26414 Federal Register / Vol. 72, No. 89 / Wednesday, May 9, 2007 / Notices 

ligand Receptor Assembly and 

Function’’ [E–095–2000/0–AU–04]; 

Australian Patent Application No. 

2006203490, filed on August 11, 2006, 

entitled ‘‘Identification of Novel Domain 

in the Tumor Necrosis Factor Receptor 

Family that Mediates Pre-ligand 

Receptor Assembly and Function’’ [E–

095–2000/0–AU–07]; and Canadian 

Patent Application No. 2399388, filed 

February 9, 2001, entitled 

‘‘Identification of Novel Domain in the 

Tumor Necrosis Factor Receptor Family 

that Mediates Pre-ligand Receptor 

Assembly and Function’’ [E–095–2000/ 

0–CA–05] to Welson Pharmaceuticals, 

Inc. 

The prospective exclusive license 

territory may be worldwide and the 

field of use may be limited to 

therapeutic applications for rheumatoid 

arthritis (RA) using Welson’s 

proprietary platform. 

DATES: Only written comments and/or 

license applications which are received 

by the National Institutes of Health on 

or before July 9, 2007 will be 

considered. 

ADDRESSES: Requests for copies of the 

patent and/or patent applications, 

inquiries, comments and other materials 

relating to the contemplated exclusive 

license should be directed to: Mojdeh 

Bahar, J.D., M.A., Technology Licensing 

Specialist, Office of Technology 

Transfer, National Institutes of Health, 

6011 Executive Boulevard, Suite 325, 

Rockville, MD 20852–3804. Telephone: 

(301) 435–2950; Facsimile: (301) 402–

0220; E-mail: baharm@od.nih.gov. 

SUPPLEMENTARY INFORMATION: The 

invention relates to methods and 

compositions that are useful for novel 

treatment of arthritis and other 

autoimmune diseases. This technology 

discloses the identification of a 

functional domain, Pre-ligand Assembly 

Domain (PLAD), an essential part in 

signaling involving receptors of the 

Tumor Necrosis Factor superfamily and 

its use in ameliorating rheumatoid 

arthritis (RA). PLAD is essential for 

signaling involving TFNR including 

TNFR–1 (p60), TNFR–2 (p80), Fas, 

TRAIL–R, LTR, CD40, CD30, CD27, 

HVEM, OX40 and DR4 and can be 

isolated as functional polypeptides 

which can be useful in inhibiting the 

first step in TNFR mediated signaling, 

ligand-independent assembly of 

members of the TNFR superfamily. The 

ability to inhibit TNFR signaling 

suggests that these PLAD polypeptides 

may be useful in development of new 

therapeutic molecules or as therapeutic 

molecules themselves used for 

modulation of immune responses, 

apoptosis, and inflammation. The 

inventors have discovered compounds 

that interfere with PLAD and can block 

the effects of TNF-alpha. 

The prospective exclusive license will 

be royalty-bearing and will comply with 

the terms and conditions of 35 U.S.C. 

209 and 37 CFR part 404.7. The 

prospective exclusive license may be 

granted unless within sixty (60) days 

from the date of this published notice, 

the NIH receives written evidence and 

argument that establish that the grant of 

the license would not be consistent with 

the requirements of 35 U.S.C. 209 and 

37 CFR part 404.7. 

Applications for a license in the field 

of use filed in response to this notice 

will be treated as objections to the grant 

of the contemplated exclusive license. 

Comments and objections submitted to 

this notice will not be made available 

for public inspection and, to the extent 

permitted by law, will not be released 

under the Freedom of Information Act, 

5 U.S.C. 552. 

Dated: April 30, 2007. 

Steven M. Ferguson, 

Director, Division of Technology Development 

and Transfer,Office of Technology 

Transfer,National Institutes of Health. 

[FR Doc. E7–8889 Filed 5–8–07; 8:45 am] 

BILLING CODE 4140–01–P 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Prospective Grant of Exclusive 

License: Treatment of Inflammatory 

Bowel Disease (IBD) Using IL–13 

Modulators and Inhibitors 

AGENCY: National Institutes of Health, 

Public Health Service, HHS. 

ACTION: Notice. 

SUMMARY: This is notice, in accordance 

with 35 U.S.C. 209(c) (1) and 37 CFR 

404.7(a)(1)(i), that the National 

Institutes of Health (NIH), Department 

of Health and Human Services (HHS), is 

contemplating the grant of an exclusive 

license to practice the invention 

embodied in: 

PCT patent application PCT/US2002/ 

018790 filed 14 June 2002, entitled: 

‘‘Methods of Treating and Preventing Colitis 

involving IL–13 and NK–T Cells’’ [HHS 

Reference Number: E–131–2002/0-PCT–01], 

to 

Wyeth Pharmaceuticals, based in 

Madison, New Jersey. The field of use 

may be limited to the use of IL–13 

modulators or NK–T cell modulators 

(such as antibodies) for the treatment or 

prevention of Inflammatory Bowel 

Disease, including ulcerative colitis and 

Crohn’s disease. The United States of 

America is an assignee of the patent 

rights in these inventions. 

