Amgen 2010 Annual Report Download - page 29

The following table reflects companies and their currently marketed products that compete with Sensipar»in
the United States and with Mimpara»in Europe in the nephrology segment for patients with CKD on dialysis. The
table and discussion below of competitor marketed products and products in development may not be exhaustive.
Territory Competitor Marketed Product Competitor
U.S. Hectorol»Genzyme Corporation (“Genzyme”)
U.S. Rocaltrol»Roche
U.S. Calcijex»Abbott
U.S. Calcium Acetate»Roxane Laboratories/Sandoz
U.S. & Europe Zemplar»Abbott
U.S. & Europe Renagel»Genzyme
U.S. & Europe Renvela»Genzyme
U.S. & Europe PhosLo»/Rephoren»Fresenius Medical Care
U.S. & Europe OsvaRen»Fresenius Medical Care
U.S. & Europe Fosrenol»Shire Pharmaceuticals Group Plc
On July 25, 2008, we filed a lawsuit against Teva Pharmaceuticals USA, Inc. and Teva Pharmaceutical
(together defined as “Teva”) and Barr Pharmaceuticals Inc. (“Barr”) for infringement of four Sensipar»patents. The
lawsuit was based on Abbreviated New Drug Applications filed by Teva and Barr that sought approval to market
generic versions of Sensipar». Following trial, on January 7, 2011, the U.S. District Court for the District of
Delaware granted an injunction prohibiting Teva and Barr from commercializing generic versions of Sensipar»in
the United States until expiration of three of those patents. (See Note 19, Contingencies and commitments to the
Consolidated Financial Statements.) These generic versions could compete with Sensipar»in the future.
Vectibix»(panitumumab)
Vectibix»is our registered trademark for panitumumab, our monoclonal antibody for the treatment of patients
with EGFr expressing mCRC after disease progression on, or following fluoropyrimidine-, oxaliplatin- and
irinotecan- containing chemotherapy regimens. EGFr is a protein that plays an important role in cancer cell
signaling and is over-expressed in many human cancers. Vectibix»binds with high affinity to EGFrs and interferes
with signals that might otherwise stimulate growth and survival of the cancer cell. We acquired full ownership of
Vectibix»with our acquisition of Abgenix, Inc. (“Abgenix”) in April 2006. In September 2006, Vectibix»received
FDA accelerated approval in the United States, based upon clinical trial data from a study demonstrating a
statistically significant improvement in progression-free survival and with the condition that Amgen conduct a
confirmatory trial to verify the clinical benefit of panitumumab through demonstration of an improvement in overall
survival. In the EU, the conditional approval of Vectibix»as monotherapy, for the treatment of patients with EGFr
expressing metastatic colorectal carcinoma with non-mutated (wild-type) KRAS genes after failure of fluoropyr-
imidine-, oxaliplatin-, and irinotecan-containing chemotherapy regimens, was received in December 2007 and is
reviewed annually by the Committee for Medicinal Products for Human Use (“CHMP”). In December 2008, 2009
and 2010, the EU conditional marketing authorization was renewed with an additional specific obligation to
conduct a clinical trial in the existing approved indication. In 2010, we began enrollment for this additional clinical
trial which compares the effect of Vectibix»versus Erbitux»(cetuximab) on overall survival for chemorefractory
mCRC patients with wild-type KRAS genes. KRAS is a protein found in all human cells. Some colorectal cancers
have mutations in the KRAS gene. Vectibix»has been shown to be ineffective in people whose tumors had KRAS
mutations in codon 12 or 13.
In 2009, we announced results from the ’203 and ’181 pivotal phase 3 trials evaluating Vectibix»in
combination with chemotherapy (FOLFOX or FOLFIRI) as a first- and second-line treatment for mCRC,
respectively. Both studies demonstrated that Vectibix»administered with chemotherapy significantly improved
progression-free survival in patients with wild-type KRAS mCRC. Additionally, both studies showed numeric
improvements in median overall survival in the same patient population. The numeric improvements in median
overall survival failed to achieve statistical significance. It was previously agreed with the FDA that the ’181 study
would serve as the confirmatory trial for establishing full approval for the mCRC indication.
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