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Chugai launches Actemra for Castleman’s disease in Japan

TokyoWednesday, June 15, 2005, 08:00 Hrs  [IST]

Chugai Pharmaceutical Co., Ltd. announced that the humanized anti-human IL-6 (interleukin-6) receptor monoclonal antibody, tocilizumab (genetical recombination) injection under the trade name Actemra 200 for intravenous infusion for the treatment of Castleman's disease, was launched. ''Actemra'' is a humanized monoclonal antibody co-developed by Osaka University and Chugai utilizing genetic recombinant technology. In order to meet the medical needs such as the development of new therapies targeting more specific disease process, Chugai completed the clinical development in a short period after receiving the orphan drug designation for Castlemen's disease in December 2000. The NDA for Castleman's disease was filed in April 2003 and was approved on April 11, 2005 as the first monoclonal antibody drug manufactured in Japan. The price was listed on the National Health Insurance reimbursement price list on June 3, 2005. The price was set at 59,879 yen per vial, a Chugai Pharmaceutical release said. ''Actemra'' is the world's first drug approved for Castleman's disease.  Chugai estimates that approximately 1,500 patients are diagnosed as Castleman's disease in Japan.  It is further estimated that among these patients, over 100 patients who cannot be treated by surgery and show resistance to traditional therapies are subject to Actemara treatment. Castleman's disease was first reported by Dr Benjamin Castleman (MD) in 1956 and is a very rare lymphoproliferative disease characterized by symptoms such as systemic lymphadenopathy, fever, general fatigue, weight loss, anaemia, splenomegaly, hepatomegaly, and various abnormal laboratory test values.  Conditions such as amyloidosis, haemolytic anaemia, or interstitial pneumonia have been reported as complications of the disease. The pathology and symptoms of Castleman's disease result from the excessive production of IL-6. ''Actemra'' has been proved through clinical trial to improve the symptoms and abnormal laboratory test values by suppressing the biological activity of IL-6. Thirty five patients with Castleman's disease received 8 mg/kg of ''Actemra'' eight times in total with two-week intervals in the phase II study, which resulted in significant improvements in inflammation markers (increased C reactive protein, increased fibrinogen, increased erythrocyte sedimentation rate), general malaise, anaemia, and hypoalbuminemia. In the subsequent long-term extension study (treatment period: maximum 1,568 days, average 1,191 days) the therapeutic effect such as improvement of the inflammation markers was maintained with good tolerability. The major adverse events were nasopharyngitis (88.6 per cent); skin rash (48.6 per cent); abdominal pain (31.4 per cent); itching (28.6 per cent); and neutropenia (25.7 per cent). As the condition for approval all patients treated with ''Actemra'' will be required to be monitored for efficacy and safety.

 
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