21774 Federal Register / Vol. 65, No. 79 / Monday, April 24, 2000 / Notices

(HGFr) pathway. In particular, the

invention described in this application

is a murine monoclonal antibody,

designated D1, which specifically binds

to an epitope in the extracellular

domain of human HGFr/met. The

monoclonal antibody can be used, for

example, to visualize HGFr/met

expression in paraffin-embedded tumor

samples and in drug screening assays

(competitive binding assays) for

antagonists/agonists of HGFr/met.

Determination of AM Binding Proteins

and the Association of Adrenomedullin

(AM) Therewith

F Cuttitta (NCI), A Martinez (NCI), R Pio

(NCI), TH Elasser (USDA–ARS),

Serial No. 60/153,397 filed 10 Sep 99

This application relates to isolation

and identification of a polypeptide

which binds to the hormone

adrenomedullin designated

adrenomedullin binding protein 1

(AMBP1). Adrenomedullin (AM), a

peptide hormone, has been implicated

in a variety of physiological functions

including the regulation of insulin

production, anti-microbial activity,

mitogenesis and angiogenesis. The

activities of AM are believed to be

mediated by a variety of binding

proteins in a manner similar to the way

in which Insulin-like Growth Factor

(IGF) is regulated. AMBP1 has been

purified to homogeneity and its amino

acid sequence determined.

The application is directed to

methods of measuring AM levels in

plasma based on the finding that

AMBP1 binds in a specific and

reversible competitive fashion with AM

and methods of treating AM related

disease by administering AMBP1. Other

aspects of the invention are complexes

of AM with AMBP1 and antibodies

which specifically bind to an epitope by

the complex of AM with AMBP1 as well

as assays for detecting the complex of

AM with AMBP1.

This work has been published in part

in Elsasser TH, et al. Endocrinology

140(10):4908–11 (Oct. 1999).

In addition to being available for

licensing the NIH is willing to consider

interest from companies who are

interested in pursuing

commercialization opportunities

through a Cooperative Research and

Development Agreement (CRADA).

AAV5 Vector and Uses Thereof

JA Chiorini, RM Kotin (NHLBI)

Serial No. PCT/US99/11958 filed 28

May 1999 based on USSN 60/087,029

filed 28 May 1998

The invention described and claimed

in this patent application provides for

novel vectors and viral particles which

comprise adeno-associated virus

serotype 5 (AAV5). AAV5 is genetically

distinct from others AAVs with respect

to its capsid proteins, VP1, VP2, and

VP3, which contributes to different

tissue tropisms for AAV5. The ITR and

Rep proteins of AAV5 are also distinct

which results in a biochemically unique

mechanism of replication compared to

the other AAVs. This difference in

replication activity contributes to the

fact that AAV5 is only able to replicate

and package AAV5 ITR containing DNA

in contrast to AAV2 which is able to

replicate and package other AAV

serotypes. Vectors produced using

AAV5 proteins may be useful in gene

therapy.

AAV5 offers several advantages which

make it attractive for use in gene

therapy: (1) increased production (10–

50 fold greater than AAV2); (2) its

distinct replication mechanism when

compared to AAV2; (3) its Rep protein

and ITR regions which do not

complement other serotypes; (4) it

appears to utilize different cell surface

attachment molecules than those of

AAV type 2; and (5) improved efficiency

of transduction of certain cell types

including airway epithelial, striated

muscle, endothelial, and neuronal cells

when compared to AAV type 2.

This work has been published, in

part, in J. Virol. 73(5): 4293–98 (May

1999) and J. Virol. 73(2): 1309–19 (Feb.

1999).

Prevention of Fetal Alcohol Syndrome

and Neuronal Cell Death with ADNF

Polypeptides

DE Brenneman (NICHD), CY Spong

(NICHD), I Gozes (TAU), M Bassan

(TAU), R Zamostiano (TAU)

Serial No. 09/267,511 filed 12 Mar 1999

This patent application describes an

extension of prior work related to

peptides derived from proteins known

as ADNF and ADNF III/ADNP. These

peptides are known as SAL (ADNFderived) and NAP (ADNP-derived). SAL

and NAP (L-isomers) have previously

been demonstrated, in in vitro work, to

be able to prevent neuronal cell death

and to protect against the toxic activities

of a cholinotoxin suggesting that they

are useful as therapeutics for

neurodegenerative diseases. The new

work presented in this EIR demonstrates

that NAP and SAL (L-isomers), alone or

in combination, prevent damage to

neurons due to oxidative stress. In

particular, the new work shows that

NAP and SAL (L-isomers) alone or

together are effective in preventing

damage due to oxidative stress in a

model for fetal alcohol syndrome. Thus,

NAP and SAL (L-isomers), alone or

together may be useful therapeutically

to treat fetal alcohol syndrome.