DATES: Only written comments and/or 

application for a license, which are 

received by the NIH Office of 

Technology Transfer on or before July 9, 

2007 will be considered. 

ADDRESSES: Requests for a copy of the 

patent application, inquiries, comments 

and other materials relating to the 

contemplated license should be directed 

to: Susan Carson, D.Phil., Office of 

Technology Transfer, National Institutes 

of Health, 6011 Executive Boulevard, 

Suite 325, Rockville, MD 20852–3804; 

E-mail: carsonsu@od.nih.gov; 

Telephone: (301) 435–5020; Facsimile: 

(301) 402–0220. 

SUPPLEMENTARY INFORMATION: Ulcerative 

colitis (UC) is a chronic inflammatory 

disease of the colorectum and affects 

approximately 400,000 people in the 

United States. The cause of UC is not 

known, although an abnormal 

immunological response by the mucosal 

T cells responsive to bacterial antigens 

in the gut microflora, is thought to be 

involved. Present treatments for UC 

include anti-inflammatory therapy using 

aminosalicylates or corticosteroids, as 

well as immunomodulators and diet. 

However, 25–40% of ulcerative colitis 

patients must eventually have their 

colons removed due to massive 

bleeding, severe illness, rupture of the 

colon, risk of cancer or due to side 

effects of corticosteroids and novel 

treatments are still actively being 

sought. NIH scientists and their 

collaborators have used a mouse model 

of experimental colitis (oxazolone 

colitis, OC) to show that IL–13, a Th2 

cytokine, is a significant pathologic 

factor in OC and that neutralizing IL–13 

in these animals effectively prevents 

colitis (Immunity (2002) 17, 629–638). 

OC is a colitis induced by intrarectal 

administration of a relatively low dose 

of the haptenating agent oxazolone 

subsequent to skin sensitization with 

oxazolone. A highly reproducible and 

chronic colonic inflammation is 

obtained that is histologically similar to 

human ulcerative colitis. Studies show 

that NKT cells rather than conventional 

CD4+T cells mediate oxazolone colitis 

and that NKT cells are the source of IL–

13, and are activated by CD1 expressing 

intestinal epithelial cells. Tissue 

removed from UC patients was also 

shown to contain increased numbers of 

nonclassical NKT cells that produce 

markedly increased amounts of IL–13 

and that in keeping with epithelial 

damage being a key factor in UC, these 

NKT cells are cytotoxic for epithelial 

cells (J Clin. Investigation (2004) 113, 


sroberts on PROD1PC70 with NOTICES
Federal Register / Vol. 72, No. 89 / Wednesday, May 9, 2007 / Notices 26415 

1490–1497). Methods of use claims are 

directed to treatments preventing the 

inflammatory response of colitis by 

modulating IL–13 and NKT cell activity 

and to methods for screening for 

therapeutic compounds effective for 

colitis. 

The prospective exclusive license will 

be royalty bearing and will comply with 

the terms and conditions of 35 U.S.C. 

209 and 37 CFR 404.7. The prospective 

exclusive license may be granted unless, 

within 60 days from the date of this 

published Notice, NIH receives written 

evidence and argument that establishes 

that the grant of the license would not 

be consistent with the requirements of 

35 U.S.C. 209 and 37 CFR 404.7. 

Properly filed competing applications 

for a license filed in response to this 

notice will be treated as objections to 

the contemplated license. Comments 

and objections submitted in response to 

this notice will not be made available 

for public inspection, and, to the extent 

permitted by law, will not be released 

under the Freedom of Information Act, 

5 U.S.C. 552. 

Dated: April 30, 2007. 

Steven M. Ferguson, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. E7–8892 Filed 5–8–07; 8:45 am] 

BILLING CODE 4140–01–P 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Office of Biotechnology Activities; 

Recombinant DNA Research: 

Proposed Actions Under the NIH 

Guidelines for Research Involving 

Recombinant DNA Molecules (NIH 

Guidelines) 

ACTION: Notice of consideration of 

proposed actions under the NIH 

Guidelines. 

SUMMARY: Proposals to conduct research 

involving the deliberate transfer of a 

tetracycline resistance trait to 

Chlamydia Trachomatis have been 

submitted to the NIH Office of 

Biotechnology Activities (OBA). The 

acquisition of this antibiotic resistance 

trait could possibly compromise the use 

of a class of antibiotics for the treatment 

of Chlamydia infections in humans. 

Under the NIH Guidelines, these 

experiments can proceed only after they 

are reviewed by the NIH Recombinant 

DNA Advisory Committee (RAC) and 

specifically approval by the NIH 

Director as Major Actions. These 

proposals will be discussed at the June 

19–21, 2007 meeting of NIH 

Recombinant DNA Advisory Committee. 

