Ortho Biotech Oncology Research & Development Unites Johnson & Johnson Biopharmaceutical Oncology R&D Assets

San Diego, California (ots/PRNewswire) -

- Newly Established Organization Presents Data on Advancing
Compounds at AACR -

Ortho Biotech Oncology Research & Development (ORD), a unit of
Johnson & Johnson Pharmaceutical Research & Development, L.L.C., will
announce results from studies of three innovative compounds--Hdm2,
c-Met, and HDAC inhibitors --here at the American Association for
Cancer Research (AACR) 2008 Annual Meeting.

"ORD is a new research and development organization that unites
the biotechnology and pharmaceutical oncology efforts of several
Johnson & Johnson companies with the goal of transforming cancer into
a chronic or curable disease," said William Hait, M.D., Senior Vice
President and Worldwide Head of Ortho Biotech Oncology Research &
Development. "The new organization harnesses broad,
multi-disciplinary capabilities and expertise in order to prioritize
existing and emerging opportunities, align cancer treatment with
modern cancer biology and improve patients' lives."

ORD's scientific approach to cancer examines the cancer cell and
the surrounding tissue, or microenvironment. Previously, researchers
often studied cancer as collections of malignant cells growing in
isolation, but now understand cancer cells depend on interactions
with the surrounding tissue to survive, grow and metastasize. ORD
seeks to identify compounds which can inhibit or block the
interaction cancer cells have with the surrounding tissues, which
compromises the cancer's ability to survive.

The organization will combine the microenvironment disruptive
agents (MDAs) resulting from this approach with classic treatments
that directly target cancer cells. MDAs represent one of the most
promising areas of drug discovery, and ORD has a pipeline of several
investigational MDAs, including some of which are first-in-class and
first-in-clinic.

Pre-clinical data presented at this year's AACR meeting
demonstrate evidence of broad-spectrum, anti-tumor activity for three
new compounds. These compounds selectively target specific pathways
and influence the interaction between cancer cells and the
microenvironment to induce cancer cell death. The presentations
include:

- JNJ-26854165, a first-in-class, first-in-clinic Hdm2 inhibitor
which induces apoptosis (programmed cell death) in a number of cancer
cell lines, and restores function of the p53 tumor suppressor protein
through a novel mechanism of action; the compound is in phase I
studies for non-small cell lung cancer and prostate cancer. (Oral
abstract #1592)

- JNJ-26481585, a novel, second-generation pan-Histone
Deacetylase (HDAC) inhibitor with anti-tumor activity against solid
and hematological malignancies, which interferes with expression of
genes that control cancer cell proliferation, angiogenesis and
metastasis; phase I trials are ongoing. (Oral abstract #2444)

- JNJ-38877605, a small molecule that selectively and potently
inhibits the c-Met receptor tyrosine kinase (c-Met RTK) pathway that
regulates inhibition of signaling from the microenvironment to block
cancer cell development and metastasis; based on promising
pre-clinical properties and clean toxicity profile of JNJ-38877605,
ORD has advanced this potent and uniquely selective c-Met inhibitor
into clinical evaluation in multiple metastasized malignancies.
(Poster abstract #4837)

"These new agents are just a few of the novel compounds from our
pipeline that we hope may lead to the control of cancer," Dr. Hait
said. "The scientific community is attempting to identify all the
genetic abnormalities within cancer cells; this has yielded a finite
number of treatment opportunities. The scientific approach of ORD has
the potential to generate new opportunities to improve cancer care."

About Our Compound Targets

Human Double Minute 2 (Hdm2)

The Hdm2 oncogene is activated in cancers through various
mechanisms, including gene amplification and deletion of upstream
tumor suppressors. Hdm2 over-expression induces tumor formation, and
Hdm2 levels correlate with sporadic tumor incidence in humans(i).
Hdm2 promotes tumor cell proliferation by associating with cell cycle
regulatory proteins, modulating their activity and stability. Key
examples include p53, p73, E2F1 and HIF1a(ii),(iii). This positions
the Hdm2 protein as an attractive target for the development of
anti-cancer agents.

