Federal Register / Vol. 71, No. 156 / Monday, August 14, 2006 / Notices 46491 

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, MD 

20852–3804; telephone: 301/496–0220. 

A signed Confidential Disclosure 

Agreement will be required to receive 

copies of the patent applications. 

Complement Regulatory Gene Variants 

as Predictive Tests for Age-related 

Macular Degeneration (AMD) 

Description of Technology 

Age-related macular degeneration 

(AMD) is complex multigenic disorder 

that affects the central region of the 

retina (macula) and is the leading cause 

of legal blindness in developed 

countries. Age, lifestyle (e.g., smoking, 

diet) and genetic predisposition are 

major risk factors for AMD and 1.75 

million adults over 40 are affected by 

advanced AMD in the United States 

with a further 7 million considered to be 

at risk (defined by the presence of large 

retinal deposits or drusen, which are the 

hallmark of this disease). A variety of 

immune-associated molecules including 

immunoglobulins, complement 

components, activators and regulators, 

etc. are associated with drusen and 

evidence suggests that AMD, like other 

age-related diseases such as Alzheimer’s 

disease and atherosclerosis, involves a 

major inflammatory component. Several 

disease-susceptibility genes have been 

identified in family studies of macular 

degeneration and in patient cohorts by 

several groups including NIH 

researchers and their collaborators, and 

variants in the factor H gene (CFH)), a 

major inhibitor of the alternative 

complement pathway, have been 

associated with the risk for developing 

AMD. 

NIH researchers and their 

collaborators have now extended this 

work to two other regulatory genes of 

this pathway, Factor B (BF) and 

complement component 2 (C2). These 

genes were screened for genetic 

variation in two independent cohorts 

comprised of ~900 AMD cases and 

~400 matched controls. Haplotype 

analyses revealed a significant common 

risk haplotype (H1) and two protective 

haplotypes (H7 and H10). Combined 

analysis of the C2/BF haplotypes and 

CFH variants shows that variation in the 

two loci can predict the clinical 

outcome in 74% of the cases and 56% 

of the controls (Nature Genetics (2006) 

38, 458). This suggests that these 

variants can be used as predictive 

genetic tests in combination with other 

potential risk factors. 

Available for licensing are methods 

for identifying a subject at increased risk 

for developing AMD by determining the 

presence of protective genotypes at 

either the BF/C2 locus and at the CFH 

locus. Microarrays and kits are also 

provided. The complex and polygenic 

nature of AMD suggests that the 

protective and risk haplotypes claimed 

here can be of great value not only to 

companies targeting Macular 

Degeneration but perhaps more broadly 

to those involved in complementmediated inflammatory disorders. 

Inventors 

Michael Dean (NCI), Bert Gold (NCI) 

et al. 

Patent Status 

U.S. Provisional Patent Application 

No. 60/772,989, filed 13 February 2006 

(HHS Reference No. E–042–2006/0–US–

01). 

Licensing Status 

Available for non-exclusive or 

exclusive licensing. 

Licensing Contract 

Susan Carson, D.Phil.; 301–435–5020; 

mail to: carsonsu@mail.nih.gov. 

Collaborative Research Opportunity 

The NCI Laboratory of Genomic 

Diversity is seeking statements of 

capability or interest from parties 

interested in collaborative research to 

further develop, evaluate, or 

commercialize functional or genetic 

tests on complement genes and proteins. 

Please contact Kathleen Higinbotham at 

301–846–5465 for more information. 

Dated: July 28, 2006. 

Steven M. Ferguson, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. 06–6879 Filed 8–11–06; 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, 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. 

Licensing Opportunity 

From the National Institutes of Health 

Target-Specific Activatable Optical 

Probes for In Vivo Imaging 

Description of Technology 

Available for licensing and 

commercial development is an optical 

imaging method capable of detecting 

living cancer cells in vivo. The method 

increases sensitivity and reduces the 

background signal to extremely low 

levels. In contrast to conventional 

fluorescent imaging, the strategy 

activates the probe after it binds to and 

is internalized within cancer cells. 

Using antibodies, reagent-receptor 

systems, or cytokines to target the agent 

to the cancer, the agent is internalized 

by the normal cellular process of 

endocytosis which in turn, leads to 

molecular changes within the probe 

itself; fluorophores are activated only in 

the living targeted cells. 

An activatable fluorophore is one that 

is normally self-quenched by 

attachment to a peptide backbone but 

which can be activated by specific 

proteases which degrade the peptide 

resulting in ‘‘de-quenching.’’ For 

example, self-quenching avidinrhodaminex, which has affinity for 

lectin on cancer cells, is activated after 

endocytosis and degradation within the 

lysosome. Cellular internalization of 

receptor-ligand pairs with subsequent 

activation of fluorescence via ‘‘dequenching’’ provides a generalizable 

and highly sensitive method of 

detecting cancer microfoci in vivo and 

has practical implications for assisting 

surgical and endoscopic procedures. 

Application(s) 

2. Optical detection of tumor cells and 

metastatic nodules 

4. Photodynamic treatment of tumors 


jlentini on PROD1PC65 with NOTICES
46492 Federal Register / Vol. 71, No. 156 / Monday, August 14, 2006 / Notices 

Market 

• Cancer Imaging 

Development Status 

• Early-stage technology with preclinical mouse models as of 18 July 

2006 

Inventors 

• Hisataka Kobayashi (NCI) 

• Peter Choyke (NCI) 

• Urano Yasuteru (University of 

Tokyo) 

Patent Status 

• U.S. Provisional Patent Application 

filed June 30, 2006 (serial number not 

assigned); closely related to HHS Ref. 

