Find out the four characteristics of outrigger canoeing that make it a sport with a unique attribute – promoting a healthy liver.
by Nicole Cutler, L.Ac.
Considered the state sport of Hawaii, outrigger canoe racing is an activity with historical roots in Southeast Asia, Polynesia and New Zealand. Over the past few decades, outrigger canoeing has steadily grown in popularity with recreational and competitive clubs strewn across the United States. While paddling an outrigger canoe may not appeal to everyone, this water sport has a number of features that make it ideal for benefiting liver health.
What Is an Outrigger Canoe?
An outrigger canoe is a type of canoe containing one or more outriggers (lateral support floats) fastened to the side of the boat. Some characteristics of this vessel, include:
· Compared to other types of canoes, outrigger canoes can move very fast.
· Most outrigger canoes seat six people, each of whom is important to the boat’s movement.
· Having an attached outrigger increases the canoe’s stability, which reduces its tendency to capsize in rough water.
Besides the canoe itself being unique, an outrigger’s paddling technique also differs from other non-motor powered boats. Different from kayaking or rowing, the outrigger paddle is single-sided, with either a straight or a double-bend shaft. Because there isn’t a dual paddle arrangement, the paddler has to alternate sides often in order to maintain stamina and stability.
Liver Reasons to Paddle
There are several reasons that outrigger canoeing is a great choice for those wanting to support their liver’s health:
1. Cardiovascular Exercise – By preventing or even reversing fatty liver disease, and helping ease portal hypertension, cardiovascular exercise helps people maintain a healthy weight and keeps blood flowing freely throughout the body (including the liver). As a vigorous cardiovascular exercise, outrigger canoeing can burn an estimated 400 calories per hour.
2. Torso Movement – Unlike most sports, outrigger paddling recruits the body’s larger muscle groups in the mid-section – exactly where the liver is housed. Because the strength to power a canoe comes mainly from twisting the torso, there is a great deal of movement in this area. Thus, paddling puts a physical demand on the body’s mid-section, which stimulates the filling and draining of the liver, the natural process necessary for the liver to cleanse the blood.
3. Optimistic Attitude – Besides its associated physical health benefits, paddling in a river, ocean, bay or lake also initiates a positive mental and emotional shift. An active way to appreciate the outdoors, paddling can be peaceful and meditative or it can be exhilarating. In addition, the breaking of the surface tension of water (by waves, falls or a canoe) releases negative hydrogen ions into the atmosphere. One of the many reported health benefits of negative hydrogen ions is to boost serotonin levels, a surefire way to lift one’s mood.
4. No Age Limit – Because it is a low-impact activity with a rich cultural history, outrigger canoeing welcomes people of all ages. Not having an age limit can be important to those who have surpassed 30 years of age and want to get involved in a team sport. In fact, competitive outrigger racing is divided into the following categories: “Open,” which includes those aged 20 to 35 (but is open to any age), “Masters,” which includes those aged 35 to 45, “Senior Masters,” which includes those aged 45 to 55 and “Kapuna,” which includes those aged 55 and up.
Outrigger Tips
If outrigger canoeing might be the sport you are looking for, these two suggestions can help guide you further:
1. Join a Club – The best way to learn about outrigger canoeing is through a local canoe club. Besides learning the proper paddling technique, a club provides the camaraderie inherent to this sport and assures safety issues are addressed.
2. Brush Up On Swimming – Since paddling involves the occasional tip into the water, it is important to be a competent swimmer. If necessary, brush up on your swimming skills so that you can feel confident in a canoe.
If keeping your liver healthy is a priority and group water sports appeals to you, consider outrigger canoeing. Because it is a low-impact cardiovascular exercise, stimulates liver activity by moving the torso, is known to lift the mood and has no age restriction, paddling in an outrigger canoe is an ultimate activity for taking care of your liver.
References:
http://en.wikipedia.org/wiki/Outrigger_canoe , Outrigger Canoe, Retrieved July 31, 2009, Wikimedia Foundation, Inc., 2009.
http://nsmc.staywellsolutionsonline.com/Features/1,2923 , Kayak Your Way to Better Health, Retrieved July 31, 2009, North Shore Medical Center, 2009.
http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Canoeing_and_kayaking?OpenDocument , Canoeing and kayaking - health benefits, Retrieved July 31, 2009, State of Victoria, March 2009.
http://www.health-benefit-of-water.com/negative-ions.html , Water generates Negative Ions, Retrieved August 1, 2009, health-benefit-of-water.com, 2009.
http://www.sheknows.com/articles/7258.htm , Benefits of canoeing and kayaking, Retrieved July 31, 2009, SheKnows LLC, 2009.
http://www.thecancerblog.com/2006/03/08/dragon-boat-races-breast-cancer-survivors-paddle-to-prevention/ , Dragon Boat Races: breast cancer survivors paddle to prevention, Dalene Entenmann, Retrieved July 31, 2009, Weblogs, Inc., 2009.
.
http://www.liversupport.com/wordpress/2010/06/a-sport-crafted-for-liver-health/
June 18, 2010
Splicing Diversity of the Human OCLN Gene and Its Biological Significance for Hepatitis C Virus Entry
Journal of Virology, July 2010, p. 6987-6994, Vol. 84, No. 14
0022-538X/10/$012.00+0 doi:10.1128/JVI.00196-10
Copyright © 2010, American Society for Microbiology. All Rights Reserved.
Indu Kohaar,1 Alexander Ploss,2 Evgenia Korol,2 Kathy Mu,2 John W. Schoggins,2 Thomas R. O'Brien,3 Charles M. Rice,2 and Ludmila Prokunina-Olsson1*
Laboratory of Translational Genomics,1 Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892,3 Center for the Study of Hepatitis C, Laboratory of Virology and Infectious Diseases, The Rockefeller University, 1230 York Avenue, Box 64, New York, New York 100652
Received 27 January 2010/ Accepted 29 April 2010
Persistent hepatitis C virus (HCV) infection is a primary etiological factor for the development of chronic liver disease, including cirrhosis and cancer. A recent study identified occludin (OCLN), an integral tight junction protein, as one of the key factors for HCV entry into cells. We explored the splicing diversity of OCLN in normal human liver and observed variable expression of alternative splice variants, including two known forms (WT-OCLN and OCLN-ex4del) and six novel forms (OCLN-ex7ext, OCLN-ex3pdel, OCLN-ex3del, OCLN-ex3-4del, OCLN-ex3p-9pdel, and OCLN-ex3p-7pdel). Recombinant protein isoforms WT-OCLN and OCLN-ex7ext, which retained the HCV-interacting MARVEL domain, were expressed on the cell membrane and were permissive for HCV infection in in vitro infectivity assays. All other forms lacked the MARVEL domain, were expressed in the cytoplasm, and were nonpermissive for HCV infection. Additionally, we observed variable expression of OCLN splicing forms across human tissues and cell lines. Our study suggests that the remarkable natural splicing diversity of OCLN might contribute to HCV tissue tropism and possibly modify the outcome of HCV infection in humans. Genetic factors crucial for regulation of OCLN expression and susceptibility to HCV infection remain to be elucidated.
* Corresponding author. Mailing address: Laboratory of Translational Genomics, National Cancer Institute, National Institutes of Health, 8717 Grovemont Circle, Bethesda, MD 20892-4605. Phone: (301) 443-5297. Fax: (301) 443-3234. E-mail: prokuninal@mail.nih.gov
Published ahead of print on 12 May 2010.
Supplemental material for this article may be found at http://jvi.asm.org/ .
Journal of Virology, July 2010, p. 6987-6994, Vol. 84, No. 14
0022-538X/10/$012.00+0 doi:10.1128/JVI.00196-10
Copyright © 2010, American Society for Microbiology. All Rights Reserved
http://jvi.asm.org/cgi/content/abstract/84/14/6987?view=short&fp=6987&vol=84&lookupType=volpage
0022-538X/10/$012.00+0 doi:10.1128/JVI.00196-10
Copyright © 2010, American Society for Microbiology. All Rights Reserved.
Indu Kohaar,1 Alexander Ploss,2 Evgenia Korol,2 Kathy Mu,2 John W. Schoggins,2 Thomas R. O'Brien,3 Charles M. Rice,2 and Ludmila Prokunina-Olsson1*
Laboratory of Translational Genomics,1 Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892,3 Center for the Study of Hepatitis C, Laboratory of Virology and Infectious Diseases, The Rockefeller University, 1230 York Avenue, Box 64, New York, New York 100652
Received 27 January 2010/ Accepted 29 April 2010
Persistent hepatitis C virus (HCV) infection is a primary etiological factor for the development of chronic liver disease, including cirrhosis and cancer. A recent study identified occludin (OCLN), an integral tight junction protein, as one of the key factors for HCV entry into cells. We explored the splicing diversity of OCLN in normal human liver and observed variable expression of alternative splice variants, including two known forms (WT-OCLN and OCLN-ex4del) and six novel forms (OCLN-ex7ext, OCLN-ex3pdel, OCLN-ex3del, OCLN-ex3-4del, OCLN-ex3p-9pdel, and OCLN-ex3p-7pdel). Recombinant protein isoforms WT-OCLN and OCLN-ex7ext, which retained the HCV-interacting MARVEL domain, were expressed on the cell membrane and were permissive for HCV infection in in vitro infectivity assays. All other forms lacked the MARVEL domain, were expressed in the cytoplasm, and were nonpermissive for HCV infection. Additionally, we observed variable expression of OCLN splicing forms across human tissues and cell lines. Our study suggests that the remarkable natural splicing diversity of OCLN might contribute to HCV tissue tropism and possibly modify the outcome of HCV infection in humans. Genetic factors crucial for regulation of OCLN expression and susceptibility to HCV infection remain to be elucidated.
