News (Updated February 15, 2003)

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Press Release Source: Roche; Trimeris

Latest Research on Fuzeon and T-1249, HIV Fusion Inhibitors, to be Presented At Upcoming Scientific Meeting

Monday February 10, 7:29 am ET

 

NUTLEY, N.J. and DURHAM, N.C., Feb. 10 /PRNewswire-FirstCall/ -- Roche and Trimeris  today announced that new clinical data on FUZEON(TM) (enfuvirtide), the most clinically advanced in an investigational class of anti-HIV drugs known as fusion inhibitors, will be presented at an upcoming scientific meeting focusing on HIV. New data will also be presented on T-1249, a second-generation fusion inhibitor being developed through the Roche/Trimeris partnership, which is currently in Phase I/II clinical testing.

Unlike existing anti-HIV drugs that work inside the cell, FUZEON and T-1249 have a unique mechanism of action that is designed to block HIV before it enters the human immune cell. Consequently, FUZEON and T-1249 are active against HIV that is resistant to the currently available classes of anti-HIV drugs.

Presentations on FUZEON

  • Combined analysis of Phase III studies. This combined analysis of 24 week data confirmed the results of the two Phase III studies -- TORO 1 (T-20 vs. Optimized Regimen Only), conducted in North America and Brazil, and TORO 2, conducted in Europe and Australia -- which have only been reported separately until now.

    In the studies, treatment-experienced patients receiving FUZEON plus an individualized regimen of standard anti-HIV drugs were twice as likely to achieve undetectable levels of HIV in the blood (less than 400 copies/mL) as patients who received an individualized drug regimen without FUZEON (32.7% vs. 15%).

    The response of patients in the FUZEON arm surpassed that of patients taking an individualized regimen alone across all subgroups studied, including age, race, baseline immune cell (CD4) count and baseline viral load. In both treatment arms, greater viral suppression was seen in patients who had more active agents in their individualized regimen, less treatment experience and less advanced disease (CD4 count greater than 100 cells/ul). The combined safety analysis included a safety update with patient exposures for longer than 24 weeks. This analysis focused on further characterizing injection site reactions and combining similar and clinically equivalent adverse event terms to identify any relevant differences between treatment arms. Injection site reactions are the most common adverse event associated with FUZEON. Injection site reactions occurred in almost all patients receiving FUZEON; most had mild to moderate pain or discomfort that did not require analgesics or limit usual activities. While the overall incidence of bacterial infections was similar across both treatment arms when adjusted for time of exposure to the individualized regimen, bacterial pneumonia was observed at increased frequency in patients in the FUZEON arm compared to patients taking an individualized regimen alone (4.5% vs. 0.3%).

    More About FUZEON

    FUZEON, a fusion inhibitor, is administered as a twice-daily subcutaneous injection. Local injection site reactions were the most frequent adverse events associated with the use of FUZEON. In Phase III clinical studies, 98 percent of patients had at least one local injection site reaction. In this treatment-experienced patient population, three percent of patients discontinued treatment with FUZEON as a result of injection site reactions.

    The addition of FUZEON to background antiretroviral therapy generally did not increase the frequency or the severity of the majority of adverse events. There was less than five percent difference in the most common adverse events seen between FUZEON plus an individualized regimen of antiretroviral drugs and individualized regimen alone. In addition to those mentioned above, the most common adverse events seen more frequently in patients receiving FUZEON plus an individualized regimen than in patients who received treatment without FUZEON were headache, peripheral neuropathy, dizziness (excluding vertigo), insomnia, depression, appetite decrease, asthenia, myalgia, constipation and pancreatitis. The majority of adverse events were of mild or moderate intensity.

    Presentation on T-1249

    New data from a short-term study (T1249-102) reveal that T-1249, the second-generation fusion inhibitor, significantly reduced levels of HIV in the blood in most patients who exhibited detectable viral replication while receiving an individualized anti-HIV drug regimen that included FUZEON.

    This study evaluated the antiviral activity and safety of T-1249 over a 10-day period in 25 patients who were participating in Phase II or Phase III studies of FUZEON and who exhibited HIV RNA levels between 5,000 and 500,000 copies/mL at two consecutive clinic visits while on treatment with FUZEON. Patients in this study discontinued FUZEON and added T-1249 to an unchanged individualized anti-HIV drug regimen. The median HIV RNA decline from baseline after 10 days of treatment was 1.1 log10. There were no serious adverse events judged possibly to be related to T-1249 in the trial. The results from this study demonstrate that fusion inhibitors constitute an expanding class of antiretroviral drugs with the potential to be used sequentially.

    More About T-1249

    In an earlier Phase I/II clinical trial of T-1249, no treatment-related, clinically important laboratory abnormalities occurred and no dose-limiting toxicities were identified. Three serious adverse events possibly related to T-1249 occurred: grade 4 neutropenia (25 mg QD), hypersensitivity reaction (25 mg BID), and fever associated with injection site reaction (150 mg QD).

