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Datum nieuwsfeit: 15-11-2005
Presentatie van evaluatie van data over vijf jaar van lange termijn therapie met Hepsera voor Hepatitis B 'e' antigeen-negatief chronische Hepatitis B op jaarlijkse bijeenkomst AASLD
( BW)(CA-GILEAD-SCIENCES)(GILD) Five-Year Data Evaluating Long-Term
Therapy with Hepsera for Hepatitis B ''e'' Antigen-Negative Chronic
Hepatitis B Presented at AASLD Annual Meeting
Business Editors/Health/Medical Writers
BIOWIRE2K
SAN FRANCISCO--(BUSINESS WIRE)--Nov. 14, 2005--
Data Indicate that Hepsera May Lead to Regression of Liver
Fibrosis in Patients Treated for up to Five Years
Gilead Sciences (Nasdaq:GILD) today presented data describing the
sustained efficacy and safety of its oral antiviral drug Hepsera(R)
(adefovir dipivoxil) for up to five years of treatment among patients
with hepatitis B "e" antigen-negative, presumed precore mutant chronic
hepatitis B. In this analysis, which includes the first prospective
set of liver biopsies following five years of oral antiviral therapy,
treatment with Hepsera resulted in regression of liver fibrosis in 75
percent of patients. Liver fibrosis is a serious consequence of
chronic liver inflammation. Study results were presented as a late
breaker poster (#LB12) at the 56th American Association for the Study
of Liver Diseases Annual Meeting in San Francisco, CA.
"This study offers long-term evidence of antiviral efficacy and
clinical benefit among patients with a difficult-to-treat form of
chronic hepatitis B," said Stephanos Hadziyannis, MD, Department of
Medicine, Henry Dunant Hospital, Athens, Greece, and a lead
investigator for Study 438. "Long-term therapy is often the rule for
patients with HBeAg-negative hepatitis B, and other oral antiviral
therapies either lack long-term data in this population or lead to the
development of genotypic resistance at high rates after only a few
years. The data presented indicate that Hepsera may be able to reverse
signs of liver damage in patients who received up to five years of
continuous treatment, with a relatively low rate of resistance."
Dr. Hadziyannis presented efficacy, tolerability, resistance and
safety data from an open-label extension of Study 438, in which
patients with HBeAg-negative chronic hepatitis B received Hepsera
monotherapy continuously for up to 240 weeks.
Liver biopsies at years one, two, four and five (240 weeks) showed
continual improvement in inflammation and regression of fibrosis.
Eighty-three percent (20/24) and 75 percent (18/24) of patients showed
improvement in inflammation and regression of fibrosis following 240
weeks of Hepsera treatment, respectively. Sixty-nine percent (38/55)
of patients who received Hepsera for 240 weeks exhibited improvement
in liver function, as measured by normalization of serum alanine
transferase (ALT) levels. Sixty-seven percent (37/55) of patients had
suppression of viral replication, indicated by undetectable levels of
serum HBV DNA (less than 1,000 copies/mL). In addition, four patients
experienced HBsAg loss. Three of the four patients showed sAg
seroconversion (complete loss of HBsAg and the development of
antibodies to the HB "surface" antigen) by the end of the evaluation.
Data from this study also showed that biochemical, virologic,
serological and histological results in the 240-week treatment group
were similar to those in a separate cohort of patients treated with
placebo for the first year and Hepsera monotherapy for four years (192
weeks), indicating that therapy with Hepsera is associated with
sustained improvements in patients with HBeAg-negative chronic
hepatitis B.
Two mutations (rtN236T and rtA181V) in the HBV polymerase enzyme
have been associated with genotypic resistance to Hepsera. According
to a life-table analysis, the cumulative probability of selecting
these viral mutations with Hepsera was 0, 3, 11, 18 and 29 percent
after 48, 96, 144, 192 and 240 weeks of treatment, respectively. These
mutations are indicators of the potential for clinical breakthrough.
