UNITED STATES
SECURITIES
AND EXCHANGE COMMISSION
Washington, D.C. 20549
FORM 8-K
CURRENT
REPORT
PURSUANT
TO SECTION 13 OR 15(d)
OF
THE SECURITIES EXCHANGE ACT OF 1934
Date of Report (Date of earliest event reported):
May 6,
2010
ImmunoGen, Inc.
(Exact name of registrant as specified in its charter)
Massachusetts
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0-17999
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04-2726691
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(State or other
jurisdiction of
incorporation)
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(Commission File
Number)
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(IRS Employer
Identification No.)
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830 Winter Street, Waltham, MA 02451
(Address of principal executive offices) (Zip Code)
Registrants telephone number, including area code:
(781) 895-0600
Check the appropriate box below if the Form 8-K filing is intended
to simultaneously satisfy the filing obligation of the registrant under any of
the following provisions (
see
General
Instruction A.2. below):
o
Written communications
pursuant to Rule 425 under the Securities Act (17 CFR 230.425)
o
Soliciting material pursuant
to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)
o
Pre-commencement communications
pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR
240.14d-2(b))
o
Pre-commencement
communications pursuant to Rule 13e-4(c) under the Exchange Act (17
CFR 240.13e-4(c))
ITEM 1.01. ENTRY INTO
A MATERIAL DEFINITIVE AGREEMENT
On
May 6, 2010, ImmunoGen, Inc. (the Company) entered into an
underwriting agreement (the Underwriting Agreement) with J.P. Morgan
Securities Inc., as representative of the several underwriters (the Underwriters)
named in Schedule 1 of the Underwriting Agreement, related to a public offering
of 9,000,000 shares of the Companys common stock, par value $0.01 per share
(the Common Stock), at a price of $8.00 per share less the underwriting discount
(the Offering). Under the terms of the Underwriting Agreement, the Company
has granted the Underwriters an option, exercisable for 30 days, to purchase up
to an additional 1,350,000 shares of Common Stock to cover over-allotments, if
any, at the same price. The
Offering is expected to close on May 12, 2010, subject to the satisfaction
of customary closing conditions. The net
proceeds to the Company are expected to be approximately $67.4 million after
deducting estimated expenses associated with the Offering.
The
Offering is being made pursuant to a prospectus supplement dated May 6,
2010 and an accompanying prospectus dated April 22, 2010, pursuant to the
Companys existing effective shelf registration statement on Form S-3
(File No. 333-165981), which was filed with the Securities and Exchange
Commission (the Commission) on April 9, 2010 and declared effective by
the Commission on April 22, 2010.
The
Underwriting Agreement contains customary representations, warranties, and
agreements by the Company, and customary conditions to closing, indemnification
obligations of the Company and the Underwriter, including for liabilities under
the Securities Act of 1933, as amended, other obligations of the parties, and
termination provisions.
A
copy of the opinion of Mintz, Levin, Cohn, Ferris, Glovsky and Popeo, P.C.
relating to the legality of the issuance and sale of the shares in the Offering
is attached as Exhibit 5.1 hereto.
A copy of the Underwriting Agreement is filed herewith as Exhibit 1.1
and is incorporated herein by reference.
The foregoing description of the Offering by the Company and the
documentation related thereto does not purport to be complete and is qualified
in its entirety by reference to such Exhibits.
ITEM 8.01. OTHER EVENTS.
On
May 6, 2010, the Company issued a press release announcing that it had
priced the public offering described in Item 1.01 of this Current Report on Form 8-K.
The Companys press release is filed as Exhibit 99.1 to this Report and is
incorporated herein by reference.
In
connection with the public offering described in Item 1.01 of this Current
Report on Form 8-K, the Company included the following updated business
overview in the prospectus supplement dated May 6, 2010.