    Roche in HIV

    Roche is at the forefront of efforts to combat HIV infection and AIDS, committed for 15 years to groundbreaking research and development of new drugs and diagnostic technology. The objective is to provide tailored treatment solutions and an improved standard of care worldwide for those people living with HIV.

    About Roche

    Hoffmann-La Roche Inc. (Roche), based in Nutley, N.J., is the U.S. prescription drug unit of the Roche Group, a leading research-based health care enterprise that ranks among the world's leaders in pharmaceuticals, diagnostics and vitamins. Roche discovers, develops, manufactures and markets numerous important prescription drugs that enhance people's health, well being and quality of life. Among the company's areas of therapeutic interest are: dermatology; genitourinary disease; infectious diseases, including influenza; inflammation, including arthritis and osteoporosis; metabolic diseases, including obesity and diabetes; neurology; oncology; transplantation; vascular diseases; and virology, including HIV/AIDS and hepatitis C.

    For more information on the Roche pharmaceuticals business in the United States, visit the company's Web site at: http://www.rocheusa.com.

    About Trimeris, Inc.

    Trimeris, Inc. is a biopharmaceutical company engaged in the discovery and development of novel therapeutic agents for the treatment of viral disease. The core technology platform is based on fusion inhibition aimed at treating disease by preventing viruses from entering host immune cells. Trimeris has two anti-HIV drug candidates in clinical development. FUZEON, currently in Phase III clinical trials, is the most advanced compound in development. A New Drug Application (NDA) and Marketing Authorisation Application (MAA) have been submitted for FUZEON with the US FDA and the EU EMEA, respectively. Trimeris' second fusion inhibitor product candidate, T- 1249, has received fast track status from the FDA and is in Phase I/II clinical testing. Trimeris is developing FUZEON and T-1249 in collaboration with F. Hoffmann-La Roche.

    For more information about Trimeris, Inc., visit the company's website at http://www.trimeris.com.

    Trimeris Safe Harbor Statement

    Note: Except for any historical information presented herein, matters presented in this release are forward-looking statements that involve risks and uncertainties. The results of Trimeris' previous clinical trials are not necessarily indicative of future clinical trials, and future results could differ materially from past results. For a more detailed description of factors that could cause or contribute to such differences, see Trimeris' filings with the Securities and Exchange Commission.


  • Source: Roche; Trimeris

     

    Invisible Condom Protects Monkeys from AIDS Virus

    Mon Feb 10, 4:30 PM ET

    By Maggie Fox, Health and Science Correspondent

    WASHINGTON (Reuters) - A gel containing antibodies to the AIDS virus protected female monkeys against infection in an experiment that suggests such a product might work as an alternative to condoms for people, researchers reported on Monday.

    The study, published in the journal Nature Medicine, helps boost claims by advocates that an "invisible condom" could be a useful way to help stop the spread of AIDS, which now infects 36 million people worldwide.

    AIDS has no cure and is always fatal, although expensive and toxic drugs can extend a patient's life for years. Condoms are the best known method for stopping its transmission.

    Half of all new cases of HIV infection are in women, and many who live in societies where a woman is not always free to demand that her partner use a condom. In addition many men refuse to use one -- whether having sex with another man or with a woman.

    Thus many experts advocate the development of a gel or cream, akin to spermicides used for birth control, that men and women alike could use quietly to prevent infection.

    John Moore of Cornell University in New York, Ronald Veazey of Tulane University in Louisiana and colleagues in the United States and Britain made a gel using one of the antibodies the human body naturally makes to the HIV virus.

    To test it they used monkeys, which do not get AIDS, Researchers have concocted a substitute virus called SHIV, which is a combination of human immunodeficiency virus and the monkey version, called SIV.

    They put the gel, or a saline solution carrying the antibodies, into the vaginas of the 12 female monkeys, then put the virus in up to two hours later. This simulated sexual transmission of the virus.

    "Only three of 12 animals ... became infected," they wrote in their report. In contrast, 12 of 13 animals given a sham treatment became infected with SHIV.

    The antibody Moore's team used does not protect against all strains of HIV, but it is an important proof of the idea, they said. "These observations support the concept that viral entry inhibitors can help prevent the sexual transmission of HIV to humans," they wrote.

    Rebekah Webb, policy development officer for the National AIDS Trust in Britain, welcomed the results.

    "It is definitely a step in the right direction but just one of many promising results from the lab confirming that microbicide is possible," she said in a telephone interview.

    "One of the huge problems in the microbicide field is funding because no big pharmaceutical company is interested in microbicide research," Webb said.

    Drug companies have suggested the market is not big enough -- a view that activists have tried hard to dispel. "We think there is a market. We think there are many emerging markets around the world and companies should be interested in that," Webb said.

    Many studies have been done on potential microbicides, and some are designed to prevent infection not only with HIV but with a range or sexually transmitted diseases, such as syphilis and gonorrhea.

    SOURCE: Nature Medicine 2003;10.1038/nm833.