In addition, a number of other patent

applications and patents related to this

technology have been filed by PHS and

are available for licensing. These

include: USP 5,767,240 (PCT/US92/

03109); 08/324,297 (PCT/US95/12929);

60/037,404 (PCT/US98/07485); 09/

187,330 (PCT/US99/26213) 60/149,956;

and 09/364,609.

Dated: April 18, 2000.

Jack Spiegel,

Director, Division of Technology Development

and Transfer, Office of Technology Transfer,

National Institutes of Health.

[FR Doc. 00–10180 Filed 4–21–00; 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, DHHS.

ACTION: Notice.

SUMMARY: The inventions listed below

are owned by agencies 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

contacting Richard U. Rodriguez,

M.B.A., at the Office of Technology

Transfer, National Institutes of Health,

6011 Executive Boulevard, Suite 325,

Rockville, Maryland 20852–3804;

telephone: 301/496–7056 ext. 287; fax:

301/402–0220; e-mail: rr154z@nih.gov.

A signed Confidential Disclosure

Agreement will be required to receive

copies of the patent applications.

Identification of a Novel Amplified

Gene, MB1, at 17q23

Anne H Kallioniemi, Maarit T Barlund,

Outi M Monni, Juha T Kononen, Olli

P Kallioniemi (NHGRI)

DHHS Reference No. E–038–00/0 filed

13 Dec 1999

DNA amplification at 17q23 is one of

the most common genetic alterations in

breast cancer. Genes affected by this

amplification may have a critical role in

Federal Register / Vol. 65, No. 79 / Monday, April 24, 2000 / Notices 21775

breast cancer development and

progression and may provide targets for

anti-cancer therapy. The inventors have

identified a novel gene from the

amplified region, named MB1, which

has no homology to any known genes.

MB1 is amplified in about 9% of

primary breast tumors and is

overexpressed in breast cancer cell lines

with amplification. MB1 may define a

critically important breast cancer gene

which could have significance for

development of improved diagnostics

against breast cancer.

The Use of Recombinant Cholera ToxinB for the Treatment of Inflammatory

Bowel Disease

Warren Strober, Monica Boirivant, Ivan

J Fuss, Brian L Kelsall (NIAID)

Serial No. 60/165,111 filed 12 Nov 1999

The present invention provides

methods of treating or preventing

inflammation in a subject, comprising

administering to the subject an effective

amount of cholera toxin subunit B (CT–

B). In particular, the present invention

provides methods of decreasing the

activity of interferon-gamma in a

subject, decreasing the activity of IL–12

in a subject, and treating or preventing

a Th1 T-cell mediated autoimmune

disorder.

Dated: April 18, 2000.

Jack Spiegel,

Director, Division of Technology Development

and Transfer, Office of Technology Transfer,

National Institutes of Health.

[FR Doc. 00–10181 Filed 4–21–00; 8:45 am]

BILLING CODE 4140–01–P

DEPARTMENT OF HEALTH AND

HUMAN SERVICES

National Institutes of Health

Government-Owned Invention

Availability for Licensing: ‘‘Therapeutic

and Diagnostic Antibodies and

Immunotoxins to a Mutant Form of

Epidermal Growth Factor Receptor,

Designated ‘‘EGFRVIII’’, Which is

Highly Expressed in Glioblastomas,

Carcinomas of the Breast and Ovary,

and Non-Small Cell Lung Carcinomas’’

AGENCY: National Institutes of Health,

Public Health Service, DHHS.

ACTION: Notice.

SUMMARY: The invention listed below is

owned by an agency of the U.S.

Government and is 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.