2
Company overview
We
develop novel, targeted therapeutics for the treatment of cancer using our
expertise in cancer biology, monoclonal antibodies, highly potent cytotoxic, or
cell-killing, agents, and the design of linkers that enable these agents to be
stably attached to the antibodies while in the blood stream and released in
their fully active form after delivery to a cancer cell. An anticancer compound
made using our Targeted Antibody Payload, or TAP, technology consists of a
monoclonal antibody that binds specifically to an antigen target found on
cancer cells with multiple copies of one of our proprietary cell-killing agents
attached using one of our engineered linkers. Its antibody component enables a
TAP compound to bind specifically to cancer cells that express a particular
target antigen, the highly potent cytotoxic agent serves to kill the cancer
cell, and the engineered linker controls the release and activation of the
cytotoxic agent inside the cancer cell. Our TAP technology is designed to
enable the creation of highly effective, well-tolerated anticancer products.
We
believe that our TAP technology and our expertise in the development and
humanization of monoclonal antibodies will enable us to become a leader in the
application of antibody-based anticancer compounds. We plan to achieve this
goal through the development of our own anticancer products and through
collaborations with other companies. There are now six TAP compounds in
clinical trials through our own programs and those of several of our
collaborators. Our collaborators currently include: Amgen, Bayer HealthCare,
Biogen Idec, Biotest, Genentech (a wholly owned member of the Roche Group) and
sanofi-aventis.
On
April 29, 2010, we reported our financial results for the third quarter of
fiscal year 2010, ended March 31, 2010, including a balance of cash and
marketable securities of approximately $42.2 million.
Our product candidates
T-DM1
The
most advanced compound in our pipeline is trastuzumab-DM1, or T-DM1, which is
in global development by Roche for the treatment of HER2+ metastatic breast
cancer, or MBC. T-DM1 consists of our DM1 cell-killing agent attached to
trastuzumab, which is the active component of the marketed anticancer compound,
Herceptin®. Herceptin was developed by Genentech, a wholly owned member of the
Roche Group.
In
April 2010, Roche reported that, based on discussions with the U.S. Food
and Drug Administration, or FDA, Roche plans to submit a marketing application
to the FDA for T-DM1 for the treatment of third-line or later HER2+ MBC in the
United States in 2010. Assuming
Roche
submits its application in 2010, we believe Roche could receive marketing
approval for T-DM1 in the United States in late 2010 or early 2011. Roche noted
that the basis for this application is to be the Phase II clinical trial that
was reported at the San Antonio Breast Cancer Symposium, or SABCS, in December 2009
that was designed to enroll 100 patients.
This
Phase II clinical trial enrolled 110 patients with advanced HER2+ MBC that had
undergone prior treatment with regimens that included an anthracycline, a
taxane, Herceptin, Tykerb® and Xeloda®. The T-DM1 objective response rate, or
ORR, was
3
32.7%,
as assessed by an independent review facility, or IRF. ORR is the proportion of
patients in the trial who had a durable complete or partial response to
treatment with T-DM1, and was the primary endpoint of the trial. The clinical
benefit rate, or CBR, was 44.5%, as assessed by an IRF. CBR includes patients
who had stable disease for six months or longer as well as patients who had an
objective response to T-DM1. The percentage of patients treated with T-DM1
whose best response was assessed to be progressive disease, which we categorize
as not having had clinical benefit, was 18.2%. Data from this clinical trial
also suggested that T-DM1 could provide better tolerability than standard
chemotherapy-containing treatment regimens. The toxicities of T-DM1 reported
were considered to be acceptable, manageable and consistent with those reported
in other T-DM1 trials.
Roche
has discussed other clinical trials that are planned or underway with T-DM1,
including:
·
A Phase III
clinical trial (EMILIA) that compares T-DM1 used alone to Tykerb used together
with Xeloda as second-line therapy for HER2+ MBC. This trial is designed to
enroll 580 patients, and its primary endpoint is progression-free survival. The
trial commenced in February 2009, and Roche has disclosed that this trial
could lead to a potential regulatory submission with the FDA and in the
European Union during 2012 for T-DM1 for second-line use in HER2+ MBC. We
believe that Roche will provide information related to this trial during 2010,
such as an update on the status of patient enrollment.
