|
|
|
|
« December 2006 | Main | February 2007 »
January 18, 2007
Announcing New Hepatitis C Treatment to Prevent Drug Resistance
A Stanford University discovery has identified certain proteins as necessary components for Hepatitis C virus replication. Presidio Pharmaceuticals has licensed the rights to use this information for developing a Hepatitis C treatment that prevents drug resistance, the leading cause of viral eradication failure.
www.endonurse.com
Presidio Pharmaceuticals Receives Exclusive License to Novel Hepatitis C Technology
January 18, 2007
SAN FRANCISCO -- Presidio Pharmaceuticals, Inc. announced today that it has licensed the exclusive worldwide rights to novel hepatitis C virus (HCV) technology from Stanford University. This technology, invented in the lab of Stanford scientist Jeffrey Glenn, targets a specific region found in the HCV proteins NS4B and NS5A, viral proteins that are absolutely required for virus replication. Disrupting the normal function of these two proteins provides for a new method of HCV treatment and should combat the emergence of drug resistance to new HCV polymerase and protease inhibitors that will be on the market in the near future.
"We are very pleased to have licensed the rights to this exciting new technology," said Omar K. Haffar, PhD, president and CEO of Presidio. "We expect to work closely with Glenn and other experts in the field to identify and test new small molecules that bind to NS4B and NS5A in order to interrupt the life cycle of the virus."
About the Hepatitis C Virus
Infections from the hepatitis C virus (HCV) have reached pandemic proportions, affecting almost 200 million people worldwide. According to the Centers for Disease Control (CDC), 3.9 million Americans have been exposed to HCV, resulting in 2.7 million cases of chronic infection, with up to 30,000 new infections occurring each year.
Source: Business Wire
Posted by Editors at 03:28 PM --- Printer-friendly version | Comments (0)
January 17, 2007
Diabetes Risk for HCV Patients Receiving Liver Transplant
Although the connection remains tentative, Hepatitis C patients who have received a liver transplant and are taking the post-transplant drug, Prograf, may be at higher risk for developing type 2 diabetes.
www.medpagetoday.com
Hepatitis C Infection Raises Diabetes Risk After Liver Transplants
VILLEJUIF, France, Jan. 8 -- Liver transplant recipients who are hepatitis C-virus (HCV) positive and receive Prograf (tacrolimus) as part of their immunosuppressant regimen are at a significantly higher risk for new-onset type 2 diabetes than HCV-negative patients, researchers here reported.
Among 211 primary liver-graft recipients, 22.7% developed new-onset diabetes, and the occurrence was higher among those treated with Prograf compared with Neoral (cyclosporine), particularly when the patients were HCV positive, found Faouzi Saliba, M.D., from the Hôpital Paul Brousse, and colleagues.
The evidence suggests that HCV status is a strong predictor of post-transplant diabetes, and that "the immunosuppressive treatment should therefore be tailored to the patient's risk, especially in case of HCV infection," the investigators wrote in the January issue of Liver Transplantation.
But the new diabetes cases may be transient, as seen by the fact that nearly all of the incident cases were taking steroids and developed diabetes within three months of their transplants, noted Paul J. Thuluvath, M.D., of Johns Hopkins in Baltimore, in an accompanying editorial.
"In a previous study, 24 of 88 patients (27%) were found to have diabetes mellitus at the end of the first postoperative year and were considered as having new-onset diabetes mellitus," Dr. Thuluvath wrote, "but at the second year after liver transplantation, only eight patients (9%) had evidence of diabetes mellitus, which implies the transient nature of diabetes mellitus in many transplant recipients."
"This may suggest that many patients in the cohort studied by Saliba et al may not have diabetes with longer follow-up, especially when corticosteroid therapy is discontinued."
Dr. Saliba and colleagues conducted a cross-sectional, multicenter retrospective study of the incidence of new-onset diabetes and potential risk factors in the 211patients who had undergone a primary liver transplant from six to 24 months earlier.
For each patient, data on demographics, immunosuppressive regimens, familial and personal histories, hepatitis status, and cardiovascular risks were collected at a single routine post-transplant visit, and the data on patients who developed new-onset diabetes were compared with those of patients in the same cohort who did not develop the disease.
They used American Diabetes Association/World Health Organization criteria to define diabetes: fasting blood glucose of more than 1.26 g/L confirmed on at least two occasions, or current treatment with an oral antidiabetic drug or insulin. They defined impaired fasting glucose as two fasting blood glucose measurements > 1.10 to < 1.26 g/L (> 6.1 and < 7.0 mmol/L) without antidiabetic therapy.