* Corresponding author. Mailing address: Laboratory of Translational Genomics, National Cancer Institute, National Institutes of Health, 8717 Grovemont Circle, Bethesda, MD 20892-4605. Phone: (301) 443-5297. Fax: (301) 443-3234. E-mail: prokuninal@mail.nih.gov
Published ahead of print on 12 May 2010.
Supplemental material for this article may be found at http://jvi.asm.org/ .
Journal of Virology, July 2010, p. 6987-6994, Vol. 84, No. 14
0022-538X/10/$012.00+0 doi:10.1128/JVI.00196-10
Copyright © 2010, American Society for Microbiology. All Rights Reserved
http://jvi.asm.org/cgi/content/abstract/84/14/6987?view=short&fp=6987&vol=84&lookupType=volpage
HCV Rapidly Develops Resistance to Directing-acting Agents, Indicating Need for Multidrug Combos
SUMMARY: The hepatitis C virus (HCV) can rapidly develop mutations that confer resistance to multiple direct-acting agents such as HCV protease and polymerase inhibitors, according to a mathematical model described in the May 5, 2010 edition of Science Translational Medicine. Researchers suggested that effective oral therapy without interferon may require as many as 4 complementary drugs to avoid resistance.
Standard therapy for chronic hepatitis C using pegylated interferon plus ribavirin can cause difficult side effects and only clears the virus about half the time, leading researchers to evaluate a large number of direct-acting oral drugs that target specific steps of the viral lifecycle.
But HCV mutates easily and rapidly as it replicates, which allows for emergence of drug resistance mutations. Recent research indicates that resistance mutations are common, and in order for these agents to have prolonged effectiveness without interferon, some people may require "cocktails" of as many as 4 drugs that work in different ways.
Below is the text of a press release issued by the University of Illinois at Chicago summarizing the modeling study.
Combination of Direct Antivirals May Be Key to Curing Hep C
Chicago -- May 5, 2010 -- A combination of antiviral drugs may be needed to combat the drug resistance that rapidly develops in potentially deadly hepatitis C infections, a new study using sophisticated computer and mathematical modeling has shown.
Using probabilistic and viral dynamic models, researchers at the University of Illinois at Chicago, Oakland University and Los Alamos National Laboratory predict why rapid resistance emerges in hepatitis C virus and show that a combination of drugs that can fight three or more mutated strains may be needed to eradicate the virus from the body. They compared their model with data from a clinical trial of the new direct-acting antiviral medication telaprevir.
The findings are published in Science Translational Medicine.
Hepatitis C is a progressive liver disease that can lead to cirrhosis and liver cancer. Current standard treatment is a combination of the antiviral drugs interferon and ribavirin for a period of 24 to 48 weeks -- a regimen that is long and expensive, carries side effects, and is successful only in about half of patients.
Intensive effort has focused on developing direct antiviral drugs. But the virus is genetically diverse, and so may be particularly prone to develop resistance, said Harel Dahari, research assistant professor of hepatology in the UIC College of Medicine and one of the paper's co-authors.
One way to combat resistance would be to administer multiple drugs, each with a different mechanism of inhibiting the virus.
"We found that rapid emergence of resistance to these types of drugs is due to a population of viruses already present, allowing the resistant virus to become the dominant strain," said Dahari.
The researchers suggest that a combination of new antiviral drugs will be needed to fight all of the resistant virus strains and achieve better cure rates for the disease.
"We are moving to a new era where we can treat these patients with direct-acting agents against the virus, in which we specifically target the life-cycle of the virus," Dahari said.
To replace the standard treatment, four or more different types of direct drugs may be needed, Dahari said. However, some patients may need fewer drugs. It depends on the level of the virus in their blood, among other factors.
It is frustrating for patients to go through a long, difficult treatment and know that they might not be cured, said Dr. Scott Cotler, associate professor of medicine at UIC and a hepatologist who treats patients at the University of Illinois Medical Center's Walter Payton Liver Center.
"Patients are looking forward to a day when they don't have to take interferon and ribavirin," said Cotler. "But as we are learning with this study, if we are going to need four different direct drugs, it is going to be awhile before we get there. Now at least we know where the goal line is."
Dahari suggests that future treatment that includes the standard treatment and direct antivirals, such as telaprevir or boceprevir, will be tailored to each patient and that using direct antivirals may also shorten the duration of treatment.
Investigator affiliations: Theoretical Biology and Biophysics, Los Alamos National Laboratory, Los Alamos, NM; Department of Mathematics and Statistics and Center for Biomedical Research, Oakland University, Rochester, MI; Department of Medicine, University of Illinois, Chicago, IL.
6/18/10
Source
University of Illinois at Chicago. HCV Rapidly Develops Resistance to Directing-acting Agents Indicating Need for Multidrug Combos. Press release. May 5, 2010.
References
L Rong, H Dahari, RM Ribeiro, and others. Rapid Emergence of Protease Inhibitor Resistance in Hepatitis C Virus. Science Translational Medicine 2(30): 30ra32 (Abstract). May 5, 2010.
DL Wyles and RT Schooley. Rong's Numbers: Accelerating Progress in HCV Therapeutic Research (Editorial). Science Translational Medicine 2(33):33ps25. May 26, 2010.
http://www.hivandhepatitis.com/hep_c/news/2010/0618_2010_b.html
Standard therapy for chronic hepatitis C using pegylated interferon plus ribavirin can cause difficult side effects and only clears the virus about half the time, leading researchers to evaluate a large number of direct-acting oral drugs that target specific steps of the viral lifecycle.
But HCV mutates easily and rapidly as it replicates, which allows for emergence of drug resistance mutations. Recent research indicates that resistance mutations are common, and in order for these agents to have prolonged effectiveness without interferon, some people may require "cocktails" of as many as 4 drugs that work in different ways.
Below is the text of a press release issued by the University of Illinois at Chicago summarizing the modeling study.
Combination of Direct Antivirals May Be Key to Curing Hep C
Chicago -- May 5, 2010 -- A combination of antiviral drugs may be needed to combat the drug resistance that rapidly develops in potentially deadly hepatitis C infections, a new study using sophisticated computer and mathematical modeling has shown.
Using probabilistic and viral dynamic models, researchers at the University of Illinois at Chicago, Oakland University and Los Alamos National Laboratory predict why rapid resistance emerges in hepatitis C virus and show that a combination of drugs that can fight three or more mutated strains may be needed to eradicate the virus from the body. They compared their model with data from a clinical trial of the new direct-acting antiviral medication telaprevir.
The findings are published in Science Translational Medicine.
Hepatitis C is a progressive liver disease that can lead to cirrhosis and liver cancer. Current standard treatment is a combination of the antiviral drugs interferon and ribavirin for a period of 24 to 48 weeks -- a regimen that is long and expensive, carries side effects, and is successful only in about half of patients.
Intensive effort has focused on developing direct antiviral drugs. But the virus is genetically diverse, and so may be particularly prone to develop resistance, said Harel Dahari, research assistant professor of hepatology in the UIC College of Medicine and one of the paper's co-authors.
One way to combat resistance would be to administer multiple drugs, each with a different mechanism of inhibiting the virus.
"We found that rapid emergence of resistance to these types of drugs is due to a population of viruses already present, allowing the resistant virus to become the dominant strain," said Dahari.
The researchers suggest that a combination of new antiviral drugs will be needed to fight all of the resistant virus strains and achieve better cure rates for the disease.
"We are moving to a new era where we can treat these patients with direct-acting agents against the virus, in which we specifically target the life-cycle of the virus," Dahari said.
To replace the standard treatment, four or more different types of direct drugs may be needed, Dahari said. However, some patients may need fewer drugs. It depends on the level of the virus in their blood, among other factors.
It is frustrating for patients to go through a long, difficult treatment and know that they might not be cured, said Dr. Scott Cotler, associate professor of medicine at UIC and a hepatologist who treats patients at the University of Illinois Medical Center's Walter Payton Liver Center.
"Patients are looking forward to a day when they don't have to take interferon and ribavirin," said Cotler. "But as we are learning with this study, if we are going to need four different direct drugs, it is going to be awhile before we get there. Now at least we know where the goal line is."
Dahari suggests that future treatment that includes the standard treatment and direct antivirals, such as telaprevir or boceprevir, will be tailored to each patient and that using direct antivirals may also shorten the duration of treatment.
Investigator affiliations: Theoretical Biology and Biophysics, Los Alamos National Laboratory, Los Alamos, NM; Department of Mathematics and Statistics and Center for Biomedical Research, Oakland University, Rochester, MI; Department of Medicine, University of Illinois, Chicago, IL.
6/18/10
Source
University of Illinois at Chicago. HCV Rapidly Develops Resistance to Directing-acting Agents Indicating Need for Multidrug Combos. Press release. May 5, 2010.
References
L Rong, H Dahari, RM Ribeiro, and others. Rapid Emergence of Protease Inhibitor Resistance in Hepatitis C Virus. Science Translational Medicine 2(30): 30ra32 (Abstract). May 5, 2010.
DL Wyles and RT Schooley. Rong's Numbers: Accelerating Progress in HCV Therapeutic Research (Editorial). Science Translational Medicine 2(33):33ps25. May 26, 2010.
http://www.hivandhepatitis.com/hep_c/news/2010/0618_2010_b.html
Idenix Begins Proof-of-Concept Study of HCV Protease Inhibitor IDX320
SUMMARY: Idenix Pharmaceuticals announced last week that it has started a 3-day proof-of-concept study of its experimental hepatitis C virus (HCV) protease inhibitor IDX320. As previously reported, researchers presented data at the recent EASL conference showing that IDX320 showed good anti-HCV activity in laboratory studies and had good pharmacokinetic and safety profiles in animals and HCV negative volunteers. If the latest study produces favorable results, the company expects to test IDX320 and its investigational HCV polymerase inhibitor IDX184 as a combination regimen.