·
A Phase III
clinical trial (MARIANNE) to assess T-DM1 as a first-line treatment for HER2+
MBC. The trial will assess T-DM1 used alone against T-DM1 used together with
pertuzumab and against Herceptin used together with a taxane and is designed to
enroll 1,092 patients. Roche has indicated that this trial is expected to
commence in the second half of 2010 and will have as a primary endpoint
progression-free survival. Roche has disclosed that this trial could lead to a
potential regulatory submission for T-DM1 use as a first-line treatment for
HER2+ MBC, and the timing would be after 2013, the latest period of its
projections.
·
A Phase II
clinical trial assessing T-DM1 as a first-line therapy for HER2+ MBC that
compares T-DM1 used alone against trastuzumab used together with docetaxel.
This trial is designed to include 120 patients, and its primary endpoint is
progression-free survival. Roche has indicated that it expects to report
preliminary data from this trial at the European Society for Medical Oncology,
or ESMO, annual meeting in October 2010.
·
A Phase Ib/II
clinical trial assessing the tolerability of T-DM1 used together with
pertuzumab. This trial was designed to enroll 40 patients. Findings from this
trial have been accepted to be reported at the American Society of Clinical
Oncology, or ASCO, meeting in June 2010.
In
addition to the trials discussed above, several studies are underway that
assess T-DM1 used in combination with other anticancer agents. We believe that
additional clinical data with T-DM1, used alone or in combination, will be
reported at SABCS in December 2010.
4
Roche
has indicated that it believes that peak T-DM1 sales, if it is approved, could
be between 2 and 5 billion Swiss francs annually. Roche has reported that there
are approximately 6,100 HER2+ MBC patients in the United States that are
eligible for second-line treatments and approximately 8,300 such patients in
five major markets in the European Union, and that there approximately 7,600
HER2+ MBC patients in the United States that are eligible for third-line and
later treatments and approximately 5,450 such patients in five major markets in
the European Union. We believe that T-DM1 has the potential to be a valuable
new pharmaceutical for the treatment of patients with HER2+ MBC.
Lorvotuzumab mertansine
Our
most advanced wholly owned compound is lorvotuzumab mertansine, which we
previously called IMGN901. The target for this TAP compound, CD56, is found on
a number of tumor types, including small-cell lung cancer, ovarian cancer,
Merkel cell carcinoma and the liquid tumor, multiple myeloma. We believe
lorvotuzumab mertansine has the potential to be the first effective
antibody-based therapy for the treatment of these targeted cancers. Based on
scientific literature and/or our own studies, we believe that CD56 is expressed
on approximately 100% of small-cell lung cancer and Merkel cell carcinoma
cases, 58% of ovarian cancer cases, and 70% of multiple myeloma cases. Based on
American Cancer Society estimates, we believe that approximately 43,900 new
cases of small-cell lung cancer, 21,550 new cases of ovarian cancer and 20,580
new cases of multiple myeloma will be diagnosed in the United States in 2010.
Based on other published data, we believe approximately 1,900 new cases of
Merkel cell carcinoma will be diagnosed in the United States in 2010. In the
case of small-cell lung cancer newly diagnosed patients generally respond to
their first treatment regimen, but typically their disease then recurs. While
many patients with recurrent small-cell lung cancer could be eligible for
additional treatment, survival at this stage is usually less than 6 months.
Metastatic Merkel cell carcinoma is also associated with a poor outcome, with a
median survival time of 6.8 months. Therefore, there is an unmet medical need
to treat these patient populations.
We
are evaluating lorvotuzumab mertansine for the treatment of CD56+ cancers,
focusing on small-cell lung cancer, Merkel cell carcinoma and ovarian cancer in
a two-phase Phase I clinical trial that we call Study 002. This trial was
designed to determine the maximum tolerated dose of lorvotuzumab mertansine
when dosed daily for three consecutive days in a 21-day cycle and then expand
into the second phase, or expansion phase, designed to gain additional
experience with lorvotuzumab mertansine when dosed at the previously determined
maximum tolerable dose. We are encouraged by the findings to date. We plan to
use data from the Phase I clinical trial, together with input gained from
regulatory agencies, to make a decision in late 2010 as to whether to commence
a pivotal Phase II clinical trial of lorvotuzumab mertansine for the treatment
of Merkel cell carcinoma in 2011. We also expect that findings from the ongoing
clinical trial will help inform our future evaluation of the compound for
ovarian cancer, a more prevalent cancer than Merkel cell carcinoma.