The authors found that the overall rate of new-onset diabetes was 22.7%, occurring in 24% of the 175 Prograf-treated patients, and in 16.7% of the 36 Neoral-treated patients. About four in five cases (81%) were diagnosed within three months of the transplant.
The occurrence was also significantly higher among HCV-positive patients compared with HCV-negative patients, at 41.7% vs. 18.9% respectively (P=0.008).
When they broke the data down by calicineurin inhibitor type, they found that in Prograf-treated patients, the rate of diabetes was 46.7% among those patients who were HCV positive, compared with 19.3% for those were HCV negative (P=0.0014).
Among Neoral-treated patients, 16.7% (one in six) of HCV-positive patients developed diabetes, as did 17.2% (five of 29) of HCV-negative patients. There was no significant difference between the groups.
In addition to HCV status, independent pretransplantation risk factors for new diabetes included impaired fasting glucose and a maximum lifetime body-mass index more than 25 kg/m2.
"Emergence of new onset diabetes mellitus after liver transplantation is related to risk factors that can be detected prior to the graft, like maximum lifetime BMI, impaired fasting glucose, and HCV status," the authors wrote. "Tacrolimus induced a significantly higher incidence of new onset diabetes mellitus in the HCV-positive compared to the HCV-negative patients."
In his editorial, Dr. Thulavath noted that the authors failed to clarify the role of corticosteroids in the development of post-transplant diabetes.
"It is unclear whether the actual dose or dose adjusted for body weight is more relevant for the development of corticosteroid-induced DM in transplant recipients," he wrote. "The authors do not provide data on median or mean corticosteroid dose when new-onset diabetes mellitus was diagnosed. Another concern with this study was that the diagnosis of new-onset diabetes mellitus was made on the basis of fasting blood glucose on two separate occasions. In a retrospective study from 10 centers, it may not be safe to assume that the blood glucose was drawn in a fasting state even in the most compliant patients."
Posted by Editors at 03:41 PM --- Printer-friendly version | Comments (0)
January 16, 2007
New HCV Botanical Drug Enters Clinical Trial
Utilizing Chinese medicine's long history of safe and therapeutic use, a pharmaceutical company has developed a drug derived from botanicals to treat Hepatitis C symptoms. Now that it has received FDA approval to begin clinical trials, this unique approach may become a new treatment option for Hepatitis C patients.
www.pharmalive.com
Phynova Obtains FDA Approval of its IND to Enter Into a Clinical Trial of PYN17 for the Treatment of Chronic Hepatitis C
OXFORDSHIRE, England, Jan. 8, 2007-Phynova Group PLC (AIM: PYN), a developer of pharmaceuticals derived from Chinese botanical drugs targeting viral and metabolic diseases and cancer, is pleased to announce that its first drug candidate will shortly enter into clinical trials in the US.
The Group has received approval from the US Food and Drug Administration (FDA) for an Investigational New Drug (IND) application in respect of its lead drug candidate PYN17, to proceed to the clinical trial phase. This trial will evaluate 40 patients in the USA with chronic hepatitis C (CHC).
Phynova's trial is expected to begin in Q2 2007 and will investigate the effect of PYN17 on safety and efficacy parameters. These include the key symptoms associated with CHC such as fatigue, poor concentration and abdominal pain leading to a marked deterioration in an individual's quality of life. There are no treatments currently available to effectively manage these disease symptoms.
PYN17 is a botanical drug derived from Chinese medicinal plants with a long history of safe use in humans.
Hepatitis C is a major viral disease with over 200 million sufferers worldwide including over four million in the USA.
Phynova's drug pipeline includes PYN18, an anti-viral drug for the treatment of hepatitis C and PYN22, an anti-obesity drug. In both cases patents have been filed to support these drug programmes.
Robert Miller, the CEO of Phynova said "This is a major milestone for us, validating our business model to shorten the time it takes to progress new drug candidates into human trials by developing products derived from Chinese
medicines which have a long history of use in humans. The US is the largest pharmaceutical market in the world and this approval sets us on the path to targeting that market."
Posted by Editors at 01:15 PM --- Printer-friendly version | Comments (0)
January 08, 2007
Coming Soon: More Affordable Hepatitis C Treatments
The 20-year patent on pegylated interferon is up, allowing an Indian pharmaceutical company to devise and offer an effective medication at a fraction of the cost of the current treatment. The long-time hope of HCV patients of an affordable Hepatitis C treatment may soon be realized.