     

     
    Press Release Source: AIDS ReSearch Alliance

    AIDS ReSearch Alliance and UCLA AIDS Institute Convene Meeting Targeting HIV Reservoirs

    Monday February 10, 3:36 pm ET

     

    BOSTON, Feb. 10 /PRNewswire/ -- AIDS ReSearch Alliance of America (ARA), in conjunction with The UCLA AIDS Institute, today convened a workshop of HIV researchers working in the area of how to eliminate HIV reservoirs in the body -- places that the AIDS virus hides and persists, and that cannot be reached by even the most powerful current drug combinations. The workshop will feature presentations on work in progress by scientists who are attempting to reach an elusive strategy for reaching these sequestered cells, in the hopes that the hidden viral material and the cells housing them can be targeted by Highly Active Antiretroviral Therapy -- HAART -- the current standard of care for those being treated. If successful, there is the possibility that depleting the reservoirs and exposing their hidden virus could lead to a combination of HAART and periodic reservoir-depleting treatments in order to eradicate HIV from the body. So far, this is only a theoretical possibility, but some believe that any outright cure to the disease must successfully target and destroy reservoir sites, such as latently infected immune cells, gut tissue, and other places the virus hides.

    "This is a unique opportunity for scientists working in the field to participate in quality scientific discussion and networking among colleagues," said. Stephen J. Brown, M.D., ARA's Medical Director. "We will be able to focus on a number of critical topics including current barriers to HIV eradication, in vivo and in vitro models of latency, and the development of potential strategies and therapeutic agents to eliminate these reservoirs."

    The HIV reservoirs are formed almost immediately after infection occurs in human. While many T helper cells are infected, essentially turning them into factories to make more copies of the virus, some of these cells are infected and then "go dormant." These dormant cells are activated when the level of virus in the blood is very low and strong medications are no longer effective. Essentially, this allows a lifelong pool of HIV for the disease to rely on even in people on current powerful drugs. Pockets of latently-infected cells include those in the brain, lymphoid tissue, bone marrow, and genital tract, among others.

    After the advent HAART in 1996, there was great optimism that HIV could be eradicated in HIV+ people who were being aggressively treated with combinations of strong drugs that interfered with HIV's ability to reproduce within cells. However, these hopes relied on the assumptions that the virus would remain completely suppressed and did not take into account the existence of the reservoirs, the nature of which was only theorized by some at the time.

    The discovery of HIV reservoirs dashed any hopes of a quick cure. It is now known that HIV can persist for decades within long-lived blood cells. In most cases observed, if someone stops their HAART medication, the latent HIV begins producing new viral copies -- flooding the body with millions of new copies within hours.

    However, recent research in the laboratory suggests that certain agents can "activate" reservoir sites. This in turn has raised hopes among some researchers that it may one day be possible to "pulse" these reservoir-activating agents with a new and improved HAART, dealing HIV a lethal blow by forcing hidden virus into the blood stream where they can then be killed by existing drugs.

    "The very fact that this meeting is happening now is exciting to us. Very few people held much hope for successfully targeting the reservoirs even a year ago. There has been a notable change in the minds of many working on this topic. This workshop offers us some hope that it is not a waste of time to continue looking for an outright cure," said Irl S. Barefield, ARA's Executive Director. Barreled notes that the meeting will help AIDS research Alliance with its own research agenda, as well. AIDS research Alliance is currently investigating a promising anti-HIV compound called prostratin under a license from the National Institutes of Health, a unique arrangement between government and the nonprofit sector to move a drug forward. Prostratin, a drug derived from a plant native to the Samoan rainforests, has activated each reservoir site it has been exposed to in the laboratory. Barefield hopes that human clinical trials of the drug will begin within a year.

    About AIDS ReSearch Alliance of America

    AIDS ReSearch Alliance of America is a non-profit medical research institution with a mission to find and accelerate the development of effective treatments for those living with HIV and AIDS. The organization leverages private funds obtained from industry sponsored clinical research into its own mission-driven research into novel compounds and approaches for treatment, and one day the elimination, of HIV-disease. See www.aidsresearch.org for more information.

    About The UCLA Institute of AIDS:

    Through research and patient care, the UCLA AIDS Institute seeks to understand HIV and its pathogenesis, and seeks to use its research for the practical ends of improving treatments and developing a vaccine for HIV/AIDS. The Institute is a think tank for collaborating scientists who translate research breakthroughs into improved treatment.


    Source: AIDS ReSearch Alliance

     


    Promising New AIDS Drugs on the Horizon

    Tue Feb 11, 4:31 PM ET

    By DANIEL Q. HANEY, AP Medical Editor

    BOSTON - A variety of highly effective new AIDS drugs are on the horizon, experts say, easing worries that the fast-mutating virus will outstrip doctors' ability to treat it.

    Ever since combinations of AIDS medicines transformed HIV into a manageable condition in the mid-1990s, doctors have worried that the virus would eventually mutate into forms that would elude their control. While HIV indeed has evolved into many drug-resistant forms, most patients are still able to find combinations that hold their virus in check.

    At the 10th Conference on Retroviruses in Boston, experts said the outlook for potent and novel medicines to control HIV has never been brighter.