5
In
November 2009, we reported interim results from Study 002 with respect to
the six patients with Merkel cell carcinoma that had received lorvotuzumab
mertansine at that time. All of these patients had received prior chemotherapy
regimens for their cancer and entered the trial with metastatic disease. Two of
these six patients had a marked, objective response to treatment with
lorvotuzumab mertansine, while a third patient had clinically relevant stable
disease for this patient population. One of these three patients had a partial
response, or PR, after the first lorvotuzumab mertansine treatment cycle and
reached a complete response, or CR, by the end of the third treatment cycle.
This patient has been in remission for more than four years. The second patient
had marked tumor reduction after the first lorvotuzumab mertansine treatment
cycle, but declined further therapy due to the occurrence of an adverse event.
This patient had a confirmed PR and based on clinical exam has shown continued
improvement in her tumors for over eight months. The third patient entered this
Phase I trial with bone metastases and had previously been treated with three
different combination regimens of chemotherapy. On treatment with lorvotuzumab
mertansine, this patient had stable disease that lasted for 79 days.
Lorvotuzumab mertansine was found to be generally well tolerated. In the
dose-escalation phase of this trial, the maximum tolerated dose was established
at 75 mg/m2/day. We are now dosing patients at 60 mg/m2/day in the expansion
phase of Study 002 to gain additional experience with the compound when
administered at that dose. We are submitting an abstract with updated findings
from Study 002 for presentation at the ESMO annual meeting in October 2010.
In
July 2009, we reported findings for the 68 small-cell lung cancer patients
that had been treated to date with lorvotuzumab mertansine in either Study 002
or in another of our Phase I trials, called Study 001. All of these patients
had received prior chemotherapy, and most had received at least two previous
regimens. The estimated clinical benefit rate was 25%, consisting of patients
with an objective response and/or sustained stable disease, defined as
non-progression for at least 77 days. An objective response was reported in a
patient whose small-cell lung cancer had recurred within four months of
treatment with cisplatin, etoposide, and topotecan plus radiation therapy. This
patient had a PR after his first lorvotuzumab mertansine treatment cycle and
reached a 91% reduction in tumor size by the end of his third cycle. His
disease progressed after his fourth cycle, which was 24 weeks after he first
received lorvotuzumab mertansine. Another patient had an objective response (an
unconfirmed PR) and no evidence of disease progression for more than 8 weeks.
This patient had previously undergone two other treatment regimens for the
cancer. Fifteen patients had sustained stable disease, with an estimated
time-to-progression, or TTP, ranging from 77 to 168 days, or 11 to 24 weeks.
Lorvotuzumab mertansine was found to be generally well tolerated.
In
December 2009, we reported at the annual meeting of the American Society
of Hematology, or ASH, interim results from our Phase I clinical trial, called
Study 003, that assesses lorvotuzumab mertansine when used alone to treat
multiple myeloma that has progressed on approved therapies. The findings
reported were for the 26 patients enrolled in this trial at that time. One
patient had a PR while receiving lorvotuzumab mertansine. This patient has
continued on treatment for more than a year. Three patients had a minimal
response, or MR, while receiving lorvotuzumab mertansine and two of these
patients remained on treatment for at least 45 weeks. The third patient
withdrew from the trial due to a broken leg while continuing to show disease
improvement. Eleven patients had stable
6
disease,
or SD, with eight of these patients remaining on treatment for at least 12
weeks at the time of data cut-off for presentation of the data. These include
four patients who have received lorvotuzumab mertansine for at least 24 weeks
and two other patients still undergoing treatment. Ten patients remained on
lorvotuzumab mertansine longer than on regimens received earlier in the course
of their disease, and eight of these patients were on lorvotuzumab mertansine
longer than on their last regimen with approved therapies. Lorvotuzumab
mertansine was found to be generally well tolerated and was not associated with
significant myelosuppression or other side effects that would limit its ability
to be administered in combination with other active agents. Lorvotuzumab
mertansine was granted orphan drug designation in the United States and similar
designation in the European Union for Merkel cell carcinoma in early 2010. If a
product that has orphan drug designation subsequently receives the first FDA
approval for the disease for which it has such designation, the product is
entitled to orphan product exclusivity, which means that the FDA may not
approve any other applications to market the same drug for the same indication,
except in very limited circumstances, for seven years.
