mediates a by a Reversible Kinase/Phosphatase variety of physiological responses and and Methods and Compositions Related has been shown to exert stimulating and Thereto trophic effects on neoplastic cells inducing its own receptors by feedback Stephen Shears (NIEHS) et al. U.S. Patent Application No. 10/508,363 mechanisms. Studies have shown that filed 16 Sep 2004 (HHS Reference No. VIP receptors are present in many E–105–2002/0–US–03), claiming epithelial cancers including breast, priority to 18 Mar 2002. colon, non-small cell lung carcinoma, Licensing Contact: Marlene Shinn-Astor; and pancreatic and prostate cancers. 301/435–4426; shinnm@mail.nih.gov. Work by NIH scientists and their collaborators has shown that VIP Receptor-dependent changes in Ins receptor antagonists such as the (3,4,5,6) P4 levels is a topic of general lipophilic VIP antagonist SNH inhibit biological significance, since this the growth of cancer cell lines in vitro regulates the activities of chloride and in vivo and potentiate the channels that in turn regulate salt and cytotoxicity of chemotherapeutic drugs. fluid and mucus secretion from For example, results have shown that epithelial cells, cell volume PO 00000 Frm 00035 Fmt 4703 Sfmt 4703 E:\FR\FM\27SEN1.SGM 27SEN1 Federal Register / Vol. 70, No. 186 / Tuesday, September 27, 2005 / Notices SNH and taxol are synergistic at inhibiting breast cell cancer growth and can potentiate the cytotoxicity of taxol in an in vivo human xenograft breast cancer mouse model. Combination therapy using these agents may therefore greatly enhance the response rate of different cancers to these drugs and may significantly reduce side effects by permitting a lower therapeutic dose to be administered. Available for licensing are compositions of matter and methods of use of VIP receptor antagonists. Dated: September 15, 2005. Steven M. Ferguson, Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health. [FR Doc. 05–19172 Filed 9–26–05; 8:45 am] BILLING CODE 4140–01–P DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health Government-Owned Inventions; Availability for Licensing National Institutes of Health, Public Health Service, HHS. ACTION: Notice. AGENCY: 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. HIV-Encoded siRNA, microRNA and Suppressor of RNA Silencing Yamina Bennasser et al. (NIAID) U.S. Provisional Application No. 60/ 677,839 filed 05 May 2005 (HHS Reference No. E–203–2005/0–US–01). Licensing Contact: Susan Ano; 301/435– 5515; anos@mail.nih.gov. VerDate Aug<31>2005 14:52 Sep 26, 2005 Jkt 205001 The present invention relates to virusencoded siRNA and miRNA species and the use of such RNAs in the diagnosis, prevention and/or treatment of retroviral infection, especially HIV or SIV infection. This invention conveys the first evidence that HIV–1 encodes viral siRNA precursors in its genome and that natural HIV–1 infection provokes nucleic acid-based immunity in human cells. To overcome this cellular defense, the HIV–1 Tat protein has evolved to include a suppressor of RNA silencing (SRS) function. Additionally, this invention identifies five microRNA (miRNA) precursor candidates that regulate cellular gene expression at a post-transcriptional level. The five miRNA precursors (21– 25 nucleotides in length) are encoded in highly conserved regions of HIV such as TAR sequence, gag, pol and nef genes. These findings indicate that viruses utilize RNA interference as a mechanism to regulate cellular gene expression. This technology is further described in: Bennasser et al., ‘‘HIV–1 encoded candidate micro-RNAs and their cellular targets,’’ Retrovirology 2004 Dec 15, 1(1):43, doi:10.1186/1742–4690–1–43; and Bennasser et al., ‘‘Evidence that HIV–1 encodes an siRNA and a suppressor of RNA silencing,’’ Immunity 2005 May, 22(5):607–619, doi:10.1016/j.immuni.2005.03.010. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. Miniature Laser-Induced Fluorescence Detector Paul Smith, Nicole Morgan, Edward Wellner, Terry Phillips (ORS) U.S. Provisional Application No. 60/ 682,847 filed 20 May 2005 (HHS Reference No. E–129–2005/0–US–01). Licensing Contact: Michael Shmilovich; 301/435–5019; shmilovm@mail.nih.gov. Available for licensing and commercial development is a miniature laser-induced fluorescence detector having an in-line microfluidic detection cell. The detection cell finds application in High Performance Liquid Chromatography (HPLC), Capillary Electrophoresis (CE) and Mass Spectroscopy (MS) applications, among others. The cell for fluorescence measurements can have a measurement volume of 1 nL or less and a sample can be excited using two excitation wavelengths. The detection cell can include a 5 mm to 5 cm long capillary tube and an excitation fiber proximate to the capillary tube. A detection fiber PO 00000 Frm 00036 Fmt 4703 Sfmt 4703 56475 is also proximate to the capillary tube, and the detection fiber has a diameter the same size or larger than the external diameter of the capillary tube. A plurality of both excitation and detection fibers can be used. In addition to licensing, the technology may be available for further development through collaborative research opportunities with the inventors. Cellular Receptor for Varicella-Zoster Virus and Cell-to-Cell Spread of Virus Jeffery Cohen et al. (NIAID) U.S. Provisional Application No. 60/ 684,526 filed 26 May 2005 (HHS Reference No. E–289–2004/0–US–01). Licensing Contact: Chekesha S. Clingman; 301/435–5018; clingmac@mail.nih.gov. This technology relates to identification of insulin degrading enzyme (IDE) as a cellular receptor for Varicella-Zoster-Virus (VZV), the etiologic agent of varicella (chickenpox) and zoster (shingles). Acute infection of VZV is followed by cell-associated viremia and the development of varicella rash. The virus establishes lifelong latency in the nervous system and can reactivate to cause zoster. The mechanism of VZV entry into target cells and spread from cell-to-cell is not well understood. The inventors have shown that antibodies to IDE and recombinant IDE partially inhibit infection with the virus in cell culture. Reducing the level of IDE in the cell (with siRNA), or blocking the ability of IDE to bind with a VZV glycoprotein, markedly diminishes cell-to-cell spread of the virus in cell culture and partially inhibits infection of cells with cell-free virus. This invention further describes molecules that may have a role in the treatment or prevention of VZV infections, including antibodies to IDE, peptides that block IDE–VZV interactions, and other molecules that block binding activity of IDE. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. A Novel Amplification Method Permits Pathogens To Be Detected With Microarrays Michael J. Brownstein, Charles Xiang, and Zhi-Qing Qi (NIMH) U.S. Provisional Application No. 60/ 635,239 filed 09 Dec 2004 (DHHS Reference No. E–184–2004/0–US–01). Licensing Contact: Cristina Thalhammer-Reyero; 301/435–4507; thalhamc@mail.nih.gov. E:\FR\FM\27SEN1.SGM 27SEN1

