Federal Register / Vol. 74, No. 60 / Tuesday, March 31, 2009 / Notices 14565 

form of trafficking in persons, a special 

needs child with a disability, a child 

who has been a victim of physical or 

sexual abuse under circumstances that 

indicate that the child’s health or 

welfare has been significantly harmed or 

threatened, or a child whose proposed 

sponsor clearly presents a risk of abuse, 

maltreatment, exploitation, or 

trafficking to the child based on all 

available objective evidence. 

9. Authority under the William 

Wilberforce Trafficking Victims 

Protection Reauthorization Act of 2008 

§ 235(c)(3)(B) to conduct follow-up 

services, during the pendency of 

removal proceedings, on children for 

whom a home study was conducted, 

and to conduct follow-up services for 

those UAC with mental health or other 

needs. 

10. Authority under the William 

Wilberforce Trafficking Victims 

Protection Reauthorization Act of 2008 

§ 235(c)(4) to cooperate with the 

Executive Office for Immigration 

Review (EOIR) to ensure that custodians 

of UAC receive legal orientation 

presentations provided through the 

Legal Orientation Program administered 

by EOIR. 

11. Authority under the William 

Wilberforce Trafficking Victims 

Protection Reauthorization Act of 2008 

§ 235(c)(5) to ensure, to the greatest 

extent practicable and consistent with 

section 292 of the Immigration and 

Nationality Act (8 U.S.C. 1362), that 

UAC who are or have been in the 

custody of the Secretary or the Secretary 

of Homeland Security, and who are not 

described in § 235(a)(2)(A), have 

counsel. To the greatest extent 

practicable, personnel in the 

Administration for Children and 

Families shall make every effort to use 

the services of pro bono counsel who 

agree to provide representation to such 

UAC without charge. 

12. Authority under the William 

Wilberforce Trafficking Victims 

Protection Reauthorization Act of 2008 

§ 235(c)(6) to appoint independent child 

advocates for child trafficking victims or 

other vulnerable UAC. 

13. Authority under the William 

Wilberforce Trafficking Victims 

Protection Reauthorization Act of 2008 

§ 235(d)(1) to specifically consent to 

juvenile court jurisdiction for an 

unaccompanied alien child who is 

applying for special immigrant status 

pursuant to 101(a)(27)(J) of the 

Immigration and Nationality Act (8 

U.S.C. 1 101(a)(27)(J)) and who is in the 

custody of the Secretary. 

14. Authority under the William 

Wilberforce Trafficking Victims 

Protection Reauthorization Act of 2008 

§ 235(d)(4)(A) to make eligible for 

placement and services under a URM 

program pursuant to § 412(d) of the 

Immigration and Nationality Act (8 

U.S.C. 1522(d)) children granted special 

immigrant status under section 

101(a)(27)(J) of the Immigration and 

Nationality Act (8 U.S.C. 1101(a)(27)(J)) 

and who were either in the custody of 

the Secretary or who were receiving 

services pursuant to section 501(a) of 

the Refugee Education Assistance Act of 

1980 (8 U.S.C. 1522 note) at the time a 

dependency order was granted. 

15. Authority under the William 

Wilberforce Trafficking Victims 

Protection Reauthorization Act of 2008 

§ 235(e) to train Federal personnel, and 

upon request, State and local personnel, 

who have substantive contact with 

UAC. 

I hereby affirmed and ratified any 

actions taken by the Assistant Secretary 

for Children and Families or any other 

Administration for Children and 

Families officials, which, in effect, 

involved the exercise of this authority 

prior to the effective date of this 

delegation. 

Limitations 

1. This delegation shall be exercised 

under the Departments’ existing 

delegation of authority and policy on 

regulations. 

2. This delegation shall be exercised 

under financial and administrative 

requirements applicable to all 

Administration for Children and 

Families authorities. 

Effective Date 

This delegation of authority is 

effective on date of signature. 

Dated: March 23, 2009. 

Charles E. Johnson, 

Acting Secretary, Department of Health and 

Human Services. 

[FR Doc. E9–6959 Filed 3–30–09; 8:45 am] 

BILLING CODE 4184–01–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. 

Cell Based Immunotherapy 

Description of Technology: The 

invention hereby offered for licensing is 

in the field of Immunotherapy and more 

specifically in therapy of autoimmune 

diseases such as Type I diabetes, 

multiple sclerosis, rheumatoid arthritis 

and systemic lupus erythematosis and 

immune mediated allergies such as 

asthma as well as in transplantationrelated disorders, such as graft 

acceptance and graft-versus-host-disease 

(GVHD). 