In
addition to the trial information discussed above, we are actively engaged in
several other planned and ongoing clinical trials with lorvotuzumab mertansine,
including:
·
A Phase I/II
clinical trial, called Study 007, to assess the safety and provide information
on the efficacy of lorvotuzumab mertansine when used in combination with
etoposide/carboplatin as a first-line treatment of small-cell lung cancer. We
plan to commence this trial by late 2010. Assuming satisfactory safety data are
obtained in the first phase of this trial, we plan to randomize patients during
the second phase of this trial to compare lorvotuzumab mertansine used with
etoposide/carboplatin against etoposide/carboplatin used alone, which is the
current standard of care for first-line treatment of small-cell lung cancer.
·
Two Phase I
clinical trials evaluating lorvotuzumab mertansine for the treatment of
multiple myeloma are underway. Study 003, as has been discussed, evaluates
lorvotuzumab mertansine when used as a single agent and is currently in the
expansion phase. Study 005 is designed to assess the tolerability of
lorvotuzumab and gain information on its efficacy when used in combination with
the standard treatment for this cancer, lenalidomide plus dexamethasone. We
expect to report interim data from one or both of these trials at the ASH
annual meeting in December 2010.
·
We plan to make
a decision in late 2010 on whether to commence a pivotal Phase II clinical
trial of lorvotuzumab mertansine for the treatment of Merkel cell carcinoma.
This decision will be informed by a number of considerations, including
additional findings in Study 002 and the input obtained from regulatory
agencies on trial design.
SAR3419
We
created SAR3419 for the treatment of non-Hodgkins lymphoma and licensed it to
sanofi-aventis as part of a broader collaboration. SAR3419 consists of our DM4
cell-killing agent attached using one of our engineered linkers to a
CD19-binding antibody that was created and humanized by us.
7
Sanofi-aventis
is evaluating SAR3419 for the treatment of non-Hodgkins lymphoma in two Phase
I clinical trials that have different dosing schedules. The first study
evaluated the compound when dosed once every three weeks and initial findings
from it have been reported. We expect data from the second Phase I trial, which
evaluates the compound when dosed weekly, to be reported at the ASH annual
meeting in December 2010. We expect SAR3419 to advance into Phase II
clinical testing in the second half of 2010.
The
findings from the first Phase I clinical trial were reported at the ASH annual
meeting in December 2009 The trial found that 17 of 27 of patients, or
63%, who were response-evaluable at the time of data cut-off for presentation
experienced a reduction in tumor size (7% to 86% reduction). These included 7
of 14 patients, or 50%, who had disease that was refractory to treatment with
rituximab. Five patients had an objective response, all of whom received
SAR3419 at its maximum tolerated dose or the next highest or lowest dose. Among
these responders was a patient with rituximab-refractory disease. All but one
of these five patients reached the best response either during the last
treatment cycle allowed under the trial protocol, which was cycle 6, or after
their last dose of SAR3419. This is consistent with the observation that the
best response to treatment typically occurred after a patient had received
several doses of SAR3419. A primary endpoint of the trial was to establish the
maximum tolerable dose of SAR3419 when administered once every three weeks.
This was determined to be 160 mg/m2. Additional patients will receive SAR3419
at this dose to gain more information on the tolerability and activity of the
compound when administered at its maximum tolerable dose.
