12316 Federal Register / Vol. 77, No. 40 / Wednesday, February 29, 2012 / Notices 

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. 

Intrathecal (IT) Administration of 

Rituximab to Treat Multiple Sclerosis 

(MS) 

Description of Technology: Multiple 

sclerosis (MS) is a chronic, neurological, 

autoimmune, demyelinating disease. 

The pathology of MS is characterized by 

an abnormal immune response directed 

against the central nervous system. In 

particular, T-lymphocytes are activated 

against the myelin sheath of the neurons 

of the central nervous system causing 

demyelination. Secondary-progressive 

multiple sclerosis (SP–MS) is the 

chronic phase of MS. The majority of 

people who have relapsing-remitting 

MS eventually develop SP–MS. There 

are currently no effective treatments for 

SP–MS patients who do not have 

evidence for focal brain inflammation 

measured by contrast enhancing lesions 

(CEL) on brain MRI. NIH investigators 

have proposed that intrathecal 

administration of Rituximab, a 

monoclonal antibody (Ab) that depletes 

B cells and effectively decreases CEL in 

relapsing-remitting MS (RR–MS) but 

does not affect progression of disability 

in progressive MS, may deplete B cells 

from the intrathecal compartment 

leading to inhibition of T cell activation 

within intrathecal compartment, and 

thereby provide a novel therapeutic 

approach to treat SP–MS. A Clinical 

trial is in progress to evaluate this novel 

approach. 

Potential Commercial Applications: 

Improved therapeutics to treat or 

prevent Secondary-progressive multiple 

sclerosis (SP–MS). 

Competitive Advantages: This 

technology would provide the first 

effective therapy for Secondaryprogressive multiple sclerosis patients 

lacking contrast enhancing lesions. 

Development Stage 

• Clinical. 

• In vivo data available (animal). 

Inventor: Bibiana Bielekova (NINDS). 

Publication: Double Blind 

Combination of Rituximab by 

Intravenous and Intrathecal Injection 

Versus Placebo in Patients With LowInflammatory Secondary Progressive 

Multiple Sclerosis (RIVITaLISe). 

ClinicalTrials.gov Identifier: 

NCT01212094 (http://clinicaltrials.gov/ 

ct2/show/NCT01212094). 

Intellectual Property: HHS Reference 

No. E–249–2011/0—U.S. Provisional 

Application No. 61/539,870 filed 27 Sep 

2011. 

Licensing Contact: Suryanarayana 

(Sury) Vepa, Ph.D., J.D.; 301–435–5020; 

vepas@mail.nih.gov. 

miR126 for the Mobilization of 

Hematopoietic Stem/Progenitor Cells 

(HSPCs) into Peripheral Blood 

Description of Technology: The NIH 

inventors have discovered that a micro 

RNA, miR126, mobilizes hematopoietic 

stem/progenitor cells (HSPCs) from the 

bone marrow into blood. These 

mobilized HSPCs can be easily collected 

from blood and used for reconstitution 

of ablated or functionally-impaired bone 

marrow. miR126 may also facilitate 

mobilization of bone-resident cancer 

cells into the circulation where they 

could be more easily targeted by cancer 

therapeutics. This discovery could 

replace bone marrow transplantation as 

we do it today. Rather than using the 

current non-selective agent G–CSF 

(which preferentially mobilizes mature 

myeloid cells rather than stem/ 

progenitor cells), miR126 could be used 

for selective mobilization of the HSPCs 

needed for hematopoietic cell 

transplantation. Additionally, miR126 

could be used to mobilize malignant 

cells from the bone marrow and render 

them more easy targets for therapy. It 

was previously shown that the bone 

marrow cavity promotes the survival of 

many cells including tumor cells, and 

that such cells may easily die when 

removed from the bone marrow niche 

and moved to the blood. Therefore, this 

discovery could also change treatment 

of many cancers that arise within the 

bone marrow or metastasize to the bone. 

Since the mechanism by which miR126 

promotes HSPCs/tumor cell 

mobilization is attributable to the 

inhibition of VCAM–1 expression, 

miR126 could be used to treat 

inflammatory states where the 

expression of VCAM1 provides an 

anchor for inflammatory cells at sites of 

inflammation. 

Potential Commercial Applications 

• Method of mobilizing 

hematopoietic stem/progenitor cells 

(HSPCs) from the bone marrow to the 

blood. 