    "The pipeline of new drugs has an impressive number of candidates in it. This is something we haven't seen in past years. It's a bumper crop," said Dr. John Mellors of the University of Pittsburgh.

    Currently, 16 drugs are approved by the Food and Drug Administration to fight AIDS. Most of the medicines are aimed at just two targets in the virus's life cycle, proteins called protease and reverse transcriptate.

    However now, doctors say, drugs are in development that are aimed at eight different points in the process by which HIV attaches itself to blood cells, enters them and finally makes new copies of the virus.

    The next new drug expected to win FDA approval is T-20, being developed by Roche and Trimeris Inc., a so-called fusion inhibitor that blocks HIV from sticking to the blood cells that it attacks.

    At the meeting Tuesday, doctors described encouraging results with the next generation of this drug, called T-1249, that is intended to be used when the virus grows resistant to T-20. Dr. Diego Miralles of Duke University said that even more versions are in the design stage to take over when T-1249 fails.

    "I am very encouraged this year that we seem to be keeping up with the virus in terms of our ability to treat resistant virus with new drugs," Mellors said.

    At least a half dozen promising drugs are in human testing, he said, and 10 or 12 more are in the pipeline.

    Furthermore, AIDS medicines have gotten much easier to take. Just a few years ago, patients had to take 20 or so pills on a carefully timed daily schedule. Now that total is down to just two or three pills taken once or twice a day.

    Among the new drugs in testing is one TNX-355, an antibody from Tanox Inc. Unlike other drugs, this one works by blocking the spot on blood cells where HIV normally attaches itself. Initial testing by Dr. Daniel Kuritzkes and others from Brigham and Women's Hospital in Boston found an injection once every one to three weeks dramatically reduced virus levels.

     
    Press Release Source: Tanox, Inc.

    TNX-355 Phase 1a Trial Results to Be Presented in Boston

    Monday February 10, 4:24 pm ET

     

    HOUSTON, Feb. 10 /PRNewswire-FirstCall/ -- Tanox, Inc. today announced that the detailed results of its Phase 1a human immunodeficiency virus (HIV) clinical trial involving TNX-355 will be presented February 11, 2003 at the 10th Conference on Retroviruses and Opportunistic Infections in Boston. The Phase 1a safety trial demonstrated that the drug is well tolerated and showed a significant decrease in viral load in patients with treatment-refractory HIV infection. TNX-355 is a humanized, non-immunosuppressive anti-CD4 monoclonal antibody being developed by Tanox for the treatment of HIV infection. TNX-355 is designed to directly block cellular infection by HIV by binding to the CD4 receptor on host cell surfaces. HIV binding to the CD4 receptor is an initial step in virus progression. This monoclonal antibody is one of a new class of drugs called viral entry inhibitors. "HIV is a growing problem, and we are excited that we may have a potential therapy to aid individuals in the fight against this life-threatening disease," said Nancy Chang, CEO of Tanox. A Phase 1b nine- week, multi-dose safety trial is currently in progress.

    About Tanox

    Tanox, Inc. is a biopharmaceutical company with demonstrated expertise in monoclonal antibody technology. The Company is engaged in the discovery and development of therapeutic monoclonal antibodies designed to address significant unmet medical needs in the areas of asthma, allergy, inflammation and other diseases affecting the human immune system. Xolair(TM), Tanox's most advanced product in development, is an anti-immunoglobulin E, or anti-IgE, antibody whose therapeutic effect has been validated through clinical trials in patients suffering from allergic asthma and seasonal allergic rhinitis (hay fever). Xolair is being developed under an agreement among Tanox, Novartis Pharma AG and Genentech, Inc. In June 2002, Xolair received marketing approval in Australia for treating adults and adolescents with moderate allergic asthma. Genentech submitted an amended Biologics License Application to the FDA in December 2002.

     
    Source: Tanox, Inc.

     

    Study shows high HIV rates for black gays

    Mon Feb 10, 7:35 PM ET

    Randy Dotinga, Gay.com / PlanetOut.com Network

    SUMMARY: A federal study shows that black gay men, both closeted and out, have significantly higher rates of HIV infection than other ethnic groups.

    New research suggests that young, black gay men are more likely to be closeted than whites, and African Americans with hidden lives appear to have much higher HIV infection rates than their counterparts from other races.

    According to a federal survey of more than 5,500 young gay and bisexual men released this month, 14 percent of black men who consider themselves closeted were found to be HIV-positive. The infection rates were less than half that for closeted whites and Hispanics.

    But even openly gay black men aren't in the clear. Their AIDS infection rates were even higher -- 24 percent.

    The study findings provide more evidence that black men feel more pressure to live gay lives "on the down low" -- in the closet.

    "African-Americans have faced a dilemma: to face the racism within the (lesbian and gay) community or the homophobia within the African-American community," said Stephen Thomas, director of the Center for Minority Health at the University of Pittsburgh, in an interview with HealthScoutNews.com.