Below is an excerpt from a recent Idenix press release describing the drugs and the new study.
Idenix Pharmaceuticals Initiates Proof-of-Concept Study for Protease Inhibitor IDX320 in Hepatitis C Patients
Cambridge, Mass. -- June 10, 2010 -- Idenix Pharmaceuticals, Inc. (Nasdaq: IDIX), a biopharmaceutical company engaged in the discovery and development of drugs for the treatment of human viral diseases, today announced that it has initiated a 3-day proof-of-concept study of IDX320, a protease inhibitor for the treatment of hepatitis C virus (HCV) infection, under a Clinical Trial Application (CTA). The study is evaluating IDX320 in treatment-naive hepatitis C genotype 1-infected patients.
"The potent and multi-genotypic activity demonstrated in vitro, as well as the favorable pharmacokinetics observed in healthy volunteers, suggests a promising profile for further development of IDX320," said Jean-Pierre Sommadossi, PhD, chief executive officer of Idenix. "The landscape for combination development in HCV is evolving quickly. Assuming favorable results from the IDX320 proof-of-concept study, we plan to discuss with regulatory agencies a direct-acting antiviral combination strategy with IDX320 and IDX184, our HCV nucleotide polymerase inhibitor."
Douglas Mayers, MD, Idenix's chief medical officer commented, "We are encouraged by the results seen to date with IDX320 and are hopeful that future clinical studies will allow us to continue advancing this program with the ultimate goal of treating a wide range of patients infected with HCV."
The proof-of-concept trial in HCV-infected patients is a Phase I/II randomized, parallel-arm, double-blind, placebo-controlled study evaluating the safety and antiviral activity of IDX320 in treatment-naive adult patients infected with chronic hepatitis C. The study will evaluate four doses of IDX320, ranging from 50 to 400 mg once-per-day, administered for three days. Each cohort of the study will evaluate eight patients randomized six to IDX320 and two to placebo.
About IDX320
IDX320, a macrocyclic HCV protease inhibitor, is an inhibitor of NS3/4A proteases from genotypes 1a, 1b, 2a and 4a (IC50 values from 0.8 to 1.9 nM), as well as from genotype 3a (IC50=23 nM). IDX320 did not inhibit nine tested cellular proteases (IC50 > 10 uM) in vitro, suggesting high selectivity. IDX320 bound tightly to the HCV protease enzyme with a long dissociation half-life (> 9 hours). After single 2 mg/kg oral doses of IDX320 in two animal species, favorable bioavailability and a long plasma half-life were observed, with substantial plasma concentrations 24 hours post dose. Comparable drug exposure was confirmed in healthy volunteers (n=6) receiving a single 200 mg oral dose. Further, no significant in vitro inhibition of human drug metabolizing enzymes, CYP450s and UGT1A1, by IDX320 suggests low potential for drug-drug interactions in patients.
About IDX184
IDX184 is a novel, liver-targeted nucleotide prodrug of 2'-methyl guanosine monophosphate, which includes Idenix's proprietary liver-targeting technology. This technology enables the delivery of nucleoside monophosphate to the liver, leading to the formation of high levels of nucleoside triphosphate, potentially maximizing drug efficacy and limiting systemic side effects with low, once-daily dosing. IDX184 in combination with pegylated interferon and ribavirin has demonstrated a generally favorable safety profile and potent antiviral activity in an ongoing Phase IIa study.
About Idenix
Idenix Pharmaceuticals, Inc., headquartered in Cambridge, Massachusetts, is a biopharmaceutical company engaged in the discovery and development of drugs for the treatment of human viral diseases. Idenix's current focus is on the treatment of patients with chronic hepatitis C infection.
For further information about Idenix, please refer to http://www.idenix.com/ .
6/8/10
Source
Idenix Pharmaceuticals. Idenix Pharmaceuticals Initiates Proof-of-Concept Study for Protease Inhibitor IDX320 in Hepatitis C Patients. Press release. June 10, 2010.
http://www.hivandhepatitis.com/hep_c/news/2010/0618_2010_a.html
Below is an excerpt from a recent Idenix press release describing the drugs and the new study.
Idenix Pharmaceuticals Initiates Proof-of-Concept Study for Protease Inhibitor IDX320 in Hepatitis C Patients
Cambridge, Mass. -- June 10, 2010 -- Idenix Pharmaceuticals, Inc. (Nasdaq: IDIX), a biopharmaceutical company engaged in the discovery and development of drugs for the treatment of human viral diseases, today announced that it has initiated a 3-day proof-of-concept study of IDX320, a protease inhibitor for the treatment of hepatitis C virus (HCV) infection, under a Clinical Trial Application (CTA). The study is evaluating IDX320 in treatment-naive hepatitis C genotype 1-infected patients.
"The potent and multi-genotypic activity demonstrated in vitro, as well as the favorable pharmacokinetics observed in healthy volunteers, suggests a promising profile for further development of IDX320," said Jean-Pierre Sommadossi, PhD, chief executive officer of Idenix. "The landscape for combination development in HCV is evolving quickly. Assuming favorable results from the IDX320 proof-of-concept study, we plan to discuss with regulatory agencies a direct-acting antiviral combination strategy with IDX320 and IDX184, our HCV nucleotide polymerase inhibitor."
Douglas Mayers, MD, Idenix's chief medical officer commented, "We are encouraged by the results seen to date with IDX320 and are hopeful that future clinical studies will allow us to continue advancing this program with the ultimate goal of treating a wide range of patients infected with HCV."
The proof-of-concept trial in HCV-infected patients is a Phase I/II randomized, parallel-arm, double-blind, placebo-controlled study evaluating the safety and antiviral activity of IDX320 in treatment-naive adult patients infected with chronic hepatitis C. The study will evaluate four doses of IDX320, ranging from 50 to 400 mg once-per-day, administered for three days. Each cohort of the study will evaluate eight patients randomized six to IDX320 and two to placebo.
About IDX320
IDX320, a macrocyclic HCV protease inhibitor, is an inhibitor of NS3/4A proteases from genotypes 1a, 1b, 2a and 4a (IC50 values from 0.8 to 1.9 nM), as well as from genotype 3a (IC50=23 nM). IDX320 did not inhibit nine tested cellular proteases (IC50 > 10 uM) in vitro, suggesting high selectivity. IDX320 bound tightly to the HCV protease enzyme with a long dissociation half-life (> 9 hours). After single 2 mg/kg oral doses of IDX320 in two animal species, favorable bioavailability and a long plasma half-life were observed, with substantial plasma concentrations 24 hours post dose. Comparable drug exposure was confirmed in healthy volunteers (n=6) receiving a single 200 mg oral dose. Further, no significant in vitro inhibition of human drug metabolizing enzymes, CYP450s and UGT1A1, by IDX320 suggests low potential for drug-drug interactions in patients.
About IDX184
IDX184 is a novel, liver-targeted nucleotide prodrug of 2'-methyl guanosine monophosphate, which includes Idenix's proprietary liver-targeting technology. This technology enables the delivery of nucleoside monophosphate to the liver, leading to the formation of high levels of nucleoside triphosphate, potentially maximizing drug efficacy and limiting systemic side effects with low, once-daily dosing. IDX184 in combination with pegylated interferon and ribavirin has demonstrated a generally favorable safety profile and potent antiviral activity in an ongoing Phase IIa study.
About Idenix
Idenix Pharmaceuticals, Inc., headquartered in Cambridge, Massachusetts, is a biopharmaceutical company engaged in the discovery and development of drugs for the treatment of human viral diseases. Idenix's current focus is on the treatment of patients with chronic hepatitis C infection.
For further information about Idenix, please refer to http://www.idenix.com/ .
6/8/10
Source
Idenix Pharmaceuticals. Idenix Pharmaceuticals Initiates Proof-of-Concept Study for Protease Inhibitor IDX320 in Hepatitis C Patients. Press release. June 10, 2010.
http://www.hivandhepatitis.com/hep_c/news/2010/0618_2010_a.html
WHEN GOOD DRUGS DO BAD THINGS
If your organs had a personality, your liver would be the strong, silent type. No matter how hard it works at filtering out toxins like alcohol and drugs, it doesn't complain until it's on the verge of collapse. And when we say drugs, we don't mean the illegal kind. We're talking about the dozens of meds with liver-damage potential. The weight-loss aid called orlistat - aka Xenical and Alli - is the latest med that has to include liver cautions on its label. Luckily for us and you, the liver has a remarkable ability to give itself a makeover. So if you do have a DILI (drug-induced liver injury), stopping the med and treating your liver right - no alcohol, for starters - usually will restore it to health, as long as it was in good shape to begin with. But since the liver isn't a whiner, the trick is to spot the damage before it makes your skin itch and turns your eyeballs yellow, your pee dark and your poop pale. Some DILI-defending tips: Read the fine print. You know those package inserts with the tiny type. Get out your magnifier and read it. Cautions about liver damage will make you more alert to warning signs (below). Don't ignore vague symptoms. Nausea, poor appetite, malaise and just not feeling great - especially shortly after starting a medication - can precede the obvious symptoms. Get the tests. Liver-function tests are advised even before treatment begins with some meds, such as terbinafine (e.g., Lamisil), the nail fungus drug. Don't blow them off.
http://telegraphjournal.canadaeast.com/magazine/article/1090306
http://telegraphjournal.canadaeast.com/magazine/article/1090306
Blueberries may benefit people with liver diseases
2010-06-18 15:30:00
Last Updated: 2010-06-18 16:11:33
Washington: A new research indicates that blueberries could provide relief to patients suffering from liver diseases - especially hepatic fibrosis.
