Results From Study of Vascular Calcification in Dialysis Patients Presented in Late-Breaking Clinical Trial Session at ERA-EDTA 2010 Congress

MUNICH, June 26, 2010 - Results from the ADVANCE study presented in a late breaking clinical
trial session at the ERA-EDTA 2010 Congress provide new insights into the
management of secondary hyperparathyroidism (SHPT) in chronic kidney disease
(CKD) patients. ADVANCE (A randomiseD VAscular calcificatioN study to
evaluate the effects of CinacalcEt) is a randomised, controlled open label
study to evaluate the effects of treatment with Mimpara(R) (cinacalcet) plus
low-dose vitamin D, compared to flexible doses of vitamin D alone, on the
progression of vascular and valvular calcification in dialysis patients with
SHPT. A trend was observed towards slower progression of vascular
calcification at all sites evaluated among patients randomised to the
cinacalcet arm, though the primary endpoint did not reach statistical
significance.

The primary endpoint for the study was percentage change in the Agatston
CAC score from baseline to week 52. Agatston CAC scores [median, (Q1, Q3)]
increased by 24 percent (-1 percent, 63 percent) from baseline in the
cinacalcet group and by 31 percent (8 percent, 81 percent) in the flexible
vitamin D group (p=0.073). Additional analyses were also performed using
volumetric scoring of CAC, an alternative method for measuring CAC, and
showed cinacalcet plus low-dose vitamin D significantly slowed the
progression of calcification compared with flexible doses of vitamin D alone.
Volume CAC scores increased by 22 percent (2 percent, 52 percent) from
baseline in the cinacalcet group and by 30 percent (10 percent, 78 percent)
in the flexible vitamin D group (p=0.009).

"Coronary artery calcification is common in dialysis patients and has
been linked to an elevated risk of cardiovascular events and mortality in
patients on dialysis," said Paolo Raggi, M.D., Professor of Medicine, Emory
University School of Medicine, Atlanta, USA. "Although the results for the
primary endpoint were not statistically significant, the findings from
ADVANCE further support the hypothesis that treatment with cinacalcet plus
low doses of vitamin D may slow the progression of this marker of risk in
patients on dialysis with SHPT."

ADVANCE also showed that cinacalcet plus low-dose vitamin D, compared to
flexible doses of vitamin D alone, provided better biochemical control of
SHPT as judged by the blood levels of parathyroid hormone (PTH), calcium, and
phosphorus from baseline to the end of the study as demonstrated in previous
studies.(1,2) Median (interquartile range) plasma PTH levels decreased by 132
pg/mL (-276,-24) from baseline to study end in the cinacalcet group and by 65
pg/mL (-184, 62) in the flexible vitamin D group (p=0.018). Mean (95 percent
CI) serum calcium decreased by 0.51 mg/dL (-0.65, -0.37) in the cinacalcet
group but increased by 0.17 mg/dL (0.06, 0.28) in the flexible vitamin D
group (p<0.001). Serum phosphorus decreased by 0.92 mg/dL (-1.28, -0.55) in
the cinacalcet group and by 0.24 mg/dL (-0.55, 0.07) in the flexible vitamin
D group (p=0.025). The incidence of adverse events was similar between the
two treatment groups.

"The results from ADVANCE, coupled with recently published data,
including an observational study showing that cinacalcet significantly
improved all-cause and cardiovascular survival in dialysis patients(3),
underscore the importance of completing the ongoing EVOLVE (EValuation Of
Cinacalcet Therapy to Lower CardioVascular Events(TM)) trial, a global,
randomised, placebo-controlled, double-blind study evaluating the impact of
cinacalcet on mortality and cardiovascular events in dialysis patients," said
Chris Mix, Executive Medical Director of Global Development at Amgen. "We
look forward to sharing those results with the nephrology community when they
become available."

Additional analyses presented at the ERA-EDTA 2010 Congress provide
further support for the hypothesis that treatment with cinacalcet plus low
doses of vitamin D may favourably affect the progression of calcification of
cardiac valves compared to vitamin D alone(4) (Abstract Number: Sa116);
highlight predictors of cardiovascular calcification in patients on
dialysis(5) (Abstract Number: OSu039) and compare cardiovascular calcium
scoring methods in the ADVANCE study(6) (Abstract Number: OM016).

ADVANCE Study Design

ADVANCE is a randomised, controlled trial to compare two treatment
strategies for SHPT and their effects on the progression of CAC among
patients on dialysis. ADVANCE studied 360 patients with SHPT and detectable
CAC who were randomised to open label treatment with cinacalcet (30-180
mg/day) plus low-dose vitamin D (less than or equal to 2 ug IV paricalcitol
equivalent/dialysis session) or to flexible vitamin D therapy. In both
groups, calcium-based phosphate binders were used exclusively, and the
therapeutic target for PTH was 150-300 pg/mL.