While the role of FOXP3+ regulatory 

T cells (Tregs) in the maintenance of 

self-tolerance and immune homeostasis 

has been established and thus their use 

in adoptive immunotherapy has been 

contemplated, there is still no good way 

to purify and expand these cells in an 

efficient and reproducible manner ex 

vivo for use in human therapy. The 

subject invention provides a method 

that allows such purification for use in 

expansion cultures to generate sufficient 

numbers of cells and purity for cellbased immunotherapy. The method is 

based on the finding that Tregs 

selectively express Latency Associated 

Peptide (LAP) and CD121b (IL–1 

Receptor Type 2) and on the ability to 

selectively separate these cells from 

other immune cells that are potentially 

hazardous, through the use of magnetic 

particles which specifically bind to 

either one of these two surface 

molecules and selectively separate those 

cells from the non-Tregs. 

Applications: 

Immunotherapy, primarily for 

autoimmune diseases such as Type I 

diabetes, hematologic disorders such as 

aplastic anemia, transplantation-related 

disorders, such as graft acceptance and 

graft-versus-host-disease (GVHD) and 

allergic diseases such as asthma. 

Facilitating detailed studies and 

analysis of human Treg function in 

health and disease. 


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Assay to differentiate thymic-derived 

versus peripheral-derived FOXP3+

Tregs. 

Potential assay to monitor disease 

status, progression and prognosis such 

as early detection or response to therapy 

of GVHD after transplantation, solid 

organ graft rejection posttransplantation or a flare-up of systemic 

lupus erythematosus. 

Advantages: The method of 

purification of FOXP3+ Tregs for human 

treatment may be superior in efficiency 

and practicality than currently existing 

techniques. After the magnetic 

separation, the final product contains 

more than 90% fully functional FOXP3+

Tregs. This novel protocol should 

facilitate the purification of Tregs for 

both cell-based therapy as well as for 

detailed studies of human Treg function 

in health and disease. It is important to 

note that most of the treatments for 

specific autoimmune diseases (i.e. 

hormone replacement therapy, enzyme 

replacement therapy, corticosteroids, 

NSAIDs, plasmaphereses, 

immunosuppressants and intravenous 

immunoglobulins) do not constitute 

cure for the specific diseases. 

Immunotherapy with Tregs has a 

potential to provide cure or prolonged 

remission for many of these diseases. 

Development Status: The purification 

protocol has been proven simple and 

efficient in a laboratory setting. 

Market: As indicated above the 

technology may be applied to allergies 

and many human diseases that are 

characterized by diminished frequency 

or dysfunction of Tregs, including 

systemic lupus erythematosus (SLE), 

type 1 diabetes, multiple sclerosis, 

aplastic anemia, idiopathic 

thrombocytopenic purpura, graft-versushost disease (GVHD) and transplant 

rejection etc. As noted above treatment 

with Tregs may have a potential to 

provide cure to many of these diseases, 

thus collectively, the commercial 

market opportunities for the technology 

are wide-ranging and the contribution to 

public health may be highly significant. 

The following information provides 

further detail concerning the potential 

market size for therapeutic use of Tregs: 

• As a group, autoimmune diseases 

afflict millions of Americans. While 

individually not very common, with the 

exception of thyroid disease, diabetes 

and systemic lupus erythematosus 

(SLE), taken as a whole, autoimmune 

diseases represent the fourth largest 

cause of disability among women in the 

United States. According to the National 

Women’s Health Centre, 75% of cases of 

autoimmune diseases occur in 

American women. 

• Similarly, Type 1 Diabetes is the 

second most common chronic disease in 

children after asthma. About 13,000 

new cases are diagnosed in the U.S. 

alone each year. Patients with Type 1 

Diabetes make up about 5% to 10% of 

all cases of diabetes. It most commonly 

appears in girls and boys when they are 

fourteen years old. 

• Multiple sclerosis is a chronic 

disease that starts early in life and as 

many as 400,000 patients are afflicted 

with this disease which lasts for 

decades. 

• More than 19,000 transplants are 

performed in the United States each 

year. That equates to 1,583 per month, 

365 per week, 52 per day, and 2 per 

hour for a rate of approximately 1 in 

14,315 or 0.01% of the U.S population. 

Inventors: Dat Q. Tran and Ethan M. 