    The statistics come from interviews between 1994 and 2000 with gay and bisexual men at bars, nightclubs and other popular gathering spots in six cities (Baltimore, Dallas, Los Angeles, Miami, New York and Seattle). The men, aged 15-29, were asked to rate their level of "outness" on a scale of one to seven. They also received HIV and hepatitis B tests.

    Researchers considered only 11 percent of all the men surveyed to be closeted because they said they were only out to a few people. But 18 percent of black men said they were closeted.

    In all ethnic groups, closeted men were much more likely than out men to consider themselves to be bisexual or even heterosexual.

    Among all races, 11 percent of the most closeted men were infected with HIV, compared to 8 percent of those who were out. Nearly one in four "out" black men were HIV-positive, compared to 14 percent of those who were closeted.

    Black men were also much more likely to be infected with hepatitis B. One in five "out" black men were infected, and 23 percent of closeted men were. By comparison, the infection rates for whites and Hispanics ranged from 9 to15 percent.

    Thomas, the Center for Minority Health director, told HealthScoutNews.com that health workers don't know the best ways to reach young, gay black men.

    "The truth of this matter is we don't have any concrete, science-based interventions for this population," he said. "This is the group that's going to not only get infected themselves but are going to drive infection into larger populations and large communities, and that should be a concern for everyone."

     

     
    Press Release Source: Progenics Pharmaceuticals, Inc.

    Progenics Presents New Findings from a Phase-2 Clinical Trial of PRO 542 HIV Entry Inhibitor

    Tuesday February 11, 5:00 am ET

    Viral-Sensitivity Test Tracked Clinical Activity, No Drug Resistance Observed

     

    BOSTON--(BUSINESS WIRE)--Feb. 11, 2003-- Progenics Pharmaceuticals, Inc.  reported encouraging new findings from a phase-2 clinical trial of its investigational drug, PRO 542, for treatment of human immunodeficiency virus (HIV) infection.

    Progenics' scientists found that the magnitude of viral load reductions observed in a previously completed clinical trial were correlated strongly with viral susceptibility to PRO 542 prior to drug treatment, as measured by the PhenoSense(TM) HIV Entry assay from ViroLogic, Inc.  The Company believes that viral-resistance testing may identify patients who will derive the greatest benefit from therapy with HIV entry inhibitors. In addition, patient viruses collected six weeks after treatment initiation showed no evidence of having developed resistance to PRO 542. The findings were presented at the 10th Conference on Retroviruses and Opportunistic Infections in Boston.

    PRO 542 belongs to a new class of drugs, viral-entry inhibitors, which are intended to prevent HIV from entering and infecting cells. Unlike currently approved therapies that block viral replication in cells already infected with HIV, PRO 542 is an antibody-like molecule that is designed to target and neutralize the virus in the bloodstream. Because of its novel mechanism of action, PRO 542 has the potential to be broadly active against viruses that have acquired resistance to existing classes of antiretroviral therapies.

    Late last year, the Company reported that, in a phase-2 clinical trial, single doses of PRO 542 reduced concentrations of HIV in the blood by 60% to 80% in a target population of highly treatment-experienced patients. The viral-load reductions were sustained throughout the six-week follow-up period, and no serious side effects were observed. Now, new laboratory studies performed in association with this trial revealed that clinical activity (cumulative viral-load reduction) was highly correlated (r = 0.97 and p = 0.0077) to in vitro viral susceptibility to PRO 542 as measured via the PhenoSense HIV Entry assay.

    The PhenoSense Entry assay was also used to compare the susceptibility of patients' viruses to PRO 542 before and after therapy. No significant change in PRO 542 sensitivity was observed for viruses collected from patients at the end of the six-week study period, during which time most patients continued to have reduced viral loads. This clinical finding supports previous laboratory studies and suggests that viral resistance to PRO 542 does not readily develop in man.

    "We are currently testing PRO 542 in multi-dose phase-2 clinical studies as therapy for HIV-infected individuals who are no longer responding to available antiretroviral therapies," explained William C. Olson, Ph.D., Progenics' Vice President of Research and Development. "The strong correlation between measurements of viral sensitivity and the magnitude of viral-load reductions, support the use of the PhenoSense assay in future clinical studies as a means of identifying and selecting those treatment-experienced patients who might benefit most from PRO 542 therapy."

    Progenics is also developing PRO 140, a second HIV entry inhibitor PRO 140 is a humanized monoclonal antibody that is designed to block HIV entry by binding to a portion of the CCR5 receptor that the virus uses to infect cells. PRO 140 has been shown to inhibit the entry of multiple strains of HIV into immune system cells, in vitro. In addition, it has demonstrated the unique ability to block HIV entry via CCR5, while leaving the normal function of this receptor unaffected. Preclinical testing and manufacturing scale-up are expected to be completed in the coming months, with the Investigational New Drug Application scheduled to be filed thereafter.