The primary endpoint for ADVANCE evaluated the percentage change in
Agatston CAC score from baseline to week 52. Secondary endpoints for ADVANCE
included:

    -- Absolute change from baseline in CAC score at week 52
    -- Absolute and percentage change from baseline in aortic calcification
       score at week 52
    -- Absolute and percentage change from baseline in aortic and mitral
       valve calcification score at week 52
    -- Proportion of patients achieving > 15% progression of CAC at week 52
    -- Absolute and percentage changes in laboratory parameters (PTH,
       calcium, phosphorus)
    -- Safety and tolerability of cinacalcet

About SHPT

SHPT is a metabolic disorder that develops in chronic kidney disease
(CKD) patients on dialysis and results in increased secretion of parathyroid
hormone (PTH), which may lead to bone disease, bone pain and fractures,
cardiovascular and soft tissue calcification and parathyroid hyperplasia.

SHPT develops as the parathyroid gland secretes increased PTH to
normalise blood levels of calcium, which are low in patients with CKD. While
SHPT initially helps to normalise serum calcium, over time, continuous PTH
secretion leads to excessive growth of the parathyroid gland, high levels of
PTH, calcium and phosphorus in the blood, and complications including bone
disease and soft tissue and vascular calcification, which increases the risk
for cardiovascular events.(7)

The majority of an estimated 324,000 CKD patients on dialysis in Europe
suffer from some degree of SHPT.

About CAC and SHPT

Cardiovascular disease and CAC are common in dialysis patients and may be
aggravated by elevated PTH levels and disturbances in calcium and phosphorus
metabolism that characterise secondary HPT. Elevated PTH was found to be a
predictor of the extent of CAC among ADVANCE patients at baseline.(8)

Additionally, CAC progresses more rapidly in patients on dialysis than
individuals with normal kidney function. Previous studies have shown that the
degree of CAC and cardiac calcification is 2.5 to 5 times greater in dialysis
patients than in non-dialysis patients with diagnosed coronary artery
disease.(9) Available methods for evaluating CAC in clinical trials are not
compliant with Good Clinical Practice. Vascular calcification is not a
validated surrogate endpoint for mortality or cardiovascular events in this
patient population.

About Mimpara(R) (cinacalcet)

Cinacalcet is a calcimimetic agent that is approved for the treatment
SHPT in patients with chronic kidney disease on dialysis and for the
reduction of hypercalcaemia in patients with parathyroid carcinoma and with
primary HPT for whom parathyroidectomy would be indicated on the basis of
serum calcium levels (as defined by relevant treatment guidelines).

Cinacalcet is a first-in-class calcimimetic that modulates the activity
of the calcium-sensing receptor (CaR). It is a small molecule that acts as an
allosteric modulator of the CaR on the parathyroid cell surface. The primary
role of the CaR is control of PTH secretion in response to extracellular
calcium concentration. Cinacalcet acts to reduce circulating PTH
concentration through activation of the CaR by increasing its sensitivity to
extracellular calcium. The reduction in PTH is associated with a concomitant
decrease in serum calcium.

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    References
    1. Messa P, Macario F, Yaqoob M, et al. The OPTIMA Study: assessing
       a new cinacalcet (Sensipar/Mimpara) treatment algorithm for
       secondary hyperparathyroidism. Clin J Am Soc Nephrol 2008;3:36-45
    2. Moe SM, Reslerova M, Ketteler M. Role of calcification inhibitors
       in the pathogenesis of vascular calcification in chronic kidney
       disease (CKD). Kidney International 2005;67:2295-2304
    3. Block GA, Zaun D, Smits G, et al. Cinacalcet hydrochloride
       treatment significantly improves all-cause and cardiovascular
       survival in a large cohort of hemodyalisis patients. Kidney
       International Advance Online Publication, June 16, 2010.
       doi:10.1038/ki.2010.167
    4. Urena P, Raggi P, Chertow G, et al. The effects of cinacalcet plus
       low-dose vitamin D on cardiac valve calcification in hemodialysis
       patients with secondary hyperparathyroidism. Data presented at ERA-
       EDTA, 25-28 June Munich 2010.
    5. Floege J, Chertow G, Block G, et al. Predictors of progression of
       cardiovascular calcification in patients on hemodialysis. Data
       presented at ERA-EDTA, 25-28 June, Munich 2010.
    6. Raggi P, Chertow G, Block G et al. Comparison of cardiovascular
       calcium scoring methods in the ADVANCE study. Data presented at ERA-
       EDTA, 25-28 June, Munich 2010
    7. Williams ME. Chronic kidney disease/bone and mineral metabolism:
       the imperfect storm. Semin Nephrol 2009;29(2):97-104
    8. Floege J, Raggi P, Block GA, et al. Study design and subject
       baseline characteristics in the ADVANCE Study: effects of cinacalcet
       on vascular calcification in haemodialysis patients. Nephrol Dial
       Transplant. 2010 Nephrol. Dial. Transplant;25:1916-1923
    9. Braun J, Oldendorf M, Moshage W, et al. Electron beam computed
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