Other product candidates under development
In
addition to T-DM1, lorvotuzumab mertansine and SAR3419, several other TAP
compounds are in development through our own programs and those of our
partners, including:
Proprietary
ImmunoGen product candidates
·
IMGN388 is a
TAP compound consisting of our DM4 cell-killing agent attached to an
integrin-targeting antibody that was developed by Centocor. IMGN388s target
occurs on many types of solid tumors and also on vascular endothelial cells in
the process of forming new blood vessels, or angiogenesis. Angiogenesis is
needed for a tumor to grow. IMGN388 is in Phase I testing and clinical data
from this trial have been accepted for poster presentation at ASCO in June 2010.
·
We have three
TAP compounds currently in or positioned to begin preclinical toxicology
studies. One of these compounds, IMGN529, is being developed for the treatment
of certain liquid tumors and we expect to submit an investigational new drug,
or IND, application to the FDA for this product candidate in 2011. One of the
other compounds is a potential treatment for certain liquid tumors and the
other is a potential treatment for certain solid tumors.
Partnered
product candidates
8
·
BT-062 was
created by Biotest under a 2006 license that grants Biotest the exclusive right
to use our maytansinoid TAP technology with antibodies that target CD138, an
antigen found on multiple myeloma and certain other cancers. BT-062 consists of
Biotests anti-CD138 antibody with our DM4 cell-killing agent attached using
one of our engineered linkers. Biotest advanced BT-062 into Phase I evaluation
in September 2008 and initial results from this trial were reported at the
ASH annual meeting in 2009. We have opt-in rights on BT-062 for the United
States.
·
BIIB015 was
created by Biogen Idec under a 2004 license that grants Biogen Idec the
exclusive right to use our maytansinoid TAP technology with antibodies that
target Cripto, an antigen found on a number of solid tumors. BIIB015 consists
of Biogen Idecs Cripto-binding antibody with our DM4 cell-killing agent
attached using one of our engineered linkers. BIIB015 advanced into Phase I
testing in the summer of 2008.
·
We expect two
compounds to advance into clinical testing in 2010 through our collaboration
with sanofi-aventis.
·
In October 2008,
we entered into a development and license agreement with Bayer HealthCare AG.
The agreement grants Bayer HealthCare exclusive rights to use our maytansinoid
TAP technology to develop and commercialize therapeutic compounds to a specific
target. We recently achieved a milestone payment for their achievement of a
preclinical event under this collaboration.
·
Amgen has taken
two licenses to use our TAP technology with antibodies to undisclosed targets,
and Genentech, now a wholly owned member of the Roche Group, has taken four
licenses in addition to the HER2 license that enabled development of T-DM1.
We
continue to conduct research to develop additional cell-killing agents and
linkers to further strengthen our position in the field, and expect over the
next several years to be involved in numerous clinical trials for existing and
new product candidates focused on various stages of development ranging from
early stage to registration trials. We believe our continued focus on
development of additional applications of our TAP technology could provide
additional opportunities for partnerships and collaborations.
Our TAP technology
We
developed our TAP technology to achieve highly effective, well tolerated
anticancer drugs. Terms used to refer to our field include armed antibodies,
empowered antibodies and antibody-drug conjugates, or ADCs. Our TAP technology
and/or antibody expertise has generated over $230 million in payments to us
from our partners since 2000. Our existing collaboration and license agreements
with partners have the potential to generate approximately $565 million in
additional payments to us in connection with potential development, clinical
and regulatory milestones.
Traditional
chemotherapy agents typically kill any rapidly dividing cell, including healthy
cells, which can result in significant adverse side effects and limit their
ability to be dosed
9
to
full efficacy. Monoclonal antibodies can be created that bind specifically to
targets found on cancer cells and, therefore, offer the potential to
selectively target cancer cells. The invention of such antibodies has led to
the creation of some successful anticancer therapeutics such as Rituxan® and Herceptin®.
For many of the antigens found on cancer cells, however, the binding of a
manufactured antibody to that antigen in and of itself has little, if any,
anticancer effect.
