Exhibit 99.1

ARIAD Presents Unique Profile of Novel Multi-Targeted Kinase Inhibitor,
          AP24534, Supporting Multiple Oncology Indications

    ATLANTA & CAMBRIDGE, Mass.--(BUSINESS WIRE)--Dec. 8, 2007--ARIAD
Pharmaceuticals, Inc. (NASDAQ: ARIA) today presented, for the first
time, results of studies on its novel multi-targeted kinase inhibitor,
AP24534, showing efficacy and oral dosing flexibility in animal models
of chronic myeloid leukemia (CML), including forms of CML caused by
clinically relevant variants of the target protein, Bcr-Abl. Further,
AP24534 demonstrated potent inhibition of selected additional kinase
targets - the receptors for vascular endothelial growth factors
(VEGFR), fibroblast growth factors (FGFR) and angiopoietin (Tie2) that
control angiogenesis, and Flt3 kinase that plays a critical role in
the pathogenesis of acute myeloid leukemia (AML). These findings
support the broad potential of AP24534 not only in drug-resistant CML,
but also in other hematological cancers, such as AML, and various
solid tumors. These data were presented today at the 49th American
Society of Hematology Annual Meeting.

    "These studies underscore the differentiated profile of AP24534,
which inhibits a select group of enzymes critical for tumor growth and
survival in various cancers, without any effect on Aurora kinases,"
said Tim Clackson, Ph.D., chief scientific officer of ARIAD. "These
data illustrate the potential for AP24534 to treat several forms of
leukemia and solid tumors based on its broad-acting and unique
profile. We are on track to enroll patients with CML and other
hematological malignancies in our first clinical trial of oral AP24534
in early 2008."

    The in vitro and in vivo studies announced today show a number of
key characteristics of AP24534:

    --  AP24534 potently inhibits all mutant forms of Bcr-Abl tested,
        including T315I, which is completely resistant to currently
        available drugs, and other partially resistant mutants, such
        as T315A;

    --  AP24534 was found to be more potent than dasatinib in animal
        models of early-stage CML (when the Bcr-Abl protein is not
        mutated);

    --  Even when given infrequently in these animal models, including
        single doses, AP24534 induced regression of tumors expressing
        unmutated or mutated forms of Bcr-Abl;

    --  AP24534 also potently inhibited the growth of primary human
        leukemia cells isolated from leukemia patients expressing
        these Bcr-Abl variants; and

    --  AP24534 does not inhibit Aurora kinases, which differentiates
        it from other investigational T315I inhibitors.

    Leukemia and Other Hematological Cancers

    Leukemia is a blood-based cancer characterized by the abnormal
proliferation and accumulation of immature, functionless blood cells
in the blood and marrow, which impede the development and function of
normal blood cells. If untreated, the cancerous blood cells overwhelm
the bone marrow, enter the bloodstream and eventually invade other
parts of the body, such as the lymph nodes, spleen, liver, and central
nervous system. According to the Leukemia and Lymphoma Society, an
estimated 44,240 new cases of leukemia will be diagnosed in the United
States in 2007. The incidence of hematological cancers, such as
leukemias, lymphomas and myelomas, is among the fastest growing
cancers due to the aging population.

    Chronic Myeloid Leukemia (CML)

    CML is characterized by an excessive and unregulated production of
white blood cells by the bone marrow due to a genetic abnormality
involving the Bcr-Abl protein. After a slow, chronic phase of
production of too many white blood cells, CML typically evolves to
more aggressive phases (i.e., "accelerated" phase or "blast crisis").
Treatment with Bcr-Abl inhibitors is initially effective but
frequently results in the emergence of Bcr-Abl mutations that confer
drug resistance. The T315I mutant of Bcr-Abl currently accounts for
15-20% of all drug resistance in CML. First-generation therapies for
CML, such as imatinib, and second-generation therapies for CML, such
as dasatinib and nilotinib, are not able to inhibit this mutated
protein and thus are not effective against all forms of CML.

    Acute Myeloid Leukemia (AML)

    AML is a fast-growing cancer in which too many abnormal and
immature white blood cells are rapidly made in the bone marrow and
interfere with the production of normal blood cells. Flt3 is a
validated target for AML. Mutation of the Flt3 protein, which is
responsible for the proliferation of normal blood cells, is the most
common genetic abnormality related to AML, present in approximately
one-third of all AML patients and associated with adverse prognoses.
The most common Flt3 mutation, the so-called internal tandem
duplication, is linked to a particularly poor disease prognosis and is
expected to be particularly susceptible to Flt3 inhibition. There are
no Flt3 inhibitors currently approved for the treatment of AML.

