A class of anti-hepatitis B drug, "the United States he Cabey," entere

September 18, from the long Australian Pharmaceutical independently developed toxic hepatitis B drug resistance of enteric capsules by the U.S. He Cabey clinical SFDA approval, marking China's independent development of new drugs to enter a new phase. Hepatitis B patients can be hung overhead in the sword of Damocles will soon be shaking.

Hepatitis B (hepatitisB), referred to as hepatitis B virus by hepatitis B (HBV) caused by liver disease and may lead to multiple organ damage mainly infectious diseases. More than 50 million people worldwide die each year of primary Hepatic carcinoma , Of which up to 80% of primary liver cancer caused by chronic hepatitis. In the 400 million chronic hepatitis B patients, 75% live in Asia, while China is a country with the highest incidence of hepatitis B. Latest figures show China's annual number of deaths due to liver disease nearly 50 million loss to society as much as 100 billion yuan.

Liver disease in our country such a big country, an effective drug against hepatitis B disease toxic hepatitis B drug entecavir enteric-coated capsules of the U.S. he appeared destined to be of concern to most people.

Market, looking forward to a hero
Current of the commonly used anti-HBV drugs which do?
European Liver Research Institute (EASL) in February this year a new version of hepatitis B prevention and treatment guidelines. "Guide" that "the purpose of treatment of hepatitis B is to prevent disease to cirrhosis, decompensated cirrhosis, end-stage liver disease, liver cancer, the death of progress, improve the patients quality of life and prolong survival. If the hepatitis B virus can be lasting suppression, the histological activity of chronic hepatitis, cirrhosis risk, decreased risk of liver cancer, hepatitis B treatment objective is reached. However, covalently closed circular DNA (cccDNA) present in the nucleus of infected liver China, HBV infection can not be removed. "

Currently used for treatment of chronic hepatitis B drugs include common interferon, pegylated interferon and nucleoside analogues. Treatment of HBV infection in nucleoside analogues are three types of: L-nucleoside (lamivudine, telbivudine and emtricitabine), deoxyguanosine analogues (entecavir) and the open-loop phosphorylation of nucleoside analogues ( Adefovir and tenofovir). Lamivudine, adefovir, entecavir, telbivudine and tenofovir have been approved by the EU for the treatment of hepatitis.

Our application of anti-hepatitis B virus is mainly: -interferon, as represented by conventional interferon and lamivudine nucleoside analogues represented, but the vast majority of anti-viral medicine due to serious The "resistance" and "rebound" phenomenon can only be "short-lived."

Are currently available and most widely used nucleoside analogues are Glaxo Wellcome's new drug lamivudine, Drugs Called lamivudine. Lamivudine is GSK developed the world's first effective oral anti-hepatitis drug market in China in 1999, 2000, the global Sell Up to 2.3 billion pounds, while sales in China reached 400 million yuan. Lamivudine in HBV infected cells

and normal metabolism of cells generated by phosphorylation of its phosphate, phosphate of the HBV polymerase and reverse transcriptase inhibited, thereby inhibiting virus replication cycle in the reverse transcription process, while can and cytidine acid (LTP) Competitive incorporation HBVDNA chain termination DNA chain extension, blocking viral DNA synthesis.

But not lamivudine inhibited covalently closed circular DNA (cccDNA), so easy to rebound after drug withdrawal, it requires long-term medication; YMDD variant strains is the main reason for resistance to chemicals, according to III clinical studies have shown that using this product after 1 year of treatment, from 14% to 32% of cases detected YMDD mutant. Addition of lamivudine to prevent the virus proteins role in the weak, the low rate of HBeAg negative.

Interferon (ordinary or pegylated interferon) The main advantage is there is no resistance, there is a potential immune-mediated anti-HBV effect, so that the end of treatment HBVDNA negative patients have the opportunity to maintain a lasting virologic response and HBsAg disappeared.

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