Histone Deacetylase (HDAC)

DNA in chromatin is wound around proteins called histones. HDACs
are a family of enzymes that influence gene expression through
selective regulation of chromatin structure. Inappropriate gene
expressions, due to changes in chromatin structure, are a hallmark of
cancer. HDAC inhibitors aim to normalize chromatin structure, thereby
restoring the activity of genes which inhibit proliferation,
angiogenesis and metastasis(iv).

c-Met Receptor Tyrosine Kinase (c-Met RTK)

Receptor tyrosine kinases (RTKs) are cell surface receptors that
regulate many key processes including invasive growth and cell
survival. The c-Met RTK pathway has been shown to be specifically
important in regulation of cell migration and invasion, cell
proliferation, survival and angiogenesis. Deregulation of c-Met RTKs
has been implicated in the development and progression of numerous
human cancers. The c-Met RTK inhibitors prevent receptor activation
and thus inhibit tumor cell development and
metastasis(v),(vi),(vii),(viii).

About ORD

Ortho Biotech Oncology Research & Development (ORD) is a new
research and development organization dedicated to oncology,
hematology and supportive care. ORD partners closely with Ortho
Biotech Products, L.P. and Janssen-Cilag companies worldwide to bring
oncology treatments and supportive medicines to patients around the
world. ORD is headquartered in Raritan, N.J., and has facilities
throughout Europe and the United States.

(This press release contains "forward-looking statements" as
defined in the Private Securities Litigation Reform Act of 1995.
These statements are based on current expectations of future events.
If underlying assumptions prove inaccurate or unknown risks or
uncertainties materialize, actual results could vary materially from
the Company's expectations and projections. Risks and uncertainties
include general industry conditions and competition; economic
conditions, such as interest rate and currency exchange rate
fluctuations; technological advances and patents attained by
competitors; challenges inherent in new product development,
including obtaining regulatory approvals; domestic and foreign health
care reforms and governmental laws and regulations; and trends toward
health care cost containment. A further list and description of these
risks, uncertainties and other factors can be found in Exhibit 99 of
Johnson & Johnson's Annual Report on Form 10-K for the fiscal year
ended December 30, 2007. Copies of this Form 10-K, as well as
subsequent filings, are available online at http://www.sec.gov,
http://www.jnj.com or on request from Johnson & Johnson. Johnson &
Johnson does not undertake to update any forward-looking statements
as a result of new information or future events or developments.)

(i) Bond GL, Hu WW, Bond EE, Robins H, Lutzker SG, Arva NC,
Bargonetti J, Bartel F, Taubert H, Wuerl P, Onel K, Yip L, Hwang SJ,
Strong LC, Lozano G, Levine AJ. A Single Nucleotide Polymorphism in
the MDM2 Promoter Attenuates the p53 Tumour Suppressor Pathway and
Accelerates Tumour Formation in Humans. Cell; 2004; 119: 591-602.

(ii) Levine, A J; Hu, W; Feng, Z. The P53 pathway: what questions
remain to be explored? Cell Death and Differentiation; 2006, 13(6),
1027-1036.

(iii) Toledo F, Wahl GM. MDM2 and MDM4: p53 regulators as targets
in anticancer therapy. International Journal of Biochemistry & Cell
Biology; 2007, 39(7-8):1476-82.

(iv) Johnstone, RW. Histone deacetylase inhibitors: novel drugs
for the treatment of cancer. Nature Reviews Drug Discovery; 2002, 1,
287 - 299.

(v) Lesko, E and Majka, M. The biological role of HGF-MET axis in
tumor growth and developmentof metastasis. Fron Biooscie; 2008, 13:
1271-80.

(vi) Sattler, M and Salgia R. c-Met and hepatocyte growth factor;
potential as novel targets in cancer theray. Curr Oncol Rep; 2007, 9
(2) 102-8.

(vii) Boccaccio C, and Comoglio, PM. Invasive growth; a MET
driven genetic programme for cancer and stem cells. Nat Rev Cancer;
2007, 6(8) 637-45.

(viii) Peruzzi, B and Bottaro, DP. Targeting the c-Met signaling
pathway in cancer. Clin Cancer Res; 2006, 12(12) 3657-60.

ots Originaltext: Ortho Biotech
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