-- 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., Oct. 23 /PRNewswire-FirstCall/ -- 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 adecatumumabīs
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
http://www.aacr.org.
About Micromet, Inc. (http://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(R) 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," "continues," "forecast,"
"designed," "goal," or the negative of those words or other comparable
words to be uncertain and 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 the
Securities Act of 1933, as amended, and Section 21E of the Securities
Exchange Act of 1934, as amended, and, as such, speak only as of the date
made. Micromet undertakes no obligation to publicly update any
forward-looking statements, whether as a result of new information, future
events or otherwise.
SOURCE Micromet, Inc.
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Related links:
http://www.micromet-inc.com
http://www.aacr.org/
CONTACT:
Christopher Schnittker, SVP & CFO, Micromet,
Inc., +1-240-752- 1421, christopher.schnittker@micromet-inc.com;
Investors, Susan Noonan, +1- 212-966-3650, susan@sanoonan.com;
Media, Andrea tenBroek, +1-781-684-0770, micromet@schwartz-pr.com
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