Clinical trials on for low-cost hepatitis C drug
www.hindustantimes.com
Posted January 2, 2007
Treatment for hepatitis C is likely to get cheaper in the near future, with clinical trials for a new drug — called PEGylated-interferon alpha molecule — beginning in India in 2007. The new affordable drug has been developed by Dr Sunil Shaunak, professor of infectious diseases at Imperial College based at Hammersmith hospital, with scientists from Imperial College and the London School of Pharmacy.
Calling their efforts “ethical pharmaceuticals, a revolutionary new model,” Shaunk said he and his colleagues have developed a cost-effective technology that allows them open up the interferon protein, drop in a sugar molecule called PEG and close the protein. The PEGylated-interferon retains its shape and cures hepatitis C infection in many of the 170 million people affected with the disease worldwide. The new method of pegylation does not infringe existing patents because it tweaks the molecular structure of an existing drug no longer under a 20-year patent to turn it into a new medicine that can be sold much cheaper.
The efforts of Shaunak and his colleague Steve Brocchini from the London School of Pharmacy will reduce the cost of treating hepatitis C to a fraction of the current cost. It will help millions in poor countries get a cure for hepatitis C, which is a leading cause of chronic liver disease and cancer.
Hyderabad-based Shantha Biotech will manufacture the drug in India. “I have been greatly inspired by Shantha Biotech founder Varaprasad Reddy, whom I met about four years ago. The company has a record of manufacturing affordable health products. If clinical trials co-sponsored by the Indian government are successful, the new drug can be supplied the world over at an affordable price,” says Shaunak.
The new molecule, a report in the journal Nature said, appeared to be as effective as the existing drug used to treat Hepatitis C. “The aim of this work is to make affordable cures for infectious diseases for the poor people by doing most of the work in universities and hospitals using funds from charitable institutions and hospitals,” Shaunak told HT.
Posted by Editors at 09:36 AM --- Printer-friendly version | Comments (0)
January 05, 2007
Race a Factor in Fatty Liver Disease in Hepatitis C Patients
Recent research has uncovered a racial disparity in regard to fat accumulation in the livers of Hepatitis C patients. The same research also indicates that levels of insulin resistance vary among races. This discovery may prove beneficial to HCV patients if modifications to insulin resistance factors lead to controlling the progression of a fatty liver.
Posted 1/2/07
www.Eurekalert.com
Racial differences seen in steatosis in patients with hepatitis C
Caucasian patients with chronic hepatitis C virus (HCV) are more likely to have hepatic steatosis, or fat in the liver, compared to African-American patients. However, steatosis is not associated with HCV treatment response. These findings are published in the January 2007 issue of Hepatology, the official journal of the American Association for the Study of Liver Diseases (AASLD). Published by John Wiley & Sons, Inc., the journal is available online via Wiley InterScience (http://www.interscience.wiley.com/journal/hepatology).
Hepatic steatosis is common among patients with HCV and often indicates more advanced disease. Researchers, led by Hari Conjeevaram, M.D., M.S. Division of Gastroenterology at the University of Michigan at Ann Arbor, sought to investigate racial differences in the prevalence and severity of hepatic steatosis in patients with HCV, genotype 1. Additionally, they investigated the relationship between steatosis and body characteristics and other measures of insulin resistance. "We also wanted to assess whether the presence and severity of hepatic steatosis and/or insulin resistance were important factors to predict virological response in this population," the authors write.
The researchers studied 194 African-American and 205 Caucasian patients with HCV, genotype 1. All patients were participating in a multi-center prospective study of peginterferon and ribavirin therapy. The researchers compared the prevalence and severity of steatosis and steatohepatitis to demographic, lifestyle and clinical characteristics. They also investigated relationships between sustained virological response and both steatosis and insulin resistance.
The researchers found hepatic steatosis in 61 percent of the African-American patients and 65 percent of Caucasian patients. In a univariable analysis, the steatosis was associated with HOMA-IR (a measure of insulin resistance), body mass index, waist circumference, serum triglycerides, aminotransferase levels, and histological scores for inflammation and fibrosis. After adjusting for those features, they found that African-Americans had a dramatically lower risk of steatosis. For a given degree of overweight and obesity or insulin resistance, African-Americans were approximately half as likely to have hepatic steatosis. After examining patient characteristics and their responsiveness to treatment, the authors report, "insulin resistance and fibrosis are important and obesity and steatosis may be less or not as important."