A study led by Ming-Liang Cheng, MD, from Department of Infectious Diseases, Guiyang Medical College, Guiyang, presented some data from their research on the effectiveness of blueberries on liver fibrosis induced in laboratory animals.
The study shows that blueberries could reduce liver indices, serum levels of hyaluronic acid and alanine aminotransferase, and increase levels of superoxide dismutase and decrease levels of malondialdehyde in liver homogenates compared with the model group. The stage of hepatic fibrosis was also significantly weakened.
The authors suggest that blueberry consumption is beneficial for hepatic diseases including fibrosis.
The study will be published on June 7, 2010 in the World Journal of Gastroenterology.
http://sify.com/news/blueberries-may-benefit-people-with-liver-diseases-news-international-kgsp4djaeef.html
Last Updated: 2010-06-18 16:11:33
Washington: A new research indicates that blueberries could provide relief to patients suffering from liver diseases - especially hepatic fibrosis.
A study led by Ming-Liang Cheng, MD, from Department of Infectious Diseases, Guiyang Medical College, Guiyang, presented some data from their research on the effectiveness of blueberries on liver fibrosis induced in laboratory animals.
The study shows that blueberries could reduce liver indices, serum levels of hyaluronic acid and alanine aminotransferase, and increase levels of superoxide dismutase and decrease levels of malondialdehyde in liver homogenates compared with the model group. The stage of hepatic fibrosis was also significantly weakened.
The authors suggest that blueberry consumption is beneficial for hepatic diseases including fibrosis.
The study will be published on June 7, 2010 in the World Journal of Gastroenterology.
http://sify.com/news/blueberries-may-benefit-people-with-liver-diseases-news-international-kgsp4djaeef.html
Improving HCV Response With Insulin Resistance
June 9, 2010
Could insulin resistance be getting in the way of your Hepatitis C treatment? To manage this possible complication, discover why many experts advise prescribing medications to manage insulin resistance in an effort to improve Hepatitis C treatment outcomes.
by Nicole Cutler, L.Ac.
Occurring in up to half of American adults, insulin resistance describes when the body can't properly use insulin to maintain normal blood sugar levels. Unfortunate for those affected, research has consistently shown that those with Hepatitis C infection and insulin resistance are more likely to suffer from liver disease progression. Thus, scientists around the globe have been focusing on how to improve the therapeutic outcome of those with insulin resistance who are battling the Hepatitis C virus.
In their search for a common denominator uniting the growing prevalence of obesity, fatty liver disease, congestive heart failure, high cholesterol, elevated blood pressure and diabetes mellitus, health officials agree that insulin resistance appears to fit the profile. Generalized descriptions of the events that lead to insulin resistance are described below:
· Released by the pancreas, insulin is dispersed into the bloodstream in response to elevated blood sugar (glucose) levels.
· By pushing glucose out of the bloodstream and into the body's cells, insulin keeps blood glucose levels from becoming too elevated and allows cells to convert glucose into energy.
· Insulin-resistant cells do not allow for the proper conversion of glucose into energy, resulting in fatigue.
· This resistance to insulin does not permit glucose to enter the cells but, rather, causes it to accumulate in the blood.
· In an attempt to reduce the glucose levels in the blood, the body signals the pancreas to produce and release even more insulin.
· The cycle of insulin-resistant cells causes even more insulin to be released, resulting in high blood insulin levels, which could potentially develop into Type 2 diabetes mellitus.
Several studies have shown that people with chronic Hepatitis C are more likely to have insulin resistance or diabetes than those without Hepatitis C. In addition, insulin resistance is associated with a poorer response to interferon-based therapy. To manage this complication, many experts advise prescribing medications to manage insulin resistance in an effort to improve Hepatitis C treatment outcomes.
As revealed at the 2008 American Association for the Study of Liver Diseases Meeting and published in the August 2009 edition of Hepatology, Spanish researchers found that metformin improved virologic response when added to Hepatitis C interferon-ribavirin therapy in those with insulin resistance. Also known by one of its brand names Glucophage, metformin is an oral medication that helps lower blood sugar in three ways:
1. It lowers the amount of glucose absorbed from food.
2. It lowers the amount of glucose produced by the liver.
3. It increases the body's response to insulin.
Led by Manuel Romero-Gomez, MD, of Valme University Hospital in Seville, 123 patients with genotype 1 Hepatitis C and insulin resistance [homeostasis model of insulin resistance (HOMA) greater than 2] received standard peginterferon-alpha-2a/ribavirin antiviral therapy plus metformin or matching placebo. After six months, the following was determined:
· 67.4 percent of the metformin group had sustained virologic response compared with 49.1 percent of the placebo group
· 57.7 percent of women in the metformin group had sustained virologic response compared with 28.6 percent of women in the placebo group
While the participants who received triple drug therapy (metformin + pegylated interferon + ribavirin) had a better outcome than those without metformin, women had a more dramatic reduction in their viral levels than men.
Adding metformin to antiviral combination therapy may not be the solution for everyone with insulin resistance and Hepatitis C infection. However, Romero-Gomez's research further confirms that taking steps toward maintaining healthy blood sugar levels hinders liver disease progression and increases the likelihood of beating the Hepatitis C virus.
References:
http://www.healthrenewal.org/nhrblog/?p=67 , Over 50% of Americans Have Insulin Resistance - Do You?, Dr. Patrick Nemecheck, Retrieved November 28, 2009, healthrenewal.org, 2009.
http://www.hivandhepatitis.com/2008icr/aasld/docs/112108_a.html, Therapies to Manage Insulin Resistance Improve Response to Interferon-based Therapy in Chronic Hepatitis C Patients, Liz Highleyman, Retrieved November 28, 2009, hivandhepatitis.com, 2009.
http://www.liversupport.com/wordpress/2007/08/the-natural-supplement-for-metabolic-health/ , The Natural Supplement for Metabolic Health, Nicole Cutler, L.Ac., Retreived November 28, 2009, Natural Wellness, 2009.
http://www.medpagetoday.com/Gastroenterology/Hepatitis/3450 , Fat Gets in the Way of Hepatitis C Therapy, Neil Osterweil, Retrieved November 24, 2009, MedPage Today, LLC, 2009.
http://www.medpagetoday.com/MeetingCoverage/AASLD/11662 , AASLD: Metformin Effective Add-On in HCV Treatment, Charles Bankhead, Retrieved November 24, 2009, MedPage Today, LLC, 2009.
http://www.ncbi.nlm.nih.gov/pubmed/19845037 , Treatment of insulin resistance with metformin in naïve genotype 1 chronic hepatitis C patients receiving peginterferon alfa-2a plus ribavirin, Romero-Gomez M, et al, Retrieved November 25, 2009, Hepatology, August 2009.
http://www.hepatitis-central.com/mt/archives/2010/06/improving_hcv_r.html
Could insulin resistance be getting in the way of your Hepatitis C treatment? To manage this possible complication, discover why many experts advise prescribing medications to manage insulin resistance in an effort to improve Hepatitis C treatment outcomes.
by Nicole Cutler, L.Ac.
Occurring in up to half of American adults, insulin resistance describes when the body can't properly use insulin to maintain normal blood sugar levels. Unfortunate for those affected, research has consistently shown that those with Hepatitis C infection and insulin resistance are more likely to suffer from liver disease progression. Thus, scientists around the globe have been focusing on how to improve the therapeutic outcome of those with insulin resistance who are battling the Hepatitis C virus.
In their search for a common denominator uniting the growing prevalence of obesity, fatty liver disease, congestive heart failure, high cholesterol, elevated blood pressure and diabetes mellitus, health officials agree that insulin resistance appears to fit the profile. Generalized descriptions of the events that lead to insulin resistance are described below:
· Released by the pancreas, insulin is dispersed into the bloodstream in response to elevated blood sugar (glucose) levels.
· By pushing glucose out of the bloodstream and into the body's cells, insulin keeps blood glucose levels from becoming too elevated and allows cells to convert glucose into energy.
· Insulin-resistant cells do not allow for the proper conversion of glucose into energy, resulting in fatigue.
· This resistance to insulin does not permit glucose to enter the cells but, rather, causes it to accumulate in the blood.
· In an attempt to reduce the glucose levels in the blood, the body signals the pancreas to produce and release even more insulin.
· The cycle of insulin-resistant cells causes even more insulin to be released, resulting in high blood insulin levels, which could potentially develop into Type 2 diabetes mellitus.
Several studies have shown that people with chronic Hepatitis C are more likely to have insulin resistance or diabetes than those without Hepatitis C. In addition, insulin resistance is associated with a poorer response to interferon-based therapy. To manage this complication, many experts advise prescribing medications to manage insulin resistance in an effort to improve Hepatitis C treatment outcomes.