Shevach (NIAID). 

Publications: 

1. J Andersson, DQ Tran, M Pesu, TS 

Davidson, H Ramsey, J O’Shea, EM 

Shevach. CD4+Foxp3+ regulatory T 

cells confer infectious tolerance in a 

TGFb-dependent manner. J Exp Med. 

2008 Sep 1;205(9):1975–1981. 

2. EM Shevach, DQ Tran, TS 

Davidson, J Andersson. The critical 

contribution of TGF-beta to the 

induction of Foxp3 expression and 

regulatory T cell function. Eur J 

Immunol. 2008 Apr;38(4):915–917. 

3. DQ Tran, R Ramsey, EM Shevach. 

Induction of FOXP3 expression in naı ̈ve 

human CD4+FOXP3- T cells by T cell 

receptor stimulation is TGFb-dependent 

but does not confer a regulatory 

phenotype. Blood. 2007 Oct 

15;110(8):2983–2990. 

Patent Status: U.S. Provisional 

Application No. 61/090,788 filed 21 

Aug 2008 (HHS Reference No. E–312– 

2008/0–US–01). 

Licensing Status: Available for 

licensing. 

Licensing Contacts: Uri Reichman, 

Ph.D., MBA; 301–435–4616; 

UR7a@nih.gov; John Stansberry, Ph.D.; 

301–435–5236; stansbej@mail.nih.gov. 

Collaborative Research Opportunity: 

The NIAID/NIH Laboratory of 

Immunology is seeking statements of 

capability or interest from parties 

interested in collaborative research to 

further develop, evaluate, or 

commercialize the use of CD121b or 

LAP to produce a Treg product for cellbased immunotherapy. Please contact 

Nicole Mahoney at 301–435–9017 for 

more information. 

Compositions and Methods for 

Inhibiting and Treating Herpes Simplex 

Virus (HSV) Infection and HSV–1 

Containing a UL3 Deletion 

Description of Technology: The 

invention offered hereby for licensing is 

in the fields of viral and cancer 

therapeutics and in particular related to 

Herpes Simplex Virus. It is based on the 

finding that Protein Disulfide Isomerase 

(PDI) family members bind in vitro to 

the herpes simplex protein UL3 and that 

HSV entry to the host cell is mediated 

through HSV’s interaction with the host 

cell’s surface protein(s) belonging to PDI 

family members. Inhibition of virus 

entry can therefore be accomplished by 

inhibitors of the PDI protein family 

members. The inventors demonstrated 

the following: 

• A small molecule such as 5,5’- 

Dithiobis(2-nitro-benzoic acid) (DTNB) 

can block HSV infection by blocking 

PDI-like activity. 

• Anti-PDI antibodies can block HSV 

infection. 

• Disulfide Isomerase family 

members bind in vitro to the herpes 

simplex protein UL3. 

Accordingly, the inventors further 

suggest that a UL3-like peptide or its 

analogues and derivatives can be 

effective as inhibitors of HSV infection. 

The invention further provides for 

methods and kits to screen for new 

inhibitors, based on the entry 

mechanism mentioned above. 

In another aspect of the invention, it 

is proposed that such PDI inhibitors or 

binding proteins can potentially serve as 

antitumor agents based on the finding 

that cancer cells express increased 

levels of PDI compared to healthy cells. 

With respect to cancer therapeutics, 

the invention further claims a 

recombinant mutant herpes simplex 

virus devoid of the capability to express 

UL3 or expressing a mutant HSV UL3 

protein. Such a virus can serve as an 

oncolytic virus for treatment of cancer. 

Applications: 

• Antiviral therapeutics. 

• Anticancer therapeutics. 

• Screening for new antiviral and 

anticancer agents. 

• Developing of Oncolytic Viruses for 

cancer therapy. 

Advantages: Herpes Simplex Viruses 

are responsible for a wide range of 

human diseases. Herpes simplex virus is 

the causative agent of oral and genital 

herpes, and is associated with sexual 

transmission. Infections with herpes 

simplex can be acute, or latent with 

recurring periodic outbreaks. An 

infection by herpes simplex is marked 

by watery blisters in the skin or mucous 

membranes of the mouth, lips or 


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Federal Register / Vol. 74, No. 60 / Tuesday, March 31, 2009 / Notices 14567 

genitals that can be painful and thus can 

severely affect the quality of life of an 

infected individual. The virus can lead 

to potentially fatal infections in babies 

whose mothers are infected, and to 

permanent neurological damage in 

adults with herpes encephalitis. The 

virus may also play a role in the spread 

of HIV as it can make people more 

susceptible to HIV infection. 