Agencies

[Federal Register Volume 70, Number 186 (Tuesday, September 27, 2005)]
[Notices]
[Pages 56473-56475]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 05-19172]


-----------------------------------------------------------------------

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

[[Page 56474]]

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.

Methods for Introducing Homologous Recombination in a Wide Variety of 
Bacteria Using Plasmids and Prophage

Donald L. Court (NCI).
U.S. Provisional Application No. 60/573,504 filed 21 May 2004 (HHS 
Reference No. E-207-2004/0-US-01; U.S. Provisional Application No. 60/
653,259 filed 14 Feb 2005 (HHS Reference No. E-207-2004/1-US-01); U.S. 
Provisional Application No. 60/655,729 filed 22 Feb 2005 (HHS Reference 
No. E-207-2004/2-US-01); U.S. Patent Application filed 20 May 2005 (HHS 
Reference No. E-207-2004/3-US-01).
Licensing Contact: Norbert Pontzer; 301/435-5502; 
pontzern@mail.nih.gov.

    Homologous recombination is the process of exchanging DNA between 
two DNA molecules through regions of identical sequence. Homologous 
recombination provides an alternative to using restriction 
endonucleases and ligases for producing recombinant DNA. Although the 
background level of homologous recombination in native E. coli is very 
low even with long homology arms, it is possible to modify or clone 
nucleic acids using homologous recombination in specific genetically 
modified strains of E. coli. Whereas, a defective prophage used in 
these recombineering strains is optimally suited for expression of the 
lambda RED functions for homologous recombination it is hard for 
experimenters not familiar with E. coli genetics to move the defective 
prophage from strain to strain. Thus, methods of introducing the 
defective prophage and its recombineering functions into other strains 
of E. coli and other bacteria, including other gram negative bacteria, 
are also needed.
    This invention provides plasmids and methods of use that confer the 
recombineering function to a variety of cells, including strains like 
DH10B of E. coli, as well as other species like Salmonella, 
Pseudomonas, Cyanobacteria, and Yeresinia, among others. These plasmids 
can be isolated in vitro and can be used to transform bacterial cells, 
such as gram negative bacteria.
    This research is described, in part, in: Thomason, L.C., 
Costantino, N., Sawitzke, JA., Datta, S., Bubunenko, M., Court, DL., 
Myers, R.S., Oppenheim, AB. 2005. Recombineering in Prokaryotes. In 
Phages: Their Role in Bacterial Pathogenesis and Biotechnology. pp. 
383-399. (MK. Waldor, DI. Friedman, and SL. Adhya) ASM Press, Herndon, 
VA.
    Also provided are Lambda phages and methods of use for their 
introduction as prophages to provide recombineering functions into E. 
coli cells (Virology 319: 185-189, 2004). These phages include 
appropriate amber mutations in genes to prevent cell death and allow 
high expression of lambda RED recombination functions. The phage also 
carry a selectable drug marker used to make lysogens. The phages can be 
used to infect an E. coli cell that includes a suppressor of the amber 
mutations which allows the phage to reproduce, lyse the infected cell, 
and produce high titers of the phage. However, the phage will not be 
able to destroy cells that do not carry the suppressor mutations and in 
these cells the phage can lysogenise and be used as a defective 
prophage to generate recombination activity in those cells. Such cells 
lacking the suppressor are DH10B cells in which genomic libraries of 
BACs are cloned. Such random libraries can be lysogenized in mass (or 
individually) with these phages by selecting for the drug marker they 
carry. These lysogens can then be manipulated for homologous 
recombination in the same way as BAC containing derivatives off DY380 
described elsewhere.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Regulation of INS (3456) P4 Signalling by a Reversible Kinase/
Phosphatase and Methods and Compositions Related Thereto