As revealed at the 2008 American Association for the Study of Liver Diseases Meeting and published in the August 2009 edition of Hepatology, Spanish researchers found that metformin improved virologic response when added to Hepatitis C interferon-ribavirin therapy in those with insulin resistance. Also known by one of its brand names Glucophage, metformin is an oral medication that helps lower blood sugar in three ways:
1. It lowers the amount of glucose absorbed from food.
2. It lowers the amount of glucose produced by the liver.
3. It increases the body's response to insulin.
Led by Manuel Romero-Gomez, MD, of Valme University Hospital in Seville, 123 patients with genotype 1 Hepatitis C and insulin resistance [homeostasis model of insulin resistance (HOMA) greater than 2] received standard peginterferon-alpha-2a/ribavirin antiviral therapy plus metformin or matching placebo. After six months, the following was determined:
· 67.4 percent of the metformin group had sustained virologic response compared with 49.1 percent of the placebo group
· 57.7 percent of women in the metformin group had sustained virologic response compared with 28.6 percent of women in the placebo group
While the participants who received triple drug therapy (metformin + pegylated interferon + ribavirin) had a better outcome than those without metformin, women had a more dramatic reduction in their viral levels than men.
Adding metformin to antiviral combination therapy may not be the solution for everyone with insulin resistance and Hepatitis C infection. However, Romero-Gomez's research further confirms that taking steps toward maintaining healthy blood sugar levels hinders liver disease progression and increases the likelihood of beating the Hepatitis C virus.
References:
http://www.healthrenewal.org/nhrblog/?p=67 , Over 50% of Americans Have Insulin Resistance - Do You?, Dr. Patrick Nemecheck, Retrieved November 28, 2009, healthrenewal.org, 2009.
http://www.hivandhepatitis.com/2008icr/aasld/docs/112108_a.html, Therapies to Manage Insulin Resistance Improve Response to Interferon-based Therapy in Chronic Hepatitis C Patients, Liz Highleyman, Retrieved November 28, 2009, hivandhepatitis.com, 2009.
http://www.liversupport.com/wordpress/2007/08/the-natural-supplement-for-metabolic-health/ , The Natural Supplement for Metabolic Health, Nicole Cutler, L.Ac., Retreived November 28, 2009, Natural Wellness, 2009.
http://www.medpagetoday.com/Gastroenterology/Hepatitis/3450 , Fat Gets in the Way of Hepatitis C Therapy, Neil Osterweil, Retrieved November 24, 2009, MedPage Today, LLC, 2009.
http://www.medpagetoday.com/MeetingCoverage/AASLD/11662 , AASLD: Metformin Effective Add-On in HCV Treatment, Charles Bankhead, Retrieved November 24, 2009, MedPage Today, LLC, 2009.
http://www.ncbi.nlm.nih.gov/pubmed/19845037 , Treatment of insulin resistance with metformin in naïve genotype 1 chronic hepatitis C patients receiving peginterferon alfa-2a plus ribavirin, Romero-Gomez M, et al, Retrieved November 25, 2009, Hepatology, August 2009.
http://www.hepatitis-central.com/mt/archives/2010/06/improving_hcv_r.html
Dude, We're running for Beaux and organ donation
Amy Donaldson
sports writer
June 18, 2010 at 9:52 a.m.
Running is hard.
It's also invigorating, refreshing and sometimes you feel so good, it almost feels like flying.
But always, there are moments that test your will, your desire, your determination. Many times you question your sanity.
And that's why taking those steps into the wind, uphill or just for miles and miles is so much easier with someone else in mind.
It is the team aspect that makes the Ragnar Relays unique. Running is a solitary endeavor. The decision to stop is yours. No referee can steal your perfect run. Only your own mind can cheat you.
So when I run I like to do it for someone else. I ran the Wasatch Back the first year the race existed, and I had never run more than a 5K at the time. It changed the way I viewed running, myself and other people. Running in the rain, alone at night, I struggled with quitting for the first time. I couldn't bring myself to give up, however, because of my abnormally upbeat teammates cheering me on. I couldn't let them down.
Every year since, and in most races, I run with someone else in my heart.
This year, our entire team - Dude, Where's My Van? - will run for a man named Beaux. None of us know him very well, but we work with his wife - Lois. What I did know of him was the usual stories colleagues offer about the men who support them, the children that make them smile. I also was recently introduced to his talent for photography. He has a website where he posts his pictures, which are, pure and simply amazing. He has a unique and beautiful perspective on life that manifests itself in his art. (http://reflectivelens.blogspot.com/)
Beaux , 49, is the father of two gorgeous girls. He was told two years ago that he'd need a new liver. After a horrific bicycle accident as a child that required more than a dozen blood transfusions, he developed Hepatitis C. He didn't know it until constant stomach aches sent him to the doctors.
Lois recently told us he'd been moved up the transplant list - a moment that gives a family hope and brings home the gravity of the diagnosis.
I was nervous about asking Lois if this group of very marginal athletes could run in her husband's honor and in hopes of raising awareness about organ donation. I mean, if you get the chance to be represented, you want it to be the person who wins. You want to have your name on Lance Armstrong's shirt, not Amy "the queen of shuffling" Donaldson's race bib.
He didn't just say yes. He was as honored to have us represent him as we are to run in his name.
He wrote a beautiful blog about our offer and his feelings, which I hope you visit.
Blog: The Paradox Syndrome
Post: Ragnar Relay's Wasatch Back
Link: theparadoxsyndrome.blogspot.com
And then I hope you take some time to consider organ donation. I know of another friend whose husband is waiting for kidneys. If you have the opportunity to offer life to a stranger, please take it. It is one last gesture of love that we can offer as members of the only team that really counts.
http://www.deseretnews.com/blog/68/10009307/Reasons-to-Run-Dude-Were-running-for-Beaux-and-organ-donation.html
sports writer
June 18, 2010 at 9:52 a.m.
Running is hard.
It's also invigorating, refreshing and sometimes you feel so good, it almost feels like flying.
But always, there are moments that test your will, your desire, your determination. Many times you question your sanity.
And that's why taking those steps into the wind, uphill or just for miles and miles is so much easier with someone else in mind.
It is the team aspect that makes the Ragnar Relays unique. Running is a solitary endeavor. The decision to stop is yours. No referee can steal your perfect run. Only your own mind can cheat you.
So when I run I like to do it for someone else. I ran the Wasatch Back the first year the race existed, and I had never run more than a 5K at the time. It changed the way I viewed running, myself and other people. Running in the rain, alone at night, I struggled with quitting for the first time. I couldn't bring myself to give up, however, because of my abnormally upbeat teammates cheering me on. I couldn't let them down.
Every year since, and in most races, I run with someone else in my heart.
This year, our entire team - Dude, Where's My Van? - will run for a man named Beaux. None of us know him very well, but we work with his wife - Lois. What I did know of him was the usual stories colleagues offer about the men who support them, the children that make them smile. I also was recently introduced to his talent for photography. He has a website where he posts his pictures, which are, pure and simply amazing. He has a unique and beautiful perspective on life that manifests itself in his art. (http://reflectivelens.blogspot.com/)
Beaux , 49, is the father of two gorgeous girls. He was told two years ago that he'd need a new liver. After a horrific bicycle accident as a child that required more than a dozen blood transfusions, he developed Hepatitis C. He didn't know it until constant stomach aches sent him to the doctors.
Lois recently told us he'd been moved up the transplant list - a moment that gives a family hope and brings home the gravity of the diagnosis.
I was nervous about asking Lois if this group of very marginal athletes could run in her husband's honor and in hopes of raising awareness about organ donation. I mean, if you get the chance to be represented, you want it to be the person who wins. You want to have your name on Lance Armstrong's shirt, not Amy "the queen of shuffling" Donaldson's race bib.
He didn't just say yes. He was as honored to have us represent him as we are to run in his name.
He wrote a beautiful blog about our offer and his feelings, which I hope you visit.
Blog: The Paradox Syndrome
Post: Ragnar Relay's Wasatch Back
Link: theparadoxsyndrome.blogspot.com
And then I hope you take some time to consider organ donation. I know of another friend whose husband is waiting for kidneys. If you have the opportunity to offer life to a stranger, please take it. It is one last gesture of love that we can offer as members of the only team that really counts.