No. E–335–2005; U.S. Provisional Patent 

Application No. 60/751,429 filed 

December 16, 2005. 

Availability 

• Available for exclusive, nonexclusive licensing or collaborative 

opportunity. 

Licensing Contact 

Chekesha S. Clingman, PhD., 

Technology Licensing Specialist, Office 

of Technology Transfer, The National 

Institutes of Health, 6011 Executive 

Blvd., Suite 325, Rockville, MD 20852, 

phone: (301) 435–5018, fax: (301) 402–

0220, clingmac@mail.nih.gov. 

Collaborative Research Opportunity 

The NCI Molecular Imaging Program 

is seeking statements of capability or 

interest from parties interested in 

collaborative research to further 

develop, evaluate, or commercialize 

target specific activatable optical probes. 

Please contact Hisataka Kobayashi or 

Peter Choyke at 301–451–4220 

pchoyke@nih.gov for more information. 

Dated: July 31, 2006. 

Steven M. Ferguson, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. 05–6881 Filed 8–11–06; 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, 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. 

Amyloid Beta Is a Ligand for FPR Class 

Receptors 

Description of Technology: 

Alzheimer’s disease is the most 

important dementing illness in the 

United States because of its high 

prevalence. Five to ten percent of the 

United States population 65 years and 

older are afflicted with the disease. In 

1990 there were approximately 4 

million individuals with Alzheimer’s, 

and this number is expected to reach 14 

million by the year 2050. It is the fourth 

leading cause of death for adults, 

resulting in more than 100,000 deaths 

annually. Amyloid beta has been 

identified as playing an important role 

in the neurodegeneration of Alzheimer’s 

disease. However, the mechanism by 

which this occurred was unknown, but 

has been postulated to be either direct 

or indirect through an induction of 

inflammatory responses. 

The NIH announces the identification 

of the 7-transmembrane, G-proteincoupled receptor, FPRL–1, in the 

cellular uptake and fibrillar aggregation 

of amyloid bb(Abb) peptides. The Abb 

peptides use the FPRL–1 receptor to 

attract and activate human monocytes 

and mouse microglial cells (publications 

referenced below), and have been 

identified as a principal component of 

the amyloid plaques associated with 

Alzheimer’s disease. In addition, the 

known anti-inflammatory drug, 

Colchicine, has been shown to inhibit 

the FPRL1 activation by amyloid bb** 

and the internalization of FPRL1/ 

amyloid beta complexes. 

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

Publications: 

1. Y Le, W Gong, L Tiffany, A 

Tumanov, S Nedospasov, W Shen, NM 

Dunlop, J-L Gao, PM Murphy, JJ 

Oppenheim, and JM Wang, ‘‘Amyloid 

(beta)42 activates a G-protein-coupled 

chemoattractant receptor, FPR-like-1,’’ J. 

Neuroscience 2001 Jan 15; 21(2):RC123. 

2. HL Tiffany, MC Lavigne, YH Cui, 

JM Wang, TL Leto, JL Gao, and PM 

Murphy, ‘‘Amyloid-beta induces 

chemotaxis and oxidant stress by acting 

at formylpeptide receptor 2, a G proteincoupled receptor expressed in 

phagocytes and brain,’’ J Biol Chem. 

2001 Jun 29;276(26):23645–52. 

3. YH Cui, Y Le, W Gong, P Proost, 

J Van Damme, WJ Murphy, and JM 

Wang, ‘‘Bacterial lipopolysaccharide 

selectively up-regulates the function of 

the chemotactic peptide receptor formyl 

peptide receptor 2 in murine microglial 

cells,’’ J Immunol. 2002 Jan 

1;168(1):434–42. 

4. H Yazawa., Z-X Yu, K Takeda, Y 

Le, W Gong, VJ Ferrans, JJ Oppenheim, 

CC Li, and JM Wang, ‘‘Beta amyloid 

peptide (Ab42) is internalized via the Gprotein coupled receptor FPRL1 and 

forms fibrillar aggregates in 

macrophages,’’ FASEB J. 2001 Nov; 

15(13):2454–2642. 

5. P Iribarren, K Chen, J Hu, G Gong, 

EH Cho, S Lockett, B Uranchimeg, and 

JM Wang, ‘‘CpG-containing 

oligodeoxynucleotide promotes 

microglial the up-take of amyloid beta 1- 

42 by up-regulating the expression of 

the G-protein coupled receptor 

mFPR2,’’.FASEB J. 2005 

Dec;19(14):2032–4. 

6. K Chen, P Iribarren, J Hu, J Chen, 

G Gong, EH Cho, S Lockett, NM Dunlop, 

and JM Wang, ‘‘Activation of Toll-like 

receptor 2 on microglia promotes cell 

uptake of Alzheimer disease-associated 

amyloid beta peptide,’’ J Biol Chem. 

2006 Feb 10;281(6):3651–9. 

Patent Status: U.S. Patent Application 

No. 10/831,524 filed 23 Apr 2004 (HHS 

Reference No. E–336–01/0–US–02), 

claiming priority to 26 Oct 2001. 

Licensing Status: Available for nonexclusive or exclusive licensing. 

Licensing Contact: 301/496–7057; 

nihott@mail.nih.gov 

Collaborative Research Opportunity: 

The National Cancer Institute, 

Laboratory of Molecular 

Immunoregulation, is seeking 

statements of capability or interest from 

parties interested in collaborative 

research to further develop, evaluate, or 

commercialized siRNA delivery 

development. Please contact Diana 

Bialozor at 301/846–5465 or 

bialozod@mail.nih.gov for more 

information. 


jlentini on PROD1PC65 with NOTICES