DATES: The public is encouraged to 

submit written comments on these 

proposed actions. Comments may be 

submitted to the OBA in paper or 

electronic form at the OBA mailing, fax, 

and e-mail addresses shown below 

under the heading FOR FURTHER

INFORMATION. The NIH will consider all 

comments submitted by June 15, 2007. 

Written comments submitted by May 

24, 2007 will be reproduced and 

distributed to the RAC for consideration 

at its June 19–21 meeting. In addition, 

an opportunity for public comment will 

be provided at that meeting. All written 

comments received in response to this 

notice will be available for public 

inspection at the NIH OBA office, 6705 

Rockledge Drive, Suite 750, Bethesda, 

MD 20892 (telephone, 301–496–9838), 

weekdays between the hours of 8:30 

a.m. and 5 p.m. 

FOR FURTHER INFORMATION CONTACT: 

Contact OBA by e-mail at 

oba@od.nih.gov, or telephone at 301–

496–9838, if you have questions, or 

require additional information about 

these proposed actions. Comments may 

be submitted to the same e-mail address 

or by fax at 301–496–9839 or sent by 

U.S. mail to the Office of Biotechnology 

Activities, National Institutes of Health, 

6705 Rockledge Drive, Suite 750, MSC 

7985, Bethesda, Maryland 20892–7985. 

For additional information about the 

RAC meeting at which these proposed 

actions will be deliberated, please visit 

the NIH OBA Web site at: http:// 

www4.od.nih.gov/oba/. 

SUPPLEMENTARY INFORMATION: OBA has 

received information from two 

Institutional Biosafety Committees 

regarding proposed experiments, which, 

to proceed, would require Major Actions 

under Section III–A–1–a of the NIH 

Guidelines. Under this section, if the 

deliberate transfer of a drug resistance 

trait to microorganisms could 

compromise the use of the drug to 

control disease in humans, veterinary 

medicine, or agriculture the experiment 

must be reviewed by the RAC. Dr. Dan 

Rockey and Dr. Walter Stamm (at 

Oregon State University and the 

University of Washington, respectively), 

are proposing to develop a genetic 

transformation system to study the 

pathogenesis of Chlamydia trachomatis, 

a human pathogen that is a leading 

cause of sexually transmitted disease 

worldwide and, mostly in the 

developing world, a preventable cause 

of blindness. Per the investigators, the 

lack of genetic tools to study the 

mechanisms of pathogenesis in these 

obligate intracellular bacterial parasites 

hinders research. The recent discovery 

of naturally occurring tetracycline 

resistant strains of C. suis (a swine 

pathogen) may provide the necessary 

genetic elements to develop such a 

transformation system. To accomplish 

this goal, experiments are planned to 

transfer tetracycline resistance from C. 

suis into C. trachomatis (a human 

pathogen). It is asserted that success in 

these proposed studies will lead to 

opportunities for ‘‘rapid developments 

in our understanding of chlamydial 

biology.’’ The investigators are 

proposing to perform these experiments 

under Biosafety Level 2 containment. 

Background information may be 

obtained by contacting NIH OBA via email at oba@od.nih.gov. Alternatively, 

information is available on the OBA 

Web site at http://www4.od.nih.gov/oba/ 

rac/latestnewsrac.htm. 

Dated: May 3, 2007. 

Amy P. Patterson, 

Director, Office of Biotechnology Activities, 

National Institutes of Health. 

[FR Doc. E7–8900 Filed 5–8–07; 8:45 am] 

BILLING CODE 4140–01–P 

DEPARTMENT OF HOMELAND 

SECURITY 

Coast Guard 

[USCG–2007–28034] 

Chemical Transportation Advisory 

Committee; Vacancies 

AGENCY: Coast Guard, DHS. 

ACTION: Request for applications. 

SUMMARY: The Coast Guard is seeking 

applications for appointment to 

membership on the Chemical 

Transportation Advisory Committee 

(CTAC). CTAC advises, consults with, 

and makes recommendations to the 

Coast Guard on matters relating to the 

safe and secure transportation and 

handling of hazardous materials in bulk 

on U.S.-flag vessels in U.S. ports and 

waterways. 

DATES: Application forms should reach 

the Coast Guard on or before August 31, 

2007. 

ADDRESSES: You may request an 

application form by writing to 

Commandant (CG–3PSO–3), U.S. Coast 

Guard, 2100 Second Street SW., 

Washington, DC 20593–0001; by calling 

(202) 372–1425/1422; or by faxing (202) 

372–1926. Submit application forms to 

the same address. This notice and the 

application form are available on the 

Internet at http://dms.dot.gov. The 

application form is also available at 


sroberts on PROD1PC70 with NOTICES