• Use in hematopoietic cell 

transplantation and treatment of 

hematopoietic deficiency, hematological 

failure, and cancer treatments. 

• To mobilize cancer cells from the 

bone marrow and thus serve as adjuvant 

cancer therapy. 

• As an anti-inflammatory agent to 

reduce inflammatory cell infiltrates at 

sites of inflammation. 

Competitive Advantages: Mobilization 

of HSPCs yielding high-level, selective 

and rapid mobilization of HSPCs to the 

peripheral blood. 

Development Stage 

• Pre-clinical. 

• In vivo data available (animal). 

Inventors: Giovanna Tosato and 

Ombretta Salvucci (NCI). 

Publication: Salvucci O, et al. 

MicroRNA126 contributes to G–CSFinduced hematopoietic progenitor cell 

mobilization by reducing VCAM–1 

expression. Haematologica. 2012 Jan 22; 

Epub ahead of print. [PMID 22271895]. 

Intellectual Property: HHS Reference 

No. E–197–2011/0—U.S. Provisional 

Application No. 61/542,468 filed 02 Oct 

2011. 

Licensing Contact: Whitney Hastings; 

301–451–7337; hastingw@mail.nih.gov. 

Collaborative Research Opportunity: 

The National Cancer Institute is seeking 

statements of capability or interest from 

parties interested in collaborative 

research to further develop, evaluate or 

commercialize miR126 and 

Mobilization of Hematopoietic Stem/ 

Progenitor Cells. For collaboration 

opportunities, please contact John 

Hewes, Ph.D. at hewesj@mail.nih.gov. 

Use of Frizzled (Fzd) as a Biomarker for 

Cancer Patient Selection and 

Therapeutic Intervention 

Description of Technology: 

Personalized medicine is becoming 

more important in the diagnosis and 

treatment of diseases, particularly 

cancer. One signaling pathway which 


tkelley on DSK3SPTVN1PROD with NOTICES
Federal Register / Vol. 77, No. 40 / Wednesday, February 29, 2012 / Notices 12317 

has been demonstrated to be involved in 

cancer is the Wnt/beta catenin signaling 

pathway. The NIH scientists associated 

with this technology have identified a 

potential new biomarker for cancer 

based on their investigation of the role 

of the secreted frizzled related proteins, 

sFRP’s, which are known to play a role 

in Wnt/beta catenin signaling. In 

particular, the scientists have 

determined that different Frizzled 

receptors (Fzd) have different and 

opposite roles in Wnt/beta catenin 

signaling with the expression of certain 

Fzd receptors, e.g. Fzd5, being 

associated with an increase in Wnt/beta 

catenin signaling and the expression of 

other Fzd receptors, e.g., Fzd2, being 

associated with a decrease in Wnt/beta 

catenin signaling. 

Potential Commercial Applications 

• As a diagnostic to identify patients 

for whom frizzled antagonists may be 

useful therapeutic agents. 

• As an aid for determining the 

appropriate level of frizzled antagonist 

to be given to a patient. 

• As an aid in drug discovery for the 

evaluation of Wnt/frizzled antagonists. 

Competitive Advantages 

• Ability to stratify clinical trials by 

identifying patients whose tumor has 

the appropriate molecular signature. 

• Ability to provide an appropriate 

dosing regimen based on the specificity 

of the drug for a particular Fzd. 

• Tool for further characterizing 

cancer drugs which target the Wnt/beta 

catenin pathway providing for more 

well characterized and specific drugs. 

Development Stage 

• Early-stage. 

• In vitro data available. 

Inventors: Jeffrey S. Rubin, Charles P. 

Xavier, and Maria Melikova (all of NCI). 

Intellectual Property 

• HHS Reference No. E–196–2011/ 

0—U.S. Provisional Application No. 61/ 

497,513 filed 15 Jun 2011. 

• HHS Reference No. E–196–2011/ 

1—U.S. Provisional Application No. 61/ 

499,684 filed 21 Jun 2011. 

Related Technologies: NIH also has 

other intellectual property (IP) related to 

sFRP which may be useful in 

conjunction with the use of the 

biomarker described above. The IP 

includes patents belonging to: 

• HHS Reference No. E–160–1997/ 

2—U.S. Patents 6,479,255 and 

7,183,377. 

• HHS Reference No. E–014–2000/ 

0—U.S. Patents 6,600,018, 7,223,853, 

and 7,947,651. 