http://www.deseretnews.com/blog/68/10009307/Reasons-to-Run-Dude-Were-running-for-Beaux-and-organ-donation.html
EASL 45th Annual Meeting
EASL 45th Annual Meeting
(European Association for the Study of the Liver)
April 14-18, 2010
April 14-18, 2010
- New HCV Drugs EASL 2010
- From Ash To Cure - EASL April 14-18 2010
- ANTIVIRAL ACTIVITY, COMBINATION AND RESISTANCE OF ACH-1625, A POTENT HCV NS3 PROTEASE INHIBITOR
- CHARACTERIZATION OF THE HEPATOSELECTIVE DISTRIBUTION OF ACH-1625: A POTENT, CLINICAL STAGE HCV NS3 PROTEASE INHIBITOR
- VIROLOGICAL RESPONSE, SAFETY, AND PHARMACOKINETIC PROFILE FOLLOWING SINGLE - AND MULTIPLE-DOSE ADMINISTRATION OF ACH-1625 PROTEASE INHIBITOR TO HEALTHY VOLUNTEERS AND HCV GENOTYPE-1 PATIENTS
- Validation of the GeneSeq HCV NS5B Sequencing Assay for Patient-Derived HCV Subtypes 1a and 1b
- Resistance Profile Of ABT-333 And Relationship To Viral Load Decrease In Patients Treated In Combination With Peg-interferon And Ribavirin For 28 Days
- Pharmacokinetics of the HCV Polymerase Inhibitor ABT-333 in US and Japanese Healthy Volunteers
- Exposure-Viral Response Analyses of the Non-nucleoside Polymerase Inhibitor ABT-333, Following Monotherapy and ABT-333 Plus Pegylated Interferon and Ribavirin Therapy
- Pharmacokinetics of the HCV Polymerase Inhibitor ABT-072 Following Single and Multiple Dosing in Healthy Adult Volunteers
- Virologic Response Rates Following 4 Weeks of Filibuvir in Combination with Pegylated Interferon Alfa-2a and Ribavirin in Chronically-Infected HCV Genotype-1 Patients
- Genotypic Characterisation of Filibuvir Resistance in Patients Receiving Four Weeks Co-administration of Filibuvir with pegIFN/RBV(12 Week Analysis)
- Exposure-response Relationship of Filibuvir in HCV-infected Patients: Application to Dose Selection for Combination Therapy
- Impact of Sustained Virological Response After Antiviral Treatment in Chronic Hepatitis C Patients on Life Expectancy and Quality-adjusted Life-years
- Locteron, controlled-release interferon alpha 2b, 3 studies at EASL 2010 Vienna - 3 company press releases
- PHASE IIB STUDY OF BALAPIRAVIR (RG1626; NUCLEOSIDE ANALOGUE INHIBITOR OF HCV POLYMERASE) PLUS PEGINTERFERON ALFA-2A (40KD) AND RIBAVIRIN FOR CHRONIC HEPATITIS C GENOTYPE 1: FINAL RESULTS
- RANDOMIZED, OPEN-LABEL, 12-WEEK COMPARISON OF CONTROLLED-RELEASE INTERFERON ALPHA2B + RIBAVRIN VS. PEGYLATED-INTERFERON ALPHA2B + RIBAVRIN IN TREATMENT-NAïVE GENOTYPE1 HEPATITIS C: 4 WEEK RESULTS FROM 480STUDY (PANEL A)
- Slow Responders Benefit From 72 Weeks Peg/Rbv - Predicting Treatment Outcome Among Slow Responders: A Retrospective Analysis of the SUCCESS Study
- Q2week Controlled Release Interferon Alpha2b + Ribavrin Reduces Flu-like Symptoms >50% And Provides Equivalent Efficacy In Comparison To Weekly Pegylated Interferon Alpha2b + Ribavirin In Treatment-naïve Genotype-1 Chronic Hepatitis C: Results From EMPOWER, A Randomized Open-label 12-week Comparison In 133 Patients
- Early Viral Response Of Controlled-release Interferon Alpha2b And Ribavirin Vs. Pegylated-interferon Alpha2b And Ribavirin In Treatment-naïve Genotype-1 Hepatitis C: 12 Week Results (SELECT-2 Trial)
- IMPACT OF LOW-DOSE RITONAVIR BOOSTING ON THE PHARMACOKINETICS OF DANOPREVIR (RG7227; ITMN-191), A HIGHLY POTENT AND SELECTIVE INHIBITOR OF THE HCV NS3/4A PROTEASE
- High Dose Pegasys/rbv can improve SVR: Impact of higher doses of peginterferon alfa-2a and ribavirin on RVR, cEVR and SVR in HCV G1 patients with viral loads ≥400 000 IU/mL weighing ≥85 kg
- Predictors of relapse among patients treated with standard- or induction-dose peginterferon alfa-2a (40KD) combined with standard- or higher-dose ribavirin in difficult-to-cure patients
- Pegasys vs Pegintron, Baseline characteristics and on-treatment predictors of responses from real-world patient cohorts: interim results of the multinational PROPHESYS cohorts
- Metabolic Syndrome (MS) [glucose/diabetes] Is a Negative Predictor of Treatment Outcome in Patients With Chronic Hepatitis C: Results From the IDEAL Study
- Improved Inflammatory Activity With Low-Dose PegIntron (PEG) Maintenance Therapy in Prior Nonresponders With METAVIR Fibrosis Scores (MFS) of F2/F3: Final Results From the EPIC3 Program
- Characterization of resistant mutants selected in vitro by the HCV NS3/4A protease inhibitor BI 201335
- Preclinical characterization of non-covalent HCV NS3/4A protease inhibitor BI 201335
- HBsAg Kinetics of Decay and Baseline Characteristics of HBeAg-Positive Patients with Chronic Hepatitis B Following 3 Years of Tenofovir Disoproxil Fumarate (TDF) Treatment
- Evaluation of Potential Virologic Resistance in HBV Polymerase Among Subjects with Persistent Viremia Following up to 144 Weeks of Therapy with Tenofovir DF
- Efficacy of Tenofovir DF Treatment in Patients with a Suboptimal Response to Adefovir Dipivoxil
- Risk and Predictors of Mortality or Hepatocellular Carcinoma among Entecavir- or Adefovir-Treated Chronic Hepatitis B Patients with Evidence of Hepatic Decompensation
- Low Rates of Nucleos(t)ide-associated Adverse Events in the Long-term Experience with Entecavir
- MK-5172, the 1st HCV Protease Inibitor with Potent Acyivity Against Resistance Mutations In Vitro
- TMC435 & Drug Interactions: Evaluation of metabolic interactions for TMC435 via cytochrome P450 (CYP) enzymes in healthy volunteers
- EARLY ON-TREATMENT RESPONSES DURING PEGYLATED INTERFERON PLUS RIBAVIRIN ARE INCREASED FOLLOWING 13 DAYS OF COMBINATION NUCLEOSIDE POLYMERASE (RG7128) AND PROTEASE (RG7227) INHIBITOR THERAPY (INFORM-1)
- Combination of TMC435 with two novel NS5B inhibitors increases anti-HCV activity and results in a higher genetic barrier in vitro
- 4 week therapy with the non-nucleosidic polymerase inhibitor BI 207127 in combination with peginterferon alfa2A and ribavirin in treatment naïve and treatment experienced chronic HCV GT1 patients
- Pharmacokinetic-pharmacodynamic (PK-PD) analyses of TMC435 in treatment-naïve hepatitis C (HCV)-infected patients in the OPERA-1 study
- Once-daily NS5A Inhibitor (BMS-790052) Plus Peginterferon-alpha-2a And Ribavirin Produces High Rates Of Extended Rapid Virologic Response In Treatment-naïve HCV-genotype 1 Subjects: Phase 2a Trial - Bristol-Myers Squibb Study AI444014
- SILEN-C2: Early antiviral activity and safety of BI 201335 combined with peginterferon alfa-2a and ribavirin (PegIFN/RBV) in chronic HCV genotype 1 patients with non-response to PegIFN/RBV
- Phase 2 Randomized, Double-Blind Placebo-Controlled Study of Nitazoxanide with Peginterferon Alfa-2a and Ribavirin in Nonresponders with Chronic Hepatitis C Genotype 1: Final Report
- Nitazoxanide + Peg/Rbv in Nonresponders
- Combination of two complementary nucleotide analogues, PSI-7977 and PSI-938, effectively clears wild type and NS5b: S282T HCV replicons - Comparison with combinations of other antiviral compounds
- Sustained Virologic Response following RG7128 1500 mg BID PEG-IFN/RBV for 28 days in HCV Genotype 2/3 prior non-responders
- Vitamin D Supplement improve SVR in Chronic Hepatitis C (Genotype 1) Naïve Patients treated with Peg Interferon and Ribavirin
- Idenix Pharmaceuticals Reports Favorable Pharmacokinetic Data for IDX320, a Potent, Multi-Genotypic Protease Inhibitor for the Treatment of Hepatitis C
- Idenix Pharmaceuticals Reports Positive Results With IDX184 nucleoside polymerase From Interim Analysis of Phase IIa Hepatitis C Study
- Triple Combinations of Direct-Acting Antiviral Agents Demonstrate Robust Anti-HCV Activity In Vitro
- Antiviral Activity, Pharmacokinetics & Safety of IDX184 in Combination with Peg/Rbv in Treatment Naïve Genotype 1
- In Vitro Antiviral Activity of IDX320, a Novel and Potent Macrocyclic HCV Protease Inhibitor
- ANA598 HCV Polymerase Inhititor Safety & Activity + Peg/Rbv in Genotype 1
- 72% OF PATIENTS RECEIVING ANA598 IN PHASE II COMBINATION STUDY WITH INTERFERON AND RIBAVIRIN ACHIEVE UNDETECTABLE LEVELS OF VIRUS AT WEEK EIGHT
- Idenix Pharmaceuticals Reports Favorable Pharmacokinetic Data for IDX320, a Potent, Multi-Genotypic Protease Inhibitor for the Treatment of Hepatitis C
- Discrepancies Between Definitions of Null Response to Treatment with Peginterferon Alfa-2a and Ribavirin: Implications for New HCV Drug Development
- On-Treatment Response-Guided Therapy with Telaprevir q8h or q12h Combined with Peginterferon Alfa-2a or Alfa-2b and Ribavirin in Treatment-Naïve Genotype 1 Hepatitis C (Study C208)
- Activity of Telaprevir Alone or in Combination with Peginterferon Alfa-2a and Ribavirin in Treatment-naïve, Genotype 2 and 3, Hepatitis C Patients: Final Results of Study C209
- On-Treatment Response-Guided Therapy with Telaprevir q8h or q12h Combined with Peginterferon Alfa-2a or Alfa-2b and Ribavirin in Treatment-Naïve Genotype 1 Hepatitis C (Study C208)
- Idenix Pharmaceuticals Reports Positive Results With IDX184 From Interim Analysis of Phase IIa Hepatitis C Study
- Silibinin as Rescue Therapy for Suboptimal Response to Peg/Rbv
- Vitamin D Improves SVR in Naïve Genotype 1 with Peg/Rbv
- InterMune Reports Virologic Response of Ritonavir-Boosted Danoprevir (RG7227/ITMN-191) in Patients with Chronic Hepatitis C
- Identification and Characterization of PPI-461, a Potent and Selective HCV NS5A Inhibitor with Activity Against all HCV Genotypes
- Dose-Ranging, Three-Day Monotherapy Study of the HCV NS3 Protease Inhibitor GS-9256
- Long-term Outcomes Following Combination Treatment with Boceprevir plus PegIntron/Ribavirin (P/R) in Patients with Chronic Hepatitis C, Genotype 1 (CHC-G1)
- Phase 2 Randomized, Double-Blind, Placebo-Controlled Study of Nitazoxanide Plus Peginterferon and Ribavirin in HCV Genotype 1 Naïve Patients: Week 12 Sustained Virologic Response Rate
- GlobeImmune GI-5005 HCV Product Candidate Improves Sustained Virologic Response by 10 Percent, Demonstrating Potential to Be First Therapeutic Vaccine for HCV
- Ritonavir boosting of low-dose danoprevir (RG7227; ITMN-191), HCV NS3/4A protease inhibitor, results in robust reduction in HCV RNA at lower exposures than provided by unboosted regimens
- Telaprevir in Null-Responders & Non-Responders
- VX-222 Vertex NNRTI Polymerase Inhibitor 3 Days Monotherapy
- Merck HCV Protease Inhibitor For Resistance
Lawmakers urge quick passage of bill to boost detection, treatment of hepatitis
By Julian Pecquet - 06/17/10 03:01 PM ET
Lawmakers on the House Oversight panel on Thursday urged Congress to quickly pass legislation to boost the detection and treatment of viral hepatitis, the leading cause of liver cancer in the United States.