    Company Profile

    Progenics Pharmaceuticals, Inc. of Tarrytown, NY, is a diversified biopharmaceutical company focusing on the development and commercialization of innovative therapeutic products to treat the unmet medical needs of patients with debilitating conditions and life-threatening diseases. The Company applies its expertise in immunology and molecular biology to develop biopharmaceuticals to fight viral diseases, such as human immunodeficiency virus (HIV) infection, and cancers, including malignant melanoma and prostate cancer. In supportive care, therapies are being developed to provide patients with an improved quality of life. Progenics' most clinically advanced product is methylnaltrexone, a compound in phase-3 clinical testing that is designed to block the debilitating side effects of opioid analgesics without interfering with pain palliation. The Company is conducting multi-dose phase-2 clinical trials with its lead HIV product, PRO 542, a viral-entry inhibitor and is in preclinical development with PRO 140 and other follow-on product candidates in HIV infection. The Company is developing cancer immunotherapies based on PSMA (prostate-specific membrane antigen) technology and currently is conducting phase-1 clinical studies of a therapeutic prostate cancer vaccine. GMK is a cancer vaccine in phase-3 clinical trials for the treatment of malignant melanoma.

    This press release contains forward-looking statements. Any statements contained herein that are not statements of historical fact may be forward-looking statements. When the Company uses the words 'anticipates,' 'plans,' 'expects' and similar expressions they are identifying forward-looking statements. Such forward-looking statements involve risks and uncertainties which may cause the Company's actual results, performance or achievements to be materially different from those expressed or implied by forward-looking statements. Such factors include, among others, the uncertainties associated with product development, the risk that clinical trials will not commence when or proceed as planned, the risks and uncertainties associated with dependence upon the actions of the Company's corporate, academic and other collaborators and of government regulatory agencies, the risk that products that appear promising in early clinical trials do not demonstrate efficacy in larger-scale clinical trials, the uncertainty of future profitability and other factors set forth more fully in the Company's Annual Report on Form 10-K for the fiscal year ended December 31, 2001 and other periodic filings with the Securities and Exchange Commission to which investors are referred for further information. In particular, the Company cannot assure you that any of the their programs will result in a commercial product. The Company does not have a policy of updating or revising forward-looking statements, and thus it should not be assumed that the Company's silence over time means that actual events are bearing out as expressed or implied in such forward-looking statements.

     

     
    Press Release Source: Gilead Sciences

    96-Week Data From Phase III Study Show Long-Term Efficacy With Reduced Risk of Lipid and Metabolic Changes for Viread Versus Stavudine in Treatment-Naive HIV Patients

    Tuesday February 11, 8:13 am ET

    Data Presented at 10th Conference on Retroviruses and Opportunistic Infections

     

    BOSTON--(BUSINESS WIRE)--Feb. 11, 2003-- Gilead Sciences  today presented 96-week data from a controlled clinical trial (Study 903) demonstrating that treatment-naive patients who received Viread® (tenofovir disoproxil fumarate) experienced substantially less lipodystrophy and lower elevations in fasting cholesterol and triglyceride levels, while achieving similar reductions in HIV viral load and increases in CD4 cell counts, compared to those who received stavudine (d4T).

    Study 903 is an ongoing three-year, randomized, double-blind trial designed to compare the efficacy and safety of a treatment regimen of Viread, lamivudine (3TC) and efavirenz to a regimen of stavudine, lamivudine and efavirenz in 600 antiretroviral-naive patients with HIV infection. The 96-week data were presented today (Abstract #564b) at the 10th Conference on Retroviruses and Opportunistic Infections in Boston, Massachusetts.

    "These data are impressive because efficacy remains strong in both arms at 96 weeks, but the Viread-containing arm has a side effect profile that has continued to improve compared to stavudine since the 48-week point," said Schlomo Staszewski, MD, University Hospital, J.W. Goethe-Universitat, Frankfurt, Germany and a lead investigator for the study. "The potential for long-term efficacy with reduced side effects compared to stavudine makes Viread an attractive antiretroviral for use in HIV therapy."

    Study Results

    The 96-week results presented today show that the Viread and stavudine arms reduced HIV RNA to less than 400 copies/mL in 82 and 78 percent of patients respectively, using the most conservative "missing equals failure" analysis. Seventy-eight and 74 percent of patients achieved HIV RNA less than 50 copies/mL. Excluding missing data, 96 and 93 percent of patients in the Viread and stavudine arms achieved HIV RNA less than 400 copies/mL and 92 and 88 percent of patients achieved HIV RNA less than 50 copies/mL. Patients in both arms of the study experienced substantial increases in mean CD4 cell counts, from the baseline mean of 276 to 537 cells/mm3 in the Viread arm and from the baseline mean of 283 to 549 cells/mm3 in the stavudine arm. Grade 3 and 4 adverse events and laboratory abnormalities were similar across treatment groups. Grade 3 and 4 adverse events were reported in less than two percent of patients and included rash, bacterial infection, depression, fever and pneumonia. There was a low discontinuation rate of approximately 15 percent in both arms.