    Angiogenesis and Solid Tumors

    Malignant tumors cannot grow beyond a certain size without
essential nutrients and oxygen. Angiogenesis is a key process in tumor
growth and spread in which tumors provoke the growth of new blood
vessels to the tumor from pre-existing vessels; these new blood
vessels provide the tumor with oxygen and nutrients, allowing these
cells to grow, invade nearby tissue and spread to other parts of the
body. To induce angiogenesis, tumors secrete various growth factors,
such as VEGF, which send chemical signals to existing blood vessels to
stimulate the growth of new blood vessels. Currently available
angiogenesis inhibitors are designed to stop the effects of the
protein VEGF on tumors, interfering with the development of new blood
vessels and blocking the supply of oxygen and nutrients that the tumor
needs to grow and spread. However, studies have shown that resistance
to VEGF inhibitors is associated with higher expression of additional
growth factors, in particular members of the FGF and angiopoietin
families. Simultaneous inhibition of VEGFR, FGFR, and the angiopoietin
1 receptor (Tie2) is expected to provide more potent inhibition of
angiogenesis that is less prone to resistance than blocking VEGF
alone.

    About AP24534

    ARIAD's second oncology product candidate, AP24534, is a novel
multi-targeted kinase inhibitor that has broad potential applications
in cancer. Specifically, in preclinical studies, AP24534 has
demonstrated potent inhibition of the kinase targets associated with
drug-resistant chronic myeloid leukemia and acute myeloid leukemia, as
well as angiogenesis in multiple solid tumors. AP24534 has completed
extensive preclinical studies, including safety assessment studies,
which indicate that the drug candidate should be well tolerated at
anticipated therapeutic dose levels in cancer patients. Phase 1
clinical development of oral AP24534 in patients with hematological
cancers is expected to begin in early 2008.

    About ARIAD

    ARIAD is engaged in the discovery and development of breakthrough
medicines to treat cancer by regulating cell signaling with small
molecules. ARIAD is developing a comprehensive approach to patients
with cancer that addresses the greatest medical need - aggressive and
advanced-stage cancers for which current treatments are inadequate.
ARIAD has a global partnership with Merck & Co., Inc. to develop and
commercialize deforolimus, ARIAD's lead cancer product candidate.
Medinol Ltd. and ICON Medical Corp. are also developing
deforolimus-eluting stents to prevent restenosis of injured vessels
following interventions in which stents are used in conjunction with
balloon angioplasty. ARIAD has an exclusive license to pioneering
technology and patents related to certain NF-(kappa)B treatment
methods, and the discovery and development of drugs to regulate
NF-(kappa)B cell-signaling activity, which may be useful in treating
certain diseases. Additional information about ARIAD can be found on
the web at http://www.ariad.com.

    This press release contains "forward-looking statements,"
including statements related to safety and efficacy of AP24534 in
various indications and the anticipated timing of clinical trials.
Forward-looking statements are based on management's expectations and
are subject to certain factors, risks and uncertainties that may cause
actual results, outcome of events, timing and performance to differ
materially from those expressed or implied by such statements. These
risks and uncertainties include, but are not limited to, the costs
associated with our research, development, manufacturing and other
activities, the conduct and results of pre-clinical and clinical
studies of our product candidates, difficulties or delays in obtaining
regulatory approvals to market products resulting from our development
efforts, our reliance on strategic partners and licensees, and other
key parties for the successful development, manufacturing and
commercialization of products, the adequacy of our capital resources
and the availability of additional funding, patent protection and
third-party intellectual property claims relating to our and any
partner's product candidates, the timing, scope, cost and outcome of
legal and patent office proceedings concerning our NF-(kappa)B patent
portfolio, the potential acquisition of or other strategic transaction
regarding the minority stockholders' interests in our 80%-owned
subsidiary, ARIAD Gene Therapeutics, Inc., future capital needs, key
employees, markets, economic conditions, prices, reimbursement rates,
competition and other factors detailed in the Company's public filings
with the U.S. Securities and Exchange Commission. The information
contained in this document is believed to be current as of the date of
original issue. The Company does not intend to update any of the
forward-looking statements after the date of this document to conform
these statements to actual results or to changes in the Company's
expectations, except as required by law.

    CONTACT: ARIAD Pharmaceuticals, Inc.
             Edward M. Fitzgerald, 617-621-2345
             or
             Pure Communications
             Sheryl Seapy, 949-608-0841