Our
TAP technology makes use of the targeting ability of monoclonal antibodies
without needing the antibody to have meaningful anticancer activity on its own.
A TAP compound consists of a tumor-targeting antibody with one of our highly
potent cell-killing agents attached using one of our engineered linkers. The
antibody serves to deliver our potent cell-killing agent specifically to cancer
cells, to help minimize damage to healthy tissue. The cell-killing agent serves
to kill the cancer cell. Our agents are far more potent than traditional
chemotherapies. Our engineered linkers serve to keep the cell-killing agent
attached to the antibody while the TAP compound is circulating in the
bloodstream and then control its release once the TAP compound has bound to and
entered a cancer cell.
We
develop our own monoclonal antibodies for use in our proprietary products and
also license to other companies the right to use our TAP technology with their
antibodies to develop products for specific targets.
Herceptin®
is a registered trademark of Genentech, a wholly owned member of the Roche Group.
Rituxan® is a registered trademark of Biogen Idec Inc. Tykerb® is a registered
trademark of GlaxoSmithKline plc. Xeloda® is a registered trademark of Roche.
Other brands, names and trademarks contained herein are the property of their
respective owners.
Special note regarding forward-looking statements
This
Current Report on Form 8-K contains forward-looking statements within the
meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E
of the Securities Exchange Act of 1934, as amended. These statements relate to
future events and our future financial performance.
These
forward-looking statements are identified by their use of terms and phrases,
such as anticipate, believe, could, estimate, expect, intend, may,
plan, predict, project, will and other similar terms and phrases,
including references to assumptions. These statements are contained in the Risk
Factors section, as well as other sections of this prospectus supplement.
Forward-looking
statements in this Current Report on Form 8-K include, but are not limited
to:
·
our and our
collaborators expectations regarding clinical trials, development timelines
and regulatory filings for T-DM1, lorvotuzumab mertansine, SAR3419, IMGN388 and
other drug candidates under development by us and our collaborators;
·
Roches plan to
submit a marketing application to the FDA for T-DM1 for the treatment of
third-line and later HER2+ MBC in the United States in 2010 on the
10
basis
of the Phase II study of T-DM1 as a third-line treatment in HER2+ MBC that was
presented at the San Antonio Breast Cancer Symposium in December 2009;
·
our belief that
Roche could receive marketing approval of T-DM1 in the United States in late
2010 or early 2011 assuming Roche submits its application in 2010;
·
Roches
expectation that it expects interim data from a Phase Ib/II clinical trial
assessing T-DM1 plus pertuzumab to be reported at ASCO in June 2010 and
that it expects preliminary data from a Phase II clinical trial comparing
T-DM1, as a single agent, against trastuzumab plus docetaxel for first-line
treatment of HER2+ MBC to be reported at the ESMO meeting in October 2010;
·
Roches
expectation to start a Phase III clinical trial to assess T-DM1 as a first-line
treatment for HER2+ MBC in the second half of 2010;
·
the expectation
that Roche could file a marketing application for T-DM1 as second-line
treatment in HER2+ MBC with the FDA and in the European Union during 2012 and as
a first-line treatment with the FDA after 2013, that Roche will provide
information related to the EMILIA trial during 2010, that additional clinical
data with T-DM1, used alone or in combination, will be reported at SABCS in December 2010,
and that peak T-DM1 sales could be between 2 and 5 billion Swiss francs
annually;
·
our belief that
T-DM1 has the potential to be a valuable new pharmaceutical for the treatment
of patients with HER2+ MBC and that lorvotuzumab mertansine has the potential
to be the first effective antibody-based therapy for certain targeted cancers;
·
our expectation