In spite of the severity of diseases 

caused by HSV and in spite of the many 

years of efforts to develop effective antiHSV medications and vaccines, there is 

still no effective cure for herpes in 

existence. The existing antiviral 

medications such as Acyclovir, 

Valacyclovir and Famciclovir that work 

by inhibiting the virus’ DNA synthesis 

(targeting the enzyme DNA Polymerase) 

cannot eradicate the virus from the 

body, but merely reduce the extent of 

the symptoms and the frequency of 

breakouts. Other small molecules in 

development also aiming at DNA 

synthesis are targeting another virus 

enzyme (Helicase-primase complex). 

The therapeutic strategy described in 

the subject technology provides a 

completely different mechanism, i.e. 

inhibition of the virus entry. Thus it 

may provide advantages compared to 

the existing drugs with respect to 

toxicity and efficacy. 

With respect to cancer therapy, the 

subject invention may offer a new class 

of drugs which act by an alternate 

mechanism in comparison to 

conventional cancer drugs. The 

technology may thus prove to be 

advantageous with respect to toxicity 

and efficacy. In addition, drugs 

developed by this technology may be 

given to patients in combination with 

existing drugs. 

Development Status: 

• The inhibition of HSV infection by 

DTNB and antibodies against the PDI 

surface protein have been demonstrated 

in vitro. 

• Pre-clinical or clinical data is not 

yet available. 

• Further development to identify 

PDI inhibitors applicable for viral 

therapy and cancer therapy is currently 

ongoing. 

• Further development and 

optimization of recombinant HSV to be 

utilized as an oncolytic virus is ongoing. 

Only in vitro data is available at present. 

Market: The market for anti-herpes 

drugs is huge. Results of a nationally 

representative study show that genital 

herpes is common in the United States. 

Nationwide, at least 50 million people 

ages 12 and older, or one of five 

adolescents and adults, have had a 

latent or acute genital HSV infection. 

There are up to 1 million new cases 

every year and according to some 

estimates genital herpes is now more 

common than diseases like diabetes and 

asthma. At the same time there is still 

no effective drug against this virus 

available, thus the commercial potential 

in developing a new effective drug is 

enormous. 

With respect to the market for cancer 

therapeutics the opportunities are also 

vast. This market has been growing in 

the last several years by an estimate of 

18% a year due to the introduction of 

many new and innovative drugs, and 

some reports forecast a market size of 

close to $90 billion by 2011. 

Inventors: Nancy S. Markovitz and 

Stephen Daniell (FDA). 

Publications: 

1. NS Markovitz. The herpes simplex 

virus type 1 UL3 transcript starts within 

the UL3 open reading frame and 

encodes a 224-amino-acid protein. J 

Virol. 2007 Oct;81(19):10524–10531. 

2. E Bar, T Kimura, M Kikuchi, NS 

Markovitz. Protein disulfide isomerase 

(PDI) family members interact with the 

UL3 protein of herpes simplex virus-1. 

31st International Herpesvirus 

Workshop, Abstract #8.51, Seattle WA, 

July 22–28, 2006. 

3. KD Nguyen, EE Bar, MJ Dambach, 

NS Markovitz. Yeast Two Hybrid 

Identification of the Herpes Simplex 

Virus-1 UL3 protein domains that 

interact with cellular target proteins. 

NIH Research Festival, Abstract #CB–19, 

Bethesda MD, October 2006. 

4. MJ Dambach, J Trecki, N Martin, 

NS Markovitz. Oncolytic viruses 

derived from the g34.5-deleted herpes 

simplex virus recombinant R3616 

encode a truncated UL3 protein. Mol 

Ther. 2006 May;13(5):891–898. 

Patent Status: U.S. Provisional 

Application No. 61/134,566 filed 11 Jul 

2008 (HHS Reference No. E–236–2008/ 

0–US–01). 

Licensing Status: Available for 

licensing. 

Licensing Contacts: Uri Reichman, 

PhD, MBA; 301–435–4616; 

UR7a@nih.gov; John Stansberry, Ph.D.; 

301–435–5236; stansbej@mail.nih.gov. 