The Oversight and Government Reform Committee held the first hearing in several years on the deadly disease, which disproportionately affects blacks and Asians, and pressed for passage of a bipartisan bill that would boost funding by $600 million over the next five years.
The hearing comes on the heels of an Institute of Medicine (IOM) report that highlighted deficiencies with the federal government's response to the epidemic. The report contains two dozen expert recommendations for improvement, including enhanced screening, physician education and the creation of a coordinated system to identify people who have the disease and refer them to care.
About 5.3 million Americans are believed to have hepatitis — the disease causes 12,000 to 15,000 deaths a year — though many don’t know it.
"The current approach [...] is not working," the IOM report says.
The legislation under consideration, introduced in October by Rep. Mike Honda (D-Calif.), has 52 bipartisan co-sponsors. The "Viral Hepatitis and Liver Cancer Control and Prevention Act" is currently in the Energy and Commerce Committee.
The bill would charge the secretary of Health and Human Services with developing and implementing a plan for the prevention, control and medical management of hepatitis B and C; it would also provide federal funding for state-based screening and early intervention programs.
Honda said the bill would eventually save billions of dollars by identifying sick people early. A study by the research firm Milliman found that without federal leadership, the cost of treating hepatitis C alone could more than triple, to $85 billion a year, by 2024.
"We can do a whole lot better than what we're doing," said Oversight panel chairman Edolphus Towns (D-N.Y.). "I think it's a disgrace to have a problem of this nature and to not commit resources."
The panel heard testimony from Honda and Reps. Bill Cassidy (R-La.) and Hank Johnson (D-Ga.). Cassidy is a hepatologist who co-sponsored the bill, and Johnson last year acknowledged he was undergoing treatment for hepatitis C.
Cassidy applauded former President Bill Clinton's children’s vaccination program and said the Honda bill would "similarly save lives." But debate quickly descended into budgetary politics.
Oversight ranking member Darrell Issa (R-Calif.) said Republicans would not vote for any new directed spending unless it's part of the budget bill, which has stalled.
Meanwhile, Democrats bristled at Issa's description of the word "earmark" to describe the bill.
A coalition of more than 175 public and private organizations launched a print ad campaign on Tuesday to coincide with the hearing. The National Viral Hepatitis Roundtable ad is made to look like a movie poster and reads "Mission: Possible."
"If Congress gets on the case now," the ad says, "the leading cause of liver cancer won't stand a chance."
Patient advocates say the Honda bill will help boost funding for hepatitis prevention efforts, which currently only get 2 percent — $19.3 million — of the budget allocated to the Centers for Disease Control and Prevention's National Center for HIV/AIDS, Viral Hepatitis, STD and TB Prevention. Advocates hope the Honda bill will eventually allow them to get $150 million a year.
Source:
http://thehill.com/blogs/healthwatch/prescription-drug-policy/103923-lawmakers-urge-quick-passage-of-bill-to-boost-detection-treatment-of-hepatitis
Lawmakers on the House Oversight panel on Thursday urged Congress to quickly pass legislation to boost the detection and treatment of viral hepatitis, the leading cause of liver cancer in the United States.
The Oversight and Government Reform Committee held the first hearing in several years on the deadly disease, which disproportionately affects blacks and Asians, and pressed for passage of a bipartisan bill that would boost funding by $600 million over the next five years.
The hearing comes on the heels of an Institute of Medicine (IOM) report that highlighted deficiencies with the federal government's response to the epidemic. The report contains two dozen expert recommendations for improvement, including enhanced screening, physician education and the creation of a coordinated system to identify people who have the disease and refer them to care.
About 5.3 million Americans are believed to have hepatitis — the disease causes 12,000 to 15,000 deaths a year — though many don’t know it.
"The current approach [...] is not working," the IOM report says.
The legislation under consideration, introduced in October by Rep. Mike Honda (D-Calif.), has 52 bipartisan co-sponsors. The "Viral Hepatitis and Liver Cancer Control and Prevention Act" is currently in the Energy and Commerce Committee.
The bill would charge the secretary of Health and Human Services with developing and implementing a plan for the prevention, control and medical management of hepatitis B and C; it would also provide federal funding for state-based screening and early intervention programs.
Honda said the bill would eventually save billions of dollars by identifying sick people early. A study by the research firm Milliman found that without federal leadership, the cost of treating hepatitis C alone could more than triple, to $85 billion a year, by 2024.
"We can do a whole lot better than what we're doing," said Oversight panel chairman Edolphus Towns (D-N.Y.). "I think it's a disgrace to have a problem of this nature and to not commit resources."
The panel heard testimony from Honda and Reps. Bill Cassidy (R-La.) and Hank Johnson (D-Ga.). Cassidy is a hepatologist who co-sponsored the bill, and Johnson last year acknowledged he was undergoing treatment for hepatitis C.
Cassidy applauded former President Bill Clinton's children’s vaccination program and said the Honda bill would "similarly save lives." But debate quickly descended into budgetary politics.
Oversight ranking member Darrell Issa (R-Calif.) said Republicans would not vote for any new directed spending unless it's part of the budget bill, which has stalled.
Meanwhile, Democrats bristled at Issa's description of the word "earmark" to describe the bill.
A coalition of more than 175 public and private organizations launched a print ad campaign on Tuesday to coincide with the hearing. The National Viral Hepatitis Roundtable ad is made to look like a movie poster and reads "Mission: Possible."
"If Congress gets on the case now," the ad says, "the leading cause of liver cancer won't stand a chance."
Patient advocates say the Honda bill will help boost funding for hepatitis prevention efforts, which currently only get 2 percent — $19.3 million — of the budget allocated to the Centers for Disease Control and Prevention's National Center for HIV/AIDS, Viral Hepatitis, STD and TB Prevention. Advocates hope the Honda bill will eventually allow them to get $150 million a year.
Source:
http://thehill.com/blogs/healthwatch/prescription-drug-policy/103923-lawmakers-urge-quick-passage-of-bill-to-boost-detection-treatment-of-hepatitis
Getz Pharma to launch therapy for Hepatitis C patients
* Biotechnology-based drug for hepatitis C will be manufactured by a Pakistani company for the first time
By Irfan Aligi
KARACHI: Getz Pharma would launch the Pegylated Interferon therapy for the treatment of hepatitis C in Pakistan. The new therapy would be highly cost-effective and easy to use as the manufacturer and presenters of the new therapy have considered patients’ care and comfort. It would also be the first time that a biotechnology-based essential drug would be manufactured by Getz Pharma, a Pakistani company. It is pertinent to mention that approximately every 20th person in Pakistan is infected with hepatitis C.
The initiative taken by Getz Pharma to invest in the local manufacturing of Pegylated Interferon (Unipeg) in the country would substantially reduce the cost of treatment for a person suffering from hepatitis C. The company has invested in research and development to formulate this molecule with the help of a team of scientists from the Netherlands, led by Dr Ben Rademaker, a PhD-holder.
Getz Pharma Managing Director and Chief Executive Officer Khalid Mehmood, during a press conference on Thursday, said the size of the country’s pharmacy market is about Rs 119 billion, which is growing by 12 to 13 percent. Henceforth, they have been able to export pharmacy goods to 45 countries around the world. The pharmacy sector in the country is the largest employment provider, with around five million people employed. Pakistan’s pharmacy industry meets 90 percent of the needs of pharmacy goods.
Pharmaceutical exports are at their highest as compared to other corporate sectors in the country and have achieved a 29 percent growth, which is four times of the country’s textile exports. Still, the country’s spending on health according to annual budgetary allocations is just 0.4 percent of the GDP, while Bangladesh is spending 0.8 percent, Khalid said.
Investment: He said Getz Pharma was set up in 1995 as a small company with only 45 employees, while today the number of its employees exceeded 2,500 worldwide, and 1,850 people in Pakistan. Getz Pharma invested Rs 4 billion in revamping existing facilities, in purchasing state-of-the-art production, quality control from 2005 to 2009. It has a plan to meet the 54 percent target of exporting medicines. According to the Federal Bureau of Revenue, Getz Pharma was the second largest taxpayer unit in terms of taxes and duties with an estimated Rs 636 million in 2009, he added.
