Micromet Data Presented at the International AACR-NCI-EORTC Conference Support the Development of Adecatumumab (MT201) in Earlier Stage Cancer Disease Settings
- Further analysis of phase 2 breast cancer data show
preferential activity of adecatumumab on inhibiting the formation
of new metastases
- Results from 169 patients treated with adecatumumab demonstrate
an apparent lack of immunogenicity of the antibody
BETHESDA, MD, October 23, 2007 - Micromet, Inc. (Nasdaq: MITI), a
biopharmaceutical company focusing on the development of novel,
proprietary antibody-based products for the treatment of cancer,
inflammation and autoimmune diseases, today announced that new data
from two previously reported phase 2 studies were presented at the
joint international meeting of the American Association for Cancer
Research (AACR), National Cancer Institute (NCI) and European
Organization for Research and Treatment of Cancer (EORTC) being
held in San Francisco, CA, from October 22-26.
Abstract A71 reports on a further analysis of data from the phase 2
trial investigating adecatumumab as single agent in metastatic
breast cancer (MBC). Previously, longer time to tumor progression
(TTP) has been shown for patients receiving higher doses of
adecatumumab and expressing high levels of EpCAM (HR = 0.433 for
the comparison of high dose/high EpCAM versus low dose/low EpCAM;
p=0.0057). All data have now been re-evaluated in order to
investigate the reasons for progression. Whereas no obvious
differences were detected for the progression of pre-existing
target lesions, a significantly lower incidence of new metastases
was observed in patients with very high EpCAM expression (only 3
out of 18 patients with new lesions at week 6; 16.7%) as compared
to those with low EpCAM (14 out of 29 patients; 48.3%; p= 0.034). A
dose-dependency of this effect was observed as patients treated
with the higher dose of adecatumumab showed less new lesions
compared to patients treated with low doses (10.0% versus 25.0% in
very high EpCAM expressing patients, and 30.8% versus 62.5% in low
EpCAM expressors, respectively).
"Adecatumumab treatment appears to decrease in a dose dependent
fashion the formation and outgrowth of new metastatic lesions in
the patient population with very high EpCAM expressing tumors. This
phenomenon fits the expected mode of action of a targeted therapy
very well," stated Prof. Christian Dittrich, former President of
the Central European Society for Anticancer Drug Research (CESAR),
and a lead investigator of the MT201-202 study, who presented the
new data at the conference. "This observation is highly encouraging
and, together with the overall good tolerability of adecatumumab,
should support the investigation of adecatumumab in earlier stage
disease settings, including adjuvant treatment."
Early and potentially prolonged treatment with adecatumumab is
further supported by data on the lack of immunogenicity of this
fully human antibody. Abstract B49 reports on the analysis of a
total of 169 patients treated with adecatumumab in the two phase 2
studies in breast and prostate cancer. Only one patient has
developed a detectable antibody response to adecatumumab, which was
not neutralizing. Potential reasons discussed for this very low
immunogenicity were closeness to germline, low tendency to
aggregate and high stability of adecatumumab.
In addition to these clinical findings, results were presented by
Olivier Gires, Ph.D. from the University Clinic of Munich in
Grosshadern, Germany, who discovered that EpCAM signals into the
cell nucleus via elements of both the notch and wnt pathways
(abstract C175). These data not only establish EpCAM as a signal
transducer of cancer cells, but could explain how the protein
induces cell proliferation and oncogene expression, and support a
critical role of EpCAM in cancer stem cell regulation.
"All of these new findings correlate well together and highlight
the prospects of EpCAM-directed immunotherapies," commented Carsten
Reinhardt, M.D., Chief Medical Officer of Micromet. "While the
findings from our collaborators in Munich may finally explain the
well-known negative prognostic potential of EpCAM, the clinical
data on adecatumumab's potential inhibitory effect on new
metastases provide a clear rationale for moving forward into
early-stage cancer settings where the goal is prevention of disease
re-occurrence rather than palliative shrinkage of large tumor
bulk."
All of the above cited abstracts can be viewed on the AACR website
at www.aacr.org.
About Micromet, Inc. (www.micromet-inc.com)
Micromet, Inc. is a biopharmaceutical company focusing on the
development of novel, proprietary antibodies for the treatment of
cancer, inflammation and autoimmune diseases. Three of its
antibodies are in clinical development. MT103 (MEDI-538), the first
antibody developed using the BiTE® technology platform to be
clinically validated in Micromet's product pipeline, is being
evaluated in a phase 1 clinical trial for the treatment of patients
with non-Hodgkin's lymphoma. BiTE antibodies represent a new class
of antibodies that activate a patient's own cytotoxic T cells to
eliminate cancer cells. Micromet is developing MT103 in
collaboration with MedImmune, a subsidiary of AstraZeneca plc. The
second clinical stage antibody is adecatumumab (MT201), a human
monoclonal antibody targeting EpCAM expressing tumors. Adecatumumab
is being developed by Micromet in collaboration with Merck Serono,
a division of Merck KGaA in Darmstadt, Germany, in a phase 1b
clinical trial evaluating MT201 in combination with docetaxel for
the treatment of patients with metastatic breast cancer. The third
clinical stage antibody is MT293 (formerly D93), also known as
TRC093, a first-in-class humanized monoclonal antibody that
inhibits angiogenesis and tumor cell growth by binding cleaved
collagen. MT293 is licensed to TRACON Pharmaceuticals, Inc.
and is being developed in a phase 1 clinical trial for the
treatment of patients with cancer and age-related macular
degeneration. In addition, Micromet has established a
collaboration with Nycomed for the development and
commercialization of MT203, Micromet's human antibody neutralizing
the activity of GM-CSF, which has potential applications in the
treatment of inflammatory diseases, such as rheumatoid arthritis,
as well as autoimmune diseases.
Forward-Looking Statements
This release contains certain forward-looking statements that
involve risks and uncertainties that could cause actual results to
be materially different from historical results or from any future
results expressed or implied by such forward-looking statements.
Such forward-looking statements include statements regarding the
intended utilization of product candidates, the conduct and results
of future clinical trials, plans regarding regulatory filings,
future research, discovery of new product candidates, and clinical
trials, and partnering activities. Factors that may cause actual
results to differ materially include the risk that product
candidates that appeared promising in early research and clinical
trials do not demonstrate safety and/or efficacy in larger-scale or
later clinical trials, the risks associated with regulatory
processes, the risks associated with reliance on outside financing
to meet capital requirements, and the risks associated with
reliance on collaborative partners for future revenues under the
terms of its existing collaboration agreements, and for further
pre-clinical and clinical studies, development and
commercialization of product candidates. You are urged to consider
statements that include the words "appear," "may," "will," "would,"
"could," "should," "believes," "estimates," "projects,"
"potential," "expects," "plans," "anticipates," "intends,"
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forward-looking. These factors and others are more fully discussed
in Micromet's periodic reports and other filings with the SEC,
including the "Risk Factors" sections of such reports.
Any forward-looking statements are made pursuant to Section 27A of
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of new information, future events or otherwise.
###
Contact Information:
Company: Investors: Media:
Christopher Schnittker, SVP & CFO Susan Noonan Andrea
tenBroek
(240) 752-1421 (212) 966-3650 (781) 684-0770
christopher.schnittker@micromet-inc.com
susan@sanoonan.com micromet@schwartz-pr.com
Posted: October 2007