    Lipid levels (triglycerides and cholesterol) measured in the fasting state were significantly different between the Viread and stavudine treatment groups. Patients receiving Viread experienced a mean increase from baseline in triglycerides of 5 mg/dL, whereas patients in the stavudine group experienced an increase of 103 mg/dL (p less than 0.001). Increases in low-density lipoprotein cholesterol (LDL or "bad" cholesterol) were 82 percent higher for patients receiving stavudine, with an increase of 11 mg/dL in the Viread arm and an increase of 20 mg/dL in the stavudine arm (p less than 0.001). Significant differences also were noted in the impact of therapy on high-density lipoprotein cholesterol (HDL or "good" cholesterol), with patients in the Viread treatment group experiencing a mean increase of 9 mg/dL in "good" cholesterol, compared with an increase of 7 mg/dL in the stavudine arm (p=0.03). In addition, 10 percent of patients in the stavudine arm added a lipid-lowering drug during the study compared to two percent in the Viread arm.

    Metabolic Changes

    The 96-week data from this study further extend the evidence of Viread's favorable metabolic profile for treatment-naive patients observed at 48 weeks. Physician-reported lipodystrophy was observed in one percent of patients receiving Viread, compared with 12 percent of patients receiving stavudine (p less than 0.001). In a separate sub-study of 250 patients, whole-body DEXA scans showed significantly more limb fat in the Viread arm than the stavudine arm at 96 weeks. Loss of limb fat, or peripheral lipoatrophy, is a crucial component of lipodystrophy -- characterized as diverse changes in metabolism and body shape -- which has been associated with long-term administration of some anti-HIV medications.

    Additionally, patients in the Viread arm experienced a favorable weight gain of 6.1 pounds from baseline versus 0.8 pounds in the stavudine arm (p=0.002). Weight gain is an important indicator of overall well being for HIV-infected patients.

    Patients who received Viread had significantly fewer adverse events associated with mitochondrial toxicity, such as peripheral neuropathy, lactic acidosis and lipodystrophy. After 96 weeks of treatment, the relative risk of these toxicities was 5.5 fold greater (95 percent confidence interval: 3.0-10.3 fold) in the stavudine-containing arm compared with the Viread-containing arm.

    "These results add to an expanding body of evidence suggesting that Viread can be broadly effective in suppressing HIV, and also may result in a lower rate of certain adverse side effects associated with other treatment regimens," said John C. Martin, PhD, President and Chief Executive Officer, Gilead Sciences. "As patients and physicians become more aware and justifiably concerned about the impact of cardiovascular problems and metabolic conditions such as lipodystrophy, these data support Viread as an increasingly important treatment option. Avoiding these potentially serious side effects helps ensure patients will be able to continue to benefit from therapy for long periods of time."

    Study 903 Continues

    Gilead designed Study 903 as a three-year trial to gather a wide variety of data on Viread's efficacy and safety profile in a controlled manner over time. Study 903 is being conducted in the United States, Europe and South America. Twenty-six percent of the study participants are women, and 36 percent are people of color. According to the U.S. Centers for Disease Control, women now account for 30 percent of new HIV infections in the United States, while nearly three-fourths of new HIV infections affect non-Caucasians.

    About Viread

    Viread is the first nucleotide analogue reverse transcriptase inhibitor (NtRTI) approved for the treatment of HIV in the United States and Europe. Since approval, approximately 85,000 patients have been prescribed Viread as part of combination therapy in the United States alone. The U.S. Food and Drug Administration approved Viread for marketing in October 2001 and the European Commission granted approval in February 2002. In clinical trials and expanded access programs, approximately 10,000 patients have been treated with Viread alone or in combination with other antiretroviral products for periods up to four years. The drug works by blocking reverse transcriptase, an enzyme involved in the replication of HIV. The approved dose of Viread for the treatment of HIV infection is 300 mg once daily taken orally with a meal.

    In the United States, Viread is indicated for use in combination with other antiretroviral agents for the treatment of HIV-1 infection. This indication is based on analyses of plasma HIV-1 RNA levels and CD4 cell counts in a controlled study of Viread of 24 weeks duration and in a controlled, dose-ranging study of Viread of 48 weeks duration. Both studies were conducted in treatment-experienced adults with evidence of HIV-1 viral replication despite ongoing antiretroviral therapy. Studies in antiretroviral-naive patients are ongoing; consequently, the risk-benefit ratio for this population has yet to be determined.

    Safety Profile

    Assessment of adverse reactions is based on two studies (902 and 907) in which 653 treatment-experienced patients received treatment with Viread 300 mg (n=443) or placebo (n=210) for 24 weeks followed by extended treatment with the drug. Adverse event rates in the Viread group were similar to those in the placebo-treated patients. The most common adverse events in these patients were mild to moderate gastrointestinal events, such as nausea, diarrhea, vomiting and flatulence. Laboratory abnormalities observed in clinical studies occurred with similar frequency in the Viread and placebo-treated groups.

    In clinical practice, a number of adverse events, including renal impairment, nausea, rash and asthenia (weakness) have been reported. Renal impairment occurred most often in patients with underlying systemic or renal disease, or in patients taking concomitant nephrotoxic agents. Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleoside analogues alone or in combination with other antiretrovirals.