ADDRESSES: Licensing information and a

copy of the U.S. patent application

referenced below may be obtained by

contacting J. R. Dixon, Ph.D., at the

Office of Technology Transfer, National

Institutes of Health, 6011 Executive

Boulevard, Suite 325, Rockville,

Maryland 20852–3804 (telephone 301/

496–7056 ext 206; fax 301/402–0220; EMail: jd212g@NIH.GOV). A signed

Confidential Disclosure Agreement is

required to receive a copy of any patent

application.

SUPPLEMENTARY INFORMATION:

Invention Title: ‘‘Anti-EGFRvIII ScFvs

with Improved Cytotoxicity and Yield,

Immunotoxins Based Thereon, and

Methods of Use Thereof’’.

Inventors: Drs. Ira H. Pastan (NCI),

Richard Beers (NCI), Partha S.

Chowdury (NCI) and Darell Bigner (EM).

USPA SN: [= DHHS Ref. No. E–009–00/

0]—Filed with the U.S.P.T.O. on

January 25, 2000.

Abstract

A mutant form of the epidermal

growth factor receptor, designated

‘‘EGFRvIII,’’ is highly expressed in some

50–60% of glioblastomas and has also

been shown to be present in some 70–

80% of carcinomas of the breast and

ovary, and about 16% of non-small cell

lung carcinomas. The mutation consists

of an in-frame deletion of exons 2–7

near the amino-terminus of the

extracellular domain which results in

the expression of an EGFR mRNA with

an 801 base deletion. The mutant

protein contains a new glycine codon at

the splice junction. The receptor has

constitutive tyrosine activity that

enhances the tumorigenicity of

glioblastomas in vivo. Because of the

tumor-specific extracellular sequence,

the mutant receptor is an attractive

potential target for cancer therapy,

particular via the use of immunotoxins

(e.g., MR1(Fv)–PE38).

Technology

The technology claimed in the patent

application is directed to antibodies to

an epidermal growth factor receptor

known as EGFRvIII. In particular, the

invention provides an antibody,

designated MR1–1, which mutates MR1

in the CDR3 of the (VH) and (VL) chains

to provide an antibody with especially

good cytotoxicity. The described

polypeptides can be coupled, attached

or otherwise linked to an effector

molecule, therapeutic moiety, or

detectable label. The patent application

provides nucleic acid molecules

encoding the polypeptides with a

mutated antibody variable heavy (VH)

chain regions or a mutated light chain

(VL) region, or both. The invention also

provides methods of killing a cell

bearing an antigen comprising

contacting the cell with an

immunotoxin comprising a toxic moiety

and a targeting moiety. The Antibodies

and Immunotoxins of claimed in this

patent application could be used to

develop cancer therapeutics and

diagnostics.

The above mentioned Invention is

available, including any available

foreign intellectual property rights, for

licensing.

Dated: April 17, 2000.

Jack Spiegel,

Director, Division of Technology Development

& Transfer, Office of Technology Transfer.

[FR Doc. 00–10182 Filed 4–21–00; 8:45 am]

BILLING CODE 4140–01–P

DEPARTMENT OF HEALTH AND

HUMAN SERVICES

National Institutes of Health

National Center for Complementary &

Alternative Medicine; Notice of Meeting

Pursuant to Section 10(a) of the

Federal Advisory Committee Act, as

amended (5 U.S.C. Appendix 2), notice

is hereby given of the National Advisory

Council for Complementary and

Alternative Medicine (NACCAM).

The meeting will be open to the

public as indicated below, with

attendance limited to space available.

Individuals who plan to attend and

need special assistance, such as sign

language interpretation or other

reasonable accommodations, should

notify the Contact Person listed below

in advance of the 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/or contract proposals and the

discussions could disclose confidential

trade secrets or commercial property

such as patentable material, and

personal information concerning

individuals associated with the grant

applications and/or contract proposals,

the disclosure of which would

constitute a clearly unwarranted

invasion of personal privacy.

Name of Committee: National Advisory

Council for Complementary and Alternative

Medicine.

Date: May 8–9, 2000.

Open: May 8, 2000, 8:30 am to

adjournment.

Agenda: The agenda includes the

Director’s Report and presentation of

NCCAM’s Draft Strategic Plan, Development

of Trans-NIH Health