Stephen Shears (NIEHS) et al.
U.S. Patent Application No. 10/508,363 filed 16 Sep 2004 (HHS Reference 
No. E-105-2002/0-US-03), claiming priority to 18 Mar 2002.
Licensing Contact: Marlene Shinn-Astor; 301/435-4426; 
shinnm@mail.nih.gov.

    Receptor-dependent changes in Ins (3,4,5,6) P4 levels is a topic of 
general biological significance, since this regulates the activities of 
chloride channels that in turn regulate salt and fluid and mucus 
secretion from epithelial cells, cell volume homeostasis, and 
electrical excitability in neurons and smooth muscle.
    The NIH announces new treatment methods for asthma, bronchitis and 
cystic fibrosis. The treatments consist of either increasing or 
decreasing the activity of inositol 1,3,4,5,6 pentakisphosphate 1-
phosphatase in a patient, thereby controlling Ins (3,4,5,6) P4-
signaling which in turn affects the chloride channels, ultimately 
regulating salt, fluid and mucus secretion. This modulation of inositol 
1,3,4,5,6 pentakisphosphate 1-phosphatase is accomplished by either 
pharmacological or genetic intervention.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Cancer Therapy Using Vasoactive Intestinal Peptide Antagonists

T. Moody (NCI), D. Brenneman (NICHD), et al.
U.S. Patent No. 5,217,953 issued 08 Jun 1993 (HHS Reference No. E-009-
1991/0-US-01); U.S. Patent No. 5,565,424 issued 15 Oct 1996 (HHS 
Reference No. E-009-1991/1-US-01); U.S. Patent No. 6,630,124 issued 07 
Oct 2003 (HHS Reference No. E-301-1998/2-US-06); Worldwide IP coverage.
Licensing Contact: Susan Carson; 301/435-5020; carsonsu@mail.nih.gov.

    The second leading cause of death in the United States is cancer 
and more than one million Americans are diagnosed with cancer each 
year, with this number likely to increase as the population ages. There 
remains a need for effective therapeutics with improved safety 
profiles, and promising results can be obtained through targeting 
receptors which are highly expressed on specific cancers. Vasoactive 
Intestinal Peptide (VIP) is a 28 amino-acid peptide hormone and one of 
several small neuropeptides that can function as autocrine growth 
factors. VIP mediates a variety of physiological responses and has been 
shown to exert stimulating and trophic effects on neoplastic cells 
inducing its own receptors by feedback mechanisms. Studies have shown 
that VIP receptors are present in many epithelial cancers including 
breast, colon, non-small cell lung carcinoma, and pancreatic and 
prostate cancers. Work by NIH scientists and their collaborators has 
shown that VIP receptor antagonists such as the lipophilic VIP 
antagonist SNH inhibit the growth of cancer cell lines in vitro and in 
vivo and potentiate the cytotoxicity of chemotherapeutic drugs. For 
example, results have shown that

[[Page 56475]]

SNH and taxol are synergistic at inhibiting breast cell cancer growth 
and can potentiate the cytotoxicity of taxol in an in vivo human 
xenograft breast cancer mouse model.
    Combination therapy using these agents may therefore greatly 
enhance the response rate of different cancers to these drugs and may 
significantly reduce side effects by permitting a lower therapeutic 
dose to be administered. Available for licensing are compositions of 
matter and methods of use of VIP receptor antagonists.

    Dated: September 15, 2005.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 05-19172 Filed 9-26-05; 8:45 am]
BILLING CODE 4140-01-P

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