Khalid said the company’s total investment in Pakistan was Rs 4 billion in the last three years, including investment in manufacturing technology of the first locally manufactured recombinant human insulin. It plans to invest an equal amount in the coming two years in new technologies that would result in local manufacturing of drugs that are currently being imported at high costs. It may be mentioned that Getz Pharma is the single largest exporter of pharmaceutical products from the country. It was estimated that the company’s exports account for approximately 40 percent of the country’s total pharmaceutical exports.
Dr Bernardus Rademaker, speaking on the occasion, said the analytical, toxicological and pharmacokinetic studies for Unipeg (Pegylated Interferon Alpha 2a) had been carried out in Europe, comparing it to the existing research molecule.
New era: He said in addition, bioactivity and potency had also been evaluated at the Centre for Applied Molecular Biology in Lahore, a premier institute of the Science and Technology Ministry. Specialised manufacturing and testing technology is required for manufacturing the Unipeg. He said Getz Pharma had acquired the technology at a substantial investment and a number of these tests were not currently available in the country’s pharmaceutical industry. Through this molecule, Getz Pharma would herald a new biotech era in the country, he added.
To a question, Dr Rademaker said since the molecule was not available in the US, it was not necessary to seek approval form the US FDA. He also said collaboration with Getz Pharma was not business-oriented, but it had been overwhelmingly planned that the hepatitis C affected population of the country should be provided with a cost-effective and latest mode of treatment.
Dr Rademaker holds a PhD in biotechnology from the State University Utrecht, Holland. He is the founder and CEO of InProPharma, a company specialising in technology platforms for the production of biologically active proteins. Prior to setting up his own company, Rephartox BV, a contract research company for the pharmaceutical industry, he was the director of Corporate Drug Development at the Rhein Biotech NV, Maastricht and the Green Cross Vaccine Company, Seoul, Korea. He is a member of the Dutch Pharmacological Society and is a registered pharmacologist. He has authored more than 50 scientific publications, and many regulatory affairs documents.
http://www.dailytimes.com.pk/default.asp?page=2010%5C06%5C18%5Cstory_18-6-2010_pg7_17
By Irfan Aligi
KARACHI: Getz Pharma would launch the Pegylated Interferon therapy for the treatment of hepatitis C in Pakistan. The new therapy would be highly cost-effective and easy to use as the manufacturer and presenters of the new therapy have considered patients’ care and comfort. It would also be the first time that a biotechnology-based essential drug would be manufactured by Getz Pharma, a Pakistani company. It is pertinent to mention that approximately every 20th person in Pakistan is infected with hepatitis C.
The initiative taken by Getz Pharma to invest in the local manufacturing of Pegylated Interferon (Unipeg) in the country would substantially reduce the cost of treatment for a person suffering from hepatitis C. The company has invested in research and development to formulate this molecule with the help of a team of scientists from the Netherlands, led by Dr Ben Rademaker, a PhD-holder.
Getz Pharma Managing Director and Chief Executive Officer Khalid Mehmood, during a press conference on Thursday, said the size of the country’s pharmacy market is about Rs 119 billion, which is growing by 12 to 13 percent. Henceforth, they have been able to export pharmacy goods to 45 countries around the world. The pharmacy sector in the country is the largest employment provider, with around five million people employed. Pakistan’s pharmacy industry meets 90 percent of the needs of pharmacy goods.
Pharmaceutical exports are at their highest as compared to other corporate sectors in the country and have achieved a 29 percent growth, which is four times of the country’s textile exports. Still, the country’s spending on health according to annual budgetary allocations is just 0.4 percent of the GDP, while Bangladesh is spending 0.8 percent, Khalid said.
Investment: He said Getz Pharma was set up in 1995 as a small company with only 45 employees, while today the number of its employees exceeded 2,500 worldwide, and 1,850 people in Pakistan. Getz Pharma invested Rs 4 billion in revamping existing facilities, in purchasing state-of-the-art production, quality control from 2005 to 2009. It has a plan to meet the 54 percent target of exporting medicines. According to the Federal Bureau of Revenue, Getz Pharma was the second largest taxpayer unit in terms of taxes and duties with an estimated Rs 636 million in 2009, he added.
Khalid said the company’s total investment in Pakistan was Rs 4 billion in the last three years, including investment in manufacturing technology of the first locally manufactured recombinant human insulin. It plans to invest an equal amount in the coming two years in new technologies that would result in local manufacturing of drugs that are currently being imported at high costs. It may be mentioned that Getz Pharma is the single largest exporter of pharmaceutical products from the country. It was estimated that the company’s exports account for approximately 40 percent of the country’s total pharmaceutical exports.
Dr Bernardus Rademaker, speaking on the occasion, said the analytical, toxicological and pharmacokinetic studies for Unipeg (Pegylated Interferon Alpha 2a) had been carried out in Europe, comparing it to the existing research molecule.
New era: He said in addition, bioactivity and potency had also been evaluated at the Centre for Applied Molecular Biology in Lahore, a premier institute of the Science and Technology Ministry. Specialised manufacturing and testing technology is required for manufacturing the Unipeg. He said Getz Pharma had acquired the technology at a substantial investment and a number of these tests were not currently available in the country’s pharmaceutical industry. Through this molecule, Getz Pharma would herald a new biotech era in the country, he added.
To a question, Dr Rademaker said since the molecule was not available in the US, it was not necessary to seek approval form the US FDA. He also said collaboration with Getz Pharma was not business-oriented, but it had been overwhelmingly planned that the hepatitis C affected population of the country should be provided with a cost-effective and latest mode of treatment.
Dr Rademaker holds a PhD in biotechnology from the State University Utrecht, Holland. He is the founder and CEO of InProPharma, a company specialising in technology platforms for the production of biologically active proteins. Prior to setting up his own company, Rephartox BV, a contract research company for the pharmaceutical industry, he was the director of Corporate Drug Development at the Rhein Biotech NV, Maastricht and the Green Cross Vaccine Company, Seoul, Korea. He is a member of the Dutch Pharmacological Society and is a registered pharmacologist. He has authored more than 50 scientific publications, and many regulatory affairs documents.
http://www.dailytimes.com.pk/default.asp?page=2010%5C06%5C18%5Cstory_18-6-2010_pg7_17
Benitec Limited (ASX:BLT) Granted Hepatitis C RNA Interference Patent In US
Melbourne, June 18, 2010 (ABN Newswire) - Benitec Limited (ASX:BLT) (PINK:BNIKF) are pleased to announce that US Patent 7727970 "Multiple promoter expression cassettes for simultaneous delivery of RNAi agents targeted to Hepatitis C virus" has been granted by the United States Patent and Trademark Office (USPTO). The granted claims cover the use of an RNA interference construct (with multiple promoters) to inhibit the level of Hepatitis C virus in animal cells, tissues and organs. Moreover, the USPTO has granted Benitec an additional 805 days patent term in recognition of the delays in examining the patent application. Additional related applications remain pending to extend the scope of protection.
Benitec has licensed the rights to use this patent for Hepatitis C exclusively to Tacere Therapeutics, Inc., who recently announced that Pfizer has exercised its option to further develop and commercialise Tacere's Hepatitis C Virus (HCV) compounds.
Benitec's Chief Scientific Officer, Dr Peter French said, "The grant of this patent is an important further recognition of our dominant global position in the transformational DNA-directed RNA interference field and provides increased depth and breadth to our patent portfolio. Benitec's ddRNAi-related patent estate (solely owned or licensed exclusively for humans from CSIRO) currently comprises over 100 patents and patent applications covering 20 jurisdictions, of which more than 30 are granted, accepted or allowed."
Link: http://www.abnnewswire.net/media/en/docs/63116-ASX-BLT-596073.pdf
About Benitec Limited
Benitec Limited (ASX:BLT) (PINK:BNIKF) is an Australian biotechnology company focused on licensing its extensive intellectual property portfolio and developing therapeutics to treat serious diseases using its proprietary ddRNAi technology. For additional information, please visit http://www.benitec.com/ .
Contact
Mel Bridges
Executive Director
Mob: +61-413-051-600
Email: mbridges@benitec.com
Peter French
Chief Executive Officer
Mob: +61-412-457-595
Email: pfrench@benitec.com
http://www.abnnewswire.net/press/en/63116/Benitec_Limited_(ASX:BLT)_Granted_Hepatitis_C_RNA_Interference_Patent_In_US.html
Benitec has licensed the rights to use this patent for Hepatitis C exclusively to Tacere Therapeutics, Inc., who recently announced that Pfizer has exercised its option to further develop and commercialise Tacere's Hepatitis C Virus (HCV) compounds.
Benitec's Chief Scientific Officer, Dr Peter French said, "The grant of this patent is an important further recognition of our dominant global position in the transformational DNA-directed RNA interference field and provides increased depth and breadth to our patent portfolio. Benitec's ddRNAi-related patent estate (solely owned or licensed exclusively for humans from CSIRO) currently comprises over 100 patents and patent applications covering 20 jurisdictions, of which more than 30 are granted, accepted or allowed."
Link: http://www.abnnewswire.net/media/en/docs/63116-ASX-BLT-596073.pdf
About Benitec Limited
Benitec Limited (ASX:BLT) (PINK:BNIKF) is an Australian biotechnology company focused on licensing its extensive intellectual property portfolio and developing therapeutics to treat serious diseases using its proprietary ddRNAi technology. For additional information, please visit http://www.benitec.com/ .
Contact
Mel Bridges
Executive Director
Mob: +61-413-051-600
Email: mbridges@benitec.com
Peter French
Chief Executive Officer
Mob: +61-412-457-595
Email: pfrench@benitec.com
http://www.abnnewswire.net/press/en/63116/Benitec_Limited_(ASX:BLT)_Granted_Hepatitis_C_RNA_Interference_Patent_In_US.html
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