Identification of Adaptive Mutations 

That Increase Infectivity of Hepatitis C 

Virus JFH1 Strain in Cell Culture 

Description of Technology: The 

technology offered for licensing is in the 

field of hepatitis C. More specifically 

the invention discloses an efficient way 

to grow the virus, a way that may 

facilitate advanced research in the field 

of hepatitis C (HCV) and its 

pathogenesis, as well as provide for 

convenient and effective ways to screen 

for new hepatitis C drugs. It also lends 

itself to the development of vaccines 

against hepatitis C. 

The invention is based on the finding 

that certain mutations in the JFH1 strain 

of HCV, as well as certain chimera of the 

mutated strain, can lead to an increase 

in production of infectious virus 

particles in cell cultures (i.e., Huh-7.5) 

between 100- to 1000-fold as compared 

to the wild type virus. Such mutations 

are introduced to a viral RNA that codes 

for hepatitis C and the latter is 

introduced to an appropriate cell to 

produce a high yield of highly infective 

virus. 

Progress in research in the field of 

HCV, as well as the development of 

drugs and vaccines to combat hepatitis 

C infections, has been hampered for 

years due to the lack of robust in vivo 

cell culture systems for the study of this 

virus. Several breakthroughs in the area 

that occurred in 2005 and thereafter 

(i.e., the isolation of HCV genotype 2a 

sequence (JFH1) and the generation of 

the unique cell line Huh-7.5) 

contributed significantly to progress in 

the field, but further optimization and 

improvements in the culture system 

have still been needed. The subject 

invention offers such improvements and 

thus may lead to enhanced progress in 

HCV research and in the development of 

the much needed drugs and vaccines 

against the virus. 

Applications: 

• Research in the field of HCV and its 

pathogenesis. 

• Screening and discovery of drugs 

that inhibit HCV infections. 

• Development of vaccines for HCV. 

Advantages: 100- to 1000-fold more 

efficient method to grow virus particles. 

Development Status: The invention is 

fully developed and requires no 

additional work. 

Market: It is estimated that 170 

million people worldwide suffer from 

HCV infection, with 3 to 4 million new 

cases each year. The primary causes of 

new HCV infections worldwide are 

unscreened blood transfusions and the 

reuse of syringes, without sterilization 

(WHO). It is estimated that nearly 4.1 

million people in the U.S. are infected 

with HCV with 3.2 million of the 4.1 

million people chronically infected. 

Approximately 70% of those 

chronically infected suffer from chronic 

liver disease (CDC). There has been a 

major decline in the number of new 

HCV infections per year in the U.S. from 

the 1980s (240,000) to 2004 (26,000) 

(CDC). In the U.S., the primary cause of 

new infections is needle-sharing by 

intravenous drug users. Despite the 

significant decrease in new HCV 

infections, the number of patients 

requiring treatment for chronic HCV is 


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14568 Federal Register / Vol. 74, No. 60 / Tuesday, March 31, 2009 / Notices 

expected to rise as patients with HCV 

infection age and progress to more 

serious liver diseases (McHutchison HG, 

et al. Chronic Hepatitis C: An Age Wave 

of Disease Burden 2005. American 

Journal of Managed Care. 11: S286– 

S295). From 2010–2019, it is estimated 

that direct medical expenditures for 

HCV will be $10.7 billion; the costs of 

decompensated HCV infection (cirrhosis 

and hepatocellular carcinoma) are 

estimated to be $21.3 billion; and 

indirect costs associated with the loss of 

life under age 65 are estimated to be 

$54.2 billion (McHutchison HG, et al. 

2005). 

Chronic hepatitis C is a serious 

disease that can result in long-term 

health problems, including liver 

damage, liver failure, liver cancer, or 

even death. It is the leading cause of 

cirrhosis and liver cancer and the most 

common reason for liver transplantation 

in the United States. Approximately 

8,000–10,000 people die every year from 

hepatitis C related liver disease. 

Of every 100 people infected with the 

hepatitis C virus, about 75–85 people 

will develop chronic hepatitis C virus 

infection; of those, 

• 60–70 people will go on to develop 

chronic liver disease. 

• 5–20 people will go on to develop 

cirrhosis over a period of 20–30 years. 

• 1–5 people will die from cirrhosis 

or liver cancer. 

In spite of the urgent public health 

need for effective drugs and vaccines 

against HCV as discussed above, and in 

spite of the huge market potential for 

such medical remedies, there are no 

effective drugs or vaccines in existence 

as of yet due to technical difficulties, 

one of them, as mentioned at the outset, 

is the difficulties in growing and 

culturing the virus. The only drugs 

available to treat HCV at the present 

time are Ribavirin and Interferon but 

none constitute a real cure for the 

disease. They also can present severe 

side effects that make the use of them 

prohibitive in many cases. The subject 

technology may therefore present an 

opportunity for drug and vaccine 

companies to accelerate their research 

and development in this area. 

