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Vectibix(R) Approved in the European Union for the Treatment of Metastatic Colorectal Cancer



    Clinically Relevant Biomarker Provides Physicians With the Ability to Predict the Patients Most Likely to Respond to Vectibix Treatment

    Amgen (NASDAQ: AMGN) today announced that the European Commission
    has granted a conditional marketing authorization for Vectibix(R)
    (panitumumab) as monotherapy for the treatment of patients with
    epidermal growth factor receptor (EGFr) expressing metastatic
    colorectal cancer (mCRC) with non-mutated (wild-type) KRAS genes after
    failure of standard chemotherapy regimens.

    Vectibix, a fully human anti-EGFr monoclonal antibody, has been
    granted a positive Commission decision in the European Union (EU)
    based upon a positive opinion from the European Committee for
    Medicinal Products for Human Use (CHMP) for marketing authorization in
    September of this year. This approval is based on a positive benefit /
    risk assessment in a patient population that currently has few
    treatment options available to them. As part of the CHMP review,
    clinical data supporting the utility of KRAS mutation status as a
    biomarker for clinical outcome were provided.

    "It is an exciting time in the oncology arena as we see a shift
    towards individualized patient care," said Willard Dere, M.D., senior
    vice president and international chief medical officer at Amgen. "We
    are pleased that Vectibix has received conditional marketing
    authorization allowing metastatic colorectal cancer patients to have
    access to a new targeted treatment option."

    These biomarker data were generated from a prospectively defined
    analysis of the Phase 3, randomized, controlled clinical trial "408"
    that investigated the treatment effect of KRAS status (non-mutated
    versus mutated) in Vectibix patients with mCRC. The analysis
    demonstrated that the effect of Vectibix on progression-free survival
    (PFS) was confined exclusively to the approximately 60 percent of
    patients whose tumors harbor normal, non-mutated (wild-type) KRAS.
    Vectibix had no clinical benefit in patients who had tumors with
    mutations in KRAS regardless of the endpoint studied. Previously
    reported pivotal results from "408" demonstrated that Vectibix
    monotherapy significantly improved PFS and response rates in heavily
    pre-treated patients with mCRC after failure of standard chemotherapy
    versus best supportive care.

    KRAS plays an important role in cell growth regulation and
    oncogenesis. Anti-EGFr therapies work by blocking the activation of
    EGFr, thereby inhibiting downstream events that lead to malignant
    signaling. However, in patients with tumors harboring a mutated or
    activated KRAS, the KRAS protein is always turned "on" regardless of
    whether EGFr has been activated or therapeutically inhibited. Thus, in
    patients with mutated KRAS, signaling continues despite anti-EGFr
    therapy. Mutant KRAS is detected in approximately 40 percent of CRC
    tumors.

    "Being able to select which patients are more likely to respond to
    therapy is an important step forward in the treatment of metastatic
    colorectal cancer," said Professor Eric Van Cutsem, Digestive Oncology
    Unit, University Hospital, Leuven, Belgium, a Vectibix investigator.
    "The ability to predict the patient population more likely to respond
    to Vectibix could potentially reduce drug exposure in patients who we
    know will not respond."

    About Vectibix

    Vectibix, the first fully human IgG2 monoclonal antibody (MAb)
    therapy, targets the EGFr, a protein that plays an important role in
    cancer cell signaling. With its demonstrated efficacy and convenient
    Q2W dosing schedule Vectibix provides an important option in the
    management of mCRC patients. Ongoing Phase 3 trials are exploring the
    potential of administering Vectibix in combination with chemotherapy
    in the first- and second-line of mCRC, as well as in the head and neck
    cancer setting.

    In the EU, Vectibix is indicated as monotherapy for the treatment
    of patients with metastatic colorectal carcinoma expressing EGFr with
    tumors with non-mutated KRAS and after failure of fluoropyrimidine-,
    oxaliplatin-, and irinotecan-containing chemotherapy regimens.

    Approved by the Food and Drug Administration (FDA) in September
    2006, Vectibix is indicated in the United States (U.S.) as a single
    agent for the treatment of patients with EGFr-expressing, metastatic
    colorectal carcinoma with disease progression on or following
    fluoropyrimidine-, oxaliplatin- and irinotecan-containing chemotherapy
    regimens. The effectiveness of Vectibix as a single agent for the
    treatment of EGFr-expressing, metastatic colorectal carcinoma is based
    on progression-free survival. Currently, no data are available that
    demonstrate an improvement in disease-related symptoms or increased
    survival with Vectibix.

    Important Product Safety Information - EU

    Dermatologic related reactions, a pharmacologic effect observed
    with epidermal growth factor receptor (EGFr) inhibitors, are
    experienced with nearly all patients (approximately 90 percent)
    treated with Vectibix. The majority of dermatological reactions are
    mild to moderate in nature. In clinical studies, subsequent to the
    development of severe dermatological reactions (including stomatitis),
    infectious complications including sepsis, in rare cases leading to
    death, and local abscesses requiring incisions and drainage were
    reported. Patients who have severe dermatologic reactions or who
    develop worsening reactions whilst receiving Vectibix should be
    monitored for the development of inflammatory or infectious sequelae,
    and appropriate treatment promptly initiated.

    Important Product Safety Information - U.S.

    Dermatologic toxicities, related to Vectibix blockade of EGF
    binding and subsequent inhibition of EGF receptor-mediated signaling
    pathways, included but were not limited to dermatitis acneiform,
    pruritus, erythema, rash, skin exfoliation, paronychia, dry skin and
    skin fissures. Dermatologic toxicities were reported in 90 percent of
    patients treated with Vectibix and were severe in 12 percent of
    patients. Severe dermatologic toxicities were complicated by
    infection, including sepsis, septic death and abscesses requiring
    incisions and drainage. Vectibix may need to be withheld or
    discontinued for severe dermatologic toxicities.

    Severe infusion reactions occurred with Vectibix in approximately
    one percent of patients. Severe infusion reactions were identified as
    anaphylactic reactions, bronchospasm, fever, chills and hypotension.
    Although fatal infusion reactions have not been reported with
    Vectibix, they have occurred with other monoclonal antibody products.
    Severe infusion reactions require stopping the infusion and possibly
    permanently discontinuing Vectibix, depending on the severity and / or
    persistence of the reaction.

    About Amgen

    Amgen discovers, develops and delivers innovative human
    therapeutics. A biotechnology pioneer since 1980, Amgen was one of the
    first companies to realize the new science´s promise by bringing safe,
    effective medicines from lab, to manufacturing plant, to patient.
    Amgen therapeutics has changed the practice of medicine, helping
    millions of people around the world in the fight against cancer,
    kidney disease, rheumatoid arthritis, and other serious illnesses.
    With a deep and broad pipeline of potential new medicines, Amgen
    remains committed to advancing science to dramatically improve
    people´s lives. To learn more about our pioneering science and our
    vital medicines, visit www.amgen.com.

    Forward Looking Statements

    This news release contains forward-looking statements that involve
    significant risks and uncertainties, including those discussed below
    and others that can be found in our Form 10-K for the year ended Dec.
    31, 2006, and in our periodic reports on Form 10-Q and Form 8-K. Amgen
    is providing this information as of the date of this news release and
    does not undertake any obligation to update any forward-looking
    statements contained in this document as a result of new information,
    future events or otherwise.

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