    About Gilead Sciences

    Gilead Sciences is a biopharmaceutical company that discovers, develops and commercializes therapeutics to advance the care of patients suffering from life-threatening diseases worldwide. The company has six marketed products and focuses its research and clinical programs on anti-infectives. Headquartered in Foster City, CA, Gilead has operations in the United States, 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 that could cause actual results to differ materially from those referred to in the forward-looking statements. These and other risks are described in detail in the Gilead Annual Report on Form 10-K for the year ended December 31, 2001 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.

     

     

     
    Press Release Source: Gilead Sciences

    Phase III Data Show Emtricitabine Maintains Viral Load Suppression as Part of Once-Daily, Protease-Sparing Anti-HIV Regimen

    Tuesday February 11, 8:14 am ET

    48-Week Data from Alize Trial Presented Today at 10th Conference on Retroviruses and Opportunistic Infections

     

    BOSTON--(BUSINESS WIRE)--Feb. 11, 2003-- French researchers presented new 48-week data from a Phase III clinical trial today. These data demonstrate that emtricitabine (FTC), an investigational once-daily nucleoside reverse transcriptase inhibitor (NRTI), suppresses HIV when taken as part of a once-daily, protease inhibitor (PI)-sparing antiretroviral regimen. Emtricitabine is being developed by Triangle Pharmaceuticals, which was acquired by Gilead Sciences in January 2003. Dr. Jean-Michel Molina presented the 48-week results of the ANRS 099 Alize trial (Abstract #551) at the 10th Conference on Retroviruses and Opportunistic Infections in Boston, Massachusetts.

    The ANRS 099 Alize trial is an ongoing three-year, open-label, multicenter study involving 355 patients who at baseline had to have HIV RNA less than 400 copies/mL while receiving PI-based antiretroviral therapy. The median duration of PI therapy was 35 months, and the median CD4 cell count was 540 cells/mm3. Patients were randomized (1:1) to continue their stable PI-based regimen or switch to an entirely once-daily regimen of emtricitabine, didanosine (another NRTI) and efavirenz (a non-nucleoside reverse transcriptase inhibitor, or NNRTI).

    "These data suggest that switching to a once-daily, PI-sparing antiretroviral regimen including emtricitabine is effective in maintaining suppression of HIV infection," said Dr. Molina. "While both arms of the study demonstrated comparable and durable antiviral response, the data may be of particular interest to physicians and patients who now have the alternative to use a convenient once-daily HAART regimen with a low pill burden."

    Study Results

    At 48 weeks, 94 percent of patients receiving the once-daily regimen of emtricitabine, didanosine and efavirenz had HIV RNA levels (viral load) less than 400 copies/mL, compared to 92 percent randomized to continue therapy in the PI-based arm (intent to treat population, assays performed at local laboratories at investigational centers). When all the samples were analyzed with a more sensitive assay at a central laboratory, the proportion of patients with HIV RNA less than 50 copies/mL at week 48 was significantly higher in the once-daily treatment group. Ninety-five percent of patients in the once-daily group achieved this result, compared to 87 percent in the PI-based arm (p=0.01). The median CD4 cell count increase was comparable in both arms, with an increase of 21 cells/mm3 for patients on the once-daily regimen and 13 cells/mm3 for those in the PI-based group.

    The discontinuation rate in the study was similar between the two arms, with 10.1 and 12.4 percent of patients in the once-daily arm and PI-based arm discontinuing, respectively. Additionally, patients switching to once-daily therapy with emtricitabine, didanosine and efavirenz experienced an increase of 7.7 mg/dL in fasting high-density lipoprotein cholesterol (HDL - or "good" cholesterol), as compared to no change in the PI-based arm (p less than 0.0001). In clinical studies of emtricitabine, the most common adverse events observed have been infection, diarrhea, headache, nausea and rash.

    "These results suggest that emtricitabine will play a key role in future anti-HIV therapy, in particular when given with other once-daily therapies such as Gilead's existing HIV medication, Viread® (tenofovir disoproxil fumarate)," said John C. Martin, PhD, President and Chief Executive Officer, Gilead Sciences. "Emtricitabine's ability to control HIV replication in different treatment combinations confirms our confidence in this compound. Today's HIV patients and physicians are demanding convenient, once-daily treatment regimens with minimal side effects. We expect that, together with Viread, emtricitabine will be important in meeting this need."

    About Emtricitabine

    Emtricitabine is a once-daily nucleoside reverse transcriptase inhibitor currently in Phase III testing for the treatment of HIV and chronic hepatitis B. Emtricitabine is chemically related to lamivudine (3TC), the most commonly-prescribed drug for HIV infection. In vitro, the drug has been shown to be four- to ten-fold more potent than lamivudine.

    Applications for marketing approval of emtricitabine for the treatment of HIV were submitted to U.S. and European regulatory authorities in September and December of 2002, respectively, by Triangle Pharmaceuticals. Emtricitabine has not been determined safe or efficacious for the treatment of HIV or chronic hepatitis B by the FDA or any other regulatory agency.


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