as to the number of cases of small-cell lung cancer, ovarian cancer, multiple
myeloma and Merkel cell carcinoma that will be diagnosed in the United States
in 2010;
·
our plan to use
data from the ongoing clinical trial of lorvotuzumab mertansine, together with
input gained from regulatory agencies, to make a decision in late 2010 as to
whether to commence a pivotal Phase II clinical trial of lorvotuzumab
mertansine for the treatment of Merkel cell carcinoma in 2011 and our
expectations as to the design of this trial;
·
our plan to
start a Phase I/II clinical trial by late 2010 to evaluate lorvotuzumab
mertansine in combination with etoposide/carboplatin, the standard care, for
first-line treatment of small-cell lung cancer;
·
our expectation
to report interim data from one or more of our clinical trials of lorvotuzumab
mertansine at the ESMO annual meeting in October 2010 and/or the ASH
annual meeting in December 2010;
·
sanofi-aventis
expectation to report certain Phase I data for SAR3419 at the ASH annual
meeting in December 2010 and to advance SAR3419 into Phase II clinical
testing in the second half of 2010;
11
·
our expectation
that IMGN388 Phase I data will be reported at ASCO in June 2010 and to
submit an IND application to the FDA for IMGN529 in 2011;
·
our expectation
that two compounds will advance into clinical testing in 2010 through our
collaboration with sanofi-aventis;
·
our expectation
that our TAP technology potentially may be used with antibodies with limited or
no anticancer activity of their own, enabling effective antibody-based
therapies to be developed for many more types of cancers and that over the next
several years we will be involved in numerous clinical trials for existing and
new product candidates focused on various stages of development ranging from
early stage to registration trials;
·
our expectation
of the amount and timing of future revenues, potential development, clinical
and regulatory milestones, expenses, investments and other items affecting the
results of our operations; and
·
our expected
uses of the net proceeds of this offering.
These
forward-looking statements involve known and unknown risks, uncertainties and
other factors that may cause actual results to be materially different from
those contemplated by our forward-looking statements. These known and unknown
risks, uncertainties and other factors are described in detail in our Annual
Report on Form 10-K for the fiscal year ended June 30, 2009 and our
subsequent Quarterly Reports on Form 10-Q. We disclaim any intention or
obligation to update or revise any forward-looking statements, whether as a
result of new information, future events or otherwise.
ITEM 9.01. FINANCIAL
STATEMENTS AND EXHIBITS
(d) The following exhibits are being filed
herewith:
Exhibit
No.
|
|
Exhibit
|
|
|
|
1.1
|
|
Underwriting
Agreement dated May 6, 2010 by and between ImmunoGen, Inc. and J.P.
Morgan Securities Inc., as representative of the several underwriters named
in Schedule 1 thereto
|
|
|
|
5.1
|
|
Opinion
of Mintz, Levin, Cohn, Ferris, Glovsky and Popeo, P.C.
|
|
|
|
23.1
|
|
Consent
of Mintz, Levin, Cohn, Ferris, Glovsky and Popeo, P.C. (included in the
opinion filed as Exhibit 5.1)
|
|
|
|
99.1
|
|
Press
release of ImmunoGen, Inc. dated May 6, 2010
|
12
SIGNATURES
Pursuant
to the requirements of the Securities Exchange Act of 1934, the Registrant has
duly caused this report to be signed on its behalf by the undersigned hereunto
duly authorized.
|
ImmunoGen, Inc.
|
|
(Registrant)
|
|
|
Date:
May 7, 2010
|
/s/
Daniel M. Junius
|
|
|
|
Daniel
M. Junius
|
|
President
and Chief Executive Officer
|
13
EXHIBIT INDEX
Exhibit
No.
|
|
Exhibit
|
|
|
|
1.1
|
|
Underwriting
Agreement dated May 6, 2010 by and between ImmunoGen, Inc. and J.P.
Morgan Securities Inc., as representative of the several underwriters named
in Schedule 1 thereto
|
|
|
|
5.1
|
|
Opinion
of Mintz, Levin, Cohn, Ferris, Glovsky and Popeo, P.C.
|
|
|
|
23.1
|
|
Consent
of Mintz, Levin, Cohn, Ferris, Glovsky and Popeo, P.C. (included in the
opinion filed as Exhibit 5.1)
|
|
|
|
99.1
|
|
Press
release of ImmunoGen, Inc. dated May 6, 2010
|
14
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