Inventors: Rodney Russell, Jens Bukh, 

Robert H. Purcell, and Suzanne U. 

Emerson (NIAID). 

Publication: RS Russell, JC Meunier, S 

Takikawa, K Faulk, RE Engle, J Bukh, 

RH Purcell, SU Emerson. Advantages of 

a single-cycle production assay to study 

cell culture-adaptive mutations of 

hepatitis C virus. Proc Natl Acad Sci 

USA. 2008 Mar 18;105(11):4370–4375. 

Patent Status: 

• U.S. Provisional Application No. 

60/931,259 filed 21 May 2007 (HHS 

Reference No. E–171–2007/0–US–01). 

• U.S. Provisional Application No. 

61/066,773 filed 22 Feb 2008 (HHS 

Reference No. E–171–2007/1–US–01). 

• PCT Application No. PCT/US2008/ 

063982 filed 16 May 2008, which 

published as WO 2008/147735 on 04 

Dec 2008 (HHS Reference No. E–171– 

2007/2–PCT–01). 

Licensing Status: Available for 

licensing. 

Licensing Contacts: Uri Reichman, 

PhD, MBA; 301–435–4616; 

UR7a@nih.gov; Rung C. Tang, JD, LLM; 

301–435–5031; tangrc@mail.nih.gov. 

Dated: March 24, 2009. 

Richard U. Rodriguez, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. E9–7207 Filed 3–30–09; 8:45 am] 

BILLING CODE 4140–01–P 

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 any 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 Antibodies to 

Human Tristetraprolin (TTP) 

Description of Technology: TTP has 

been implicated in autoimmune and 

inflammatory diseases through its role 

as a regulator of the transcripts encoding 

several pro-inflammatory cytokines, 

including tumor necrosis factor alpha. 

However, it has been difficult to study 

endogenous TTP in man and other 

animals because it is expressed at very 

low levels in most cells and tissues, and 

because of the lack of mouse 

monoclonal antibodies directed at the 

human protein. 

Scientists at the NIH have developed 

three mouse monoclonal antibodies 

(TTP–16, TTP–214 and TTP–409) that 

react to different regions of the human 

TTP to allow for the identification and 

localization of the TTP protein by 

standard protocols. Although validation 

has only been conducted at the level of 

western blotting to date, they do not 

appear to cross-react with other human 

members of the TTP protein family. 

Potential Applications: Mouse 

monoclonal antibodies to human TTP 

will be useful in both clinical and basic 

research on a variety of inflammatory 

diseases and studies of mRNA 

destabilization. They can be used to 

identify or isolate TTP in cells or tissues 

by Western blotting, 

immunoprecipitation, 

immunohistochemistry, 

immunofluorescence, flow cytometry, 

and RNA super-shift assays, and can 

also be used in cross-linking and 

immunoprecipitation protocols. 

Inventors: Elizabeth A. Kennington 

and Perry J. Blackshear (NIEHS). 

Patent Status: HHS Reference No. E– 

123–2009/0—Research Tool. Patent 

protection is not being pursued for this 

technology. 

Licensing Status: Available for 

licensing. 

Licensing Contact: Fatima Sayyid, 

M.H.P.M.; 301–435–4521; 

Fatima.Sayyid@hhs.nih.gov. 

Use of Anthrax Lethal Factor To Treat 

Cancer and Screening Methods for 

MAPK Kinase Protease Activity 

Description of Technology: Anthrax 

toxin, produced by Bacillus anthracis, is 

composed of three proteins; protective 

antigen (PA), edema factor (EF), and 

lethal factor (LF). PA by itself has little 

or no toxic effect upon cells, but serves 

to bind cell surface receptors and 

mediate the entry of EF and LF into the 

cell. EF has been identified as an 

adenylate cyclase and together with PA 

forms a toxin (edema toxin; EdTx) 

which can induce edema formation 

when injected subcutaneously. LF and 

PA together form a toxin (lethal toxin; 

LeTx) which can cause rapid lysis of 

certain macrophage-derived cell lines in 

vitro as well as death when injected 

intravenously. 

Indirect evidence had suggested that 

LF was a metalloprotease. However, the 


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