The results may have been confounded by patients taking oral anti-diabetic agents, and by the possibility that HOMA underestimated the degree of insulin resistance in overtly diabetic patients.
Still, "the importance of these findings is that insulin resistance is a potentially modifiable factor, so that responses to antiviral therapy in hepatitis C may be improved by modulation of insulin signaling and improvements in insulin resistance and glucose control. These possibilities deserve prospective evaluation," they conclude.
Posted by Editors at 10:35 AM --- Printer-friendly version | Comments (0)
January 04, 2007
Hepatitis C Immune Response Breakthrough
University of Texas researchers have recently identified the mechanism controlling the body's fight against Hepatitis C. This groundbreaking research is already being utilized to design new treatments allowing the body to clear this and other viruses.
Posted 12/29/06
Star Community Newspapers
www.carrolltonleader.com
DALLAS — Much like flipping a light switch, the hepatitis C virus turns on human immune defenses upon entering the body but also turns off those defenses by manipulating interaction of key cellular proteins, UT Southwestern Medical Center researchers have found.
This same molecular “on/off switch” controls immunity against many viruses, highlighting a potential new target for novel therapeutics to fight viruses, the researchers report.
In a study available online and in an upcoming issue of the “Proceedings of the National Academy of Sciences,” UT Southwestern scientists describe how the proteins RIG-I and LGP2 normally interact to turn on and off immune response to hepatitis C.
It’s known that when a virus invades a cell, the RIG-I protein triggers the body to generate an immune response. Once the virus has been cleared out, the LGP2 protein turns off the RIG-I signals.
This interaction between RIG-I and LGP2 is vital for properly regulating immunity, but viruses such as hepatitis C can disrupt the normal process to shut down immune defenses early, the research team found.
“This knowledge will help us design drugs that mimic the viral effects on these proteins to either activate a host’s immune response or shut it down,” said Dr. Michael Gale, associate professor of microbiology and the study’s senior author. “This holds great potential in developing new disease therapies, because the tactics employed by hepatitis C to trigger immune response are similar to those employed by other viruses such as West Nile, influenza and the common cold.”
Dr. Gale’s research centers on studying the mechanisms viruses use to evade immune defenses. Of particular interest is the hepatitis C virus, a blood-borne infection transmitted by intravenous drug use, blood transfusions and sexual contact. It affects 4 million U.S. residents and is the nation’s leading cause of cirrhosis and liver cancer.
In 2005 Dr. Gale, of Carrollton, and his team completed several breakthrough studies on hepatitis C, discovering that the RIG-I protein binds to viral genetic material. Then, RIG-I changes its shape and sends signals to other proteins that spur production of interferon, a molecule that stops viral replication. The researchers also found that the virus launches a counterattack on RIG-I, producing a protein called a protease to disrupt the signaling process, preventing interferon production and allowing viral replication.
Just how RIG-I signaling is normally regulated, however, hadn’t been known.
In the current study, UT Southwestern researchers found that RIG-I and LGP2 each contain a repressor domain, a sort of docking site that controls the actions of each protein. The domain is the key site that regulates the ability of RIG-I to bind to its signaling partners, including LGP2, acting as a switch for controlling immune response, Dr. Gale said.
“Hepatitis C and others viruses hijack this signaling pathway to stop immune defenses,” he said.
His research team and others are working to design novel therapeutics and drugs that could mimic viral effects on RIG-I to spur antiviral response or, conversely, mimic viral effects on LGP2 to shut down RIG-I activity. RIG-I shutdown would be necessary in cases when the immune system’s response to a virus is dangerously overactive, which happened in many flu cases during the 1918 pandemic.
“Fine-tuning immune response to infection is where antiviral or immune regulatory drugs are headed,” said Dr. Gale, a Nancy Cain and Jeffrey A. Marcus Scholar in Medical Research, in Honor of Dr. Bill S. Vowell.
Other UT Southwestern researchers involved in the study were microbiology postdoctoral researcher and lead author Dr. Takeshi Saito; microbiology postdoctoral researcher Dr. Yueh-Ming Loo; graduate student researchers Cynthia Johnson and David Owen; and Dr. Sangita Sinha, an instructor in internal medicine. Researchers from Kyoto University and Osaka University in Japan also were involved in the study.
The National Institutes of Health, the Burroughs Wellcome Fund and Mr. and Mrs. R. Batcheldor supported the study.
Posted by Editors at 11:57 AM --- Printer-friendly version | Comments (0)