• HHS Reference No. E–060–2000/ 

1—U.S. Patent 7,488,710; Foreign patent 

protection is also available (PCT/US02/ 

00869, published as WO 02/055547). 

Licensing Contact: Susan S. Rucker; 

301–435–4478; ruckersu@mail.nih.gov. 

Collaborative Research Opportunity: 

The National Cancer Institute is seeking 

statements of capability or interest from 

parties interested in collaborative 

research to further develop, evaluate or 

commercialize Regulation of Wnt and 

Frizzled signaling by secreted Frizzledrelated proteins. For collaboration 

opportunities, please contact John 

Hewes, Ph.D. at hewesj@mail.nih.gov. 

A Highly Potent Human sRAGE Protein 

for Treating Vascular Disease, Injury, 

or Inflammation 

Description of Technology: The 

receptor for advanced glycation end 

products (RAGE) is a cell surface 

protein that triggers signaling pathways 

leading to inflammation. RAGEstimulated inflammation can contribute 

to adverse vascular conditions, such as 

atherosclerosis and restenosis. The 

soluble version of RAGE (sRAGE) binds 

the same target molecules (advanced 

glycation end products), but cannot 

activate inflammatory signaling 

pathways. For this reason, sRAGE is 

thought to act as a decoy for RAGE. 

sRAGE reduces inflammation and 

pathogenic consequences associated 

with RAGE signaling. The 

administration of sRAGE has been used 

to treat atherosclerosis and arterial 

restenosis in animal models. The 

inventors established a way to produce 

human sRAGE with more than 1000- 

fold greater potency than current 

methods. Production of full length 

human sRAGE in cultured mammalian 

cells enables addition of mammalian 

post-translational modifications that 

dramatically enhance potency. This 

invention covers methods of 

production, the resulting modified 

sRAGE molecules, and methods of using 

this highly potent sRAGE for treating 

adverse vascular conditions. 

Potential Commercial Applications 

• Atherosclerosis therapeutics. 

• Prevention of vascular 

inflammation. 

• Treating vascular injuries due to 

angioplasty or traumatic injury. 

• Treating vascular complications of 

diabetes mellitus. 

• Alzheimer’s disease treatment 

based on amyloid-beta protein binding. 

Competitive Advantages 

• Greater than 1000-fold increased 

potency over sRAGE produced in insect 

cells. 

• Readily scalable production as a 

recombinant protein secreted from CHO 

cells. 

• Simple affinity purification method. 

Development Stage 

• Early-stage. 

• Pre-clinical. 

• In vitro data available. 

• In vivo data available (animal). 

Inventors: Li Lin, Sungha Park, Wen 

Wei, Rui-ping Xiao, and Mark Talan 

(NIA). 

Publication: Lin L, et al. RAGE 

signaling in inflammation and arterial 

aging. Front Biosci. 2009 Jan 1;14:1403– 

1413. [PMID 19273137]. 

Intellectual Property: HHS Reference 

No. E–165–2011/0—U.S. Provisional 

Application No. 61/582,574 filed 03 Jan 

2012. 

Related Technology: HHS Reference 

No. E–016–2009/0—U.S. Patent 

Application No. 12/652,395 filed 05 Jan 

2010. 

Licensing Contact: Betty B. Tong, 

Ph.D.; 301–594–6565; 

tongb@mail.nih.gov. 

Collaborative Research Opportunity: 

The National Institute on Aging, 

Laboratory of Cardiovascular Science, is 

seeking statements of capability or 

interest from parties interested in 

collaborative research to further 

develop, evaluate, or commercialize 

sRAGE. For collaboration opportunities, 

please contact Vio Conley, M.S. at 

conleyv@mail.nih.gov. 

Dated: February 23, 2012. 

Richard U. Rodriguez, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. 2012–4736 Filed 2–28–12; 8:45 am] 

BILLING CODE 4140–01–P 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Center for Scientific Review; Notice of 

Closed Meeting 

Pursuant to section 10(d) of the 

Federal Advisory Committee Act, as 

amended (5 U.S.C. App.), notice is 

hereby given of the following meeting. 

The meeting will be closed to the 

public in accordance with the 

provisions set forth in sections 

552b(c)(4) and 552b(c)(6), Title 5 U.S.C., 

as amended. The grant applications and 

the discussions could disclose 

confidential trade secrets or commercial 

property such as patentable material, 

and personal information concerning 

individuals associated with the grant 


tkelley on DSK3SPTVN1PROD with NOTICES