The safety profile of Hepsera remained favorable through 240 weeks
of treatment. Four patients (3 percent) had a confirmed increase in
serum creatinine of greater than or equal to 0.5 mg/dL from baseline
by week 240 and of those one patient discontinued the study. One
patient had a serum phosphorous level less than 2.0 mg/dL, which was
observed after discontinuation of therapy. Serious adverse events were
reported in 19 percent (24/125) of patients in the study; none were
determined to be related to Hepsera. Three patients (2 percent)
discontinued from the study due to adverse events.
About Hepsera
Hepsera, a nucleotide analogue for the treatment of chronic
hepatitis B, works by inhibiting HBV DNA polymerase, an enzyme
involved in the replication of the virus in the body.
In the United States, Hepsera is indicated for the treatment of
chronic hepatitis B in adults with evidence of active viral
replication and either evidence of persistent elevations in serum
aminotransferases (ALT or AST) or histologically active disease.
Clinical and laboratory evidence of exacerbations of hepatitis
have occurred after discontinuation of treatment with antiviral
therapies for hepatitis B, including Hepsera. Special warnings and
precautions for use are included in the package insert regarding
monitoring of renal function, post-treatment exacerbations of
hepatitis, and the occurrence of lactic acidosis and severe
hepatomegaly with steatosis. The adverse reactions considered at least
possibly related to treatment reported in 3 percent or greater of
patients in the first 48 weeks in Hepsera pivotal clinical studies
were asthenia, headache, abdominal pain, nausea, flatulence, diarrhea
and dyspepsia. Patients who received Hepsera beyond 48 weeks reported
adverse reactions similar in nature and severity to those reported in
the first 48 weeks of treatment with only a slight increase in
incidence. By week 96, increases in serum creatinine were observed in
patients with chronic hepatitis B and compensated liver disease
treated with Hepsera. Changes in serum creatinine were more prevalent
in patients pre- and post-transplantation with lamivudine-resistant
liver disease and multiple risk factors for changes in renal function
who were treated with Hepsera for up to 129 weeks, with a median time
on treatment of 19 and 56 weeks, respectively. Dosing instructions for
patients with underlying renal impairment and for patients co-infected
with HIV are also provided in the package insert, which is available
for download online at www.hepsera.com.
About Chronic Hepatitis B
Chronic hepatitis B is a serious disease that can lead to
potentially fatal complications such as cirrhosis and liver cancer.
More than 400 million people are estimated to be chronically infected
with HBV worldwide, with approximately 1.25 million people infected in
the United States alone. HBeAg-negative hepatitis B accounts for
approximately 14 to 33 percent of chronic hepatitis B cases worldwide.
About Gilead
Gilead Sciences is a biopharmaceutical company that discovers,
develops and commercializes innovative therapeutics in areas of unmet
medical need. The company's mission is to advance the care of patients
suffering from life-threatening diseases worldwide. Headquartered in
Foster City, California, Gilead has operations in North America,
Europe and Australia.
This press release includes forward-looking statements, within the
meaning of the Private Securities Litigation Reform Act of 1995, that
are subject to risks, uncertainties and other factors. These risks and
uncertainties could cause actual results to differ materially from
those referred to in the forward-looking statements. Risks are
described in detail in the Gilead Annual Report on Form 10-K for the
year ended December 31, 2004 and in Gilead's Quarterly Reports on Form
10-Q, all of which are on file with the U.S. Securities and Exchange
Commission. All forward-looking statements are based on information
currently available to Gilead and Gilead assumes no obligation to
update any such forward-looking statements.
Hepsera is a registered trademark of Gilead Sciences, Inc.
For more information on Gilead, please call the Gilead Public
Affairs Department at 1-800-GILEAD-5 (1-800-445-3235) or visit
www.gilead.com.
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CONTACT: Gilead Sciences, Inc.
Susan Hubbard, 650-522-5715 (Investors)
Erin Edgley, 650-522-5635 (Media)