Drug – bio-affecting and body treating compositions – Antigen – epitope – or other immunospecific immunoeffector – Conjugate or complex
Patent
1999-04-06
2000-09-05
Reamer, James H.
Drug, bio-affecting and body treating compositions
Antigen, epitope, or other immunospecific immunoeffector
Conjugate or complex
A61K 3578
Patent
active
061139092
DESCRIPTION:
BRIEF SUMMARY
This application is the national phase under 35 U.S.C. .sctn.371 of PCT International Application No. PCT/KP98/00214 which has an International filing date of Jul. 15, 1998, which designated the United States of America.
TECHNICAL FIELD
The present invention relates to a pharmaceutical composition for treatment of hepatitis C which contains a mixed extract of Phellodendron amurense RUPRECHT cortex and Patrinia scabiosaefolia FISCH. as an active ingredient. More specifically, the present invention relates to a pharmaceutical composition which contains a mixed extract obtained from the mixture of Phellodendron amurense RUPRECHT cortex and Patrinia scabiosaefolia FISCH. in water or alcohol extraction, as an active ingredient, which can be used effectively for the treatment of hepatitis C and hepatic cirrhosis originated from hepatitis C due to its anti-viral activity against hepatitis C virus and, at the same time, its ability to retrieve the damaged T helper cells to reinforce the host immune system.
BACKGROUND ART
Chronic hepatitis C is a disease characterized in that the infection of hepatitis C viruses (HCV) continuously induces inflammation in liver centering around the area of portal vein, and advances to hepatic cirrhosis or primary hepatocellular carcinoma. Contrary to hepatitis A or B, about 90% of hepatitis C shows abnormal GPT (glutamic-pyruvic transaminase) level, even at the primary infection, and develops into chronic illness. Recently, it is reported that hepatitis C virus may directly participate in the induction of hepatocellular carcinoma [see, Sakamuro, Furukawa and Takegami, J. Virol. 69: 3893-3896, 1995; Ray, Logging, Meyer and Ray, J. Virol. 70: 4438-4443, 1996]. In addition, it is also reported that hepatitis C virus is detected in 30% of patients with hepatocellular carcinoma in western countries [see, Mangia, Vallari and Bisceglie, J. Med. Virol. 43, 125-128, 1994].
According to the development of HCV antibody (C100-3 antibody) detection system by Chiron Inc. (U.S.A.) in 1988, it has been revealed that the majority of non-A, non-B hepatitis are caused by hepatitis C virus. In Japan, the screening assay using antibody detection system has allowed to demonstrate that hepatitis C virus is detected in 70% of patients suffering from non-A, non-B hepatitis and in 90% or more of hepatoma patients.
In 1989, the nature of hepatitis C virus was first identified by separating a part of virus gene from the serum of chimpanzee suffering from non-A, non-B hepatitis. That is, hepatitis C virus belongs to Flaviviridae having 9.5 kb positive(+)-stranded RNA as a gene, and synthesizes viral polypeptide precursor in host cells. The precursor protein is transformed into structural proteins (core, E1, E2), which are directly comprised to make up the viral structure, and non-structural proteins (NS2, NS3, NS4A, NS4B, NS5A, NS5B) having enzymatic activities after the post-translational modification by the signal peptidase of a host, and by metalloprotease and serine protease produced from hepatitis C virus. Particularly, numerous variants can be produced due to the presence of two hypervariable regions (HVR1 and HVR2) on the 5' end of E2 gene.
Although the mechanism related to the progression from chronic hepatitis C to hepatocellular carcinoma has not been yet established, chronic inflammation and the intensity of inflammation may be closely related. That is, although the host immune system produces neutralizing antibody against hepatitis C virus, the neutralizing antibody affects only the limited types of viruses, and the variants resistant to the neutralizing antibody are produced quickly (genetic mutation at high rate). In spite of the presence of the neutralizing antibody, the variants may continuously induce inflammation in the host (immune escape). Further, the regeneration ability of host liver cells from the continuous infectious damages may cause tumorigenesis. Recently, it has been reported that double strand RNA-dependent protein kinase R (PKR) of host cells can phosphorylate elF-2a to sti
REFERENCES:
patent: 5244662 (1993-09-01), Han et al.
Japanese Abstract: JP 01-272581A, vol. 14, No. 37, 1990.
Japanese Abstract: JP 01-224317A, vol. 13, No. 549, 1989.
Derwent Publications Ltd. AN 97-527439, CN 1 127 125.
Chung Young Shin
Han Young Bok
Hong Eun Kyung
Kim Sang Geon
Lee Kyung Yung
Reamer James H.
Young Bok Han
Young Hee Kim
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