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Mar 24, 2003: ADVR Granted
Therapeutic Composition Patent For Product R; U.S. Patent Awarded for
Chemical Structure of Novel Peptide Nucleic Acid YONKERS, N.Y., March 24 /PRNewswire-FirstCall/ -- Advanced Viral Research Corp. (OTC Bulletin Board: ADVR) today announced that it has been awarded U.S. Patent Number 6,528,098, entitled "Preparation of a Therapeutic Composition," for Product R, the peptide nucleic acid immunomodulator currently in clinical trials in Israel. The claims of the newly issued patent focus on the chemical structures of the two unique peptides that constitute Product R. The patent describes the amino acid compositions and sequences of peptides A and B. In addition, the claims include the nature of the polynucleotide conjugate of peptide B. Product R is composed of two peptides that, in combination, produce a stable biopolymeric structure highly resistant to degradative enzymes such as nucleases and peptidases. "This new patent is a significant and important addition to the intellectual property of Advanced Viral Research Corp. The chemical structure of the peptide nucleic acid described in this patent unfolds a rich, new chemistry that may yield important future therapeutic agents related to Product R," said Shalom Z. Hirschman, M.D. President and CEO. "The patent describes the unique chemical structure of the two peptides present in Product R, including the peptide that is a novel peptide nucleic acid conjugate. The chemical structures of the peptides of Product R were filed in our Drug Master File submitted with our investigational new drug (IND) application to the US FDA in 2001." "We believe that Product R may one day play a broad role in the treatment of a variety of diseases," said Eli Wilner, Chairman of the Board of Advanced Viral. "We are committed to ensuring that the intellectual property associated with the ultimate commercialization of Product R is broadly and adequately protected." In October 2001 the company was granted a U.S. Patent for the preparation and overall composition of Product R. ADVR holds 10 U.S. patents related to Product R that cover such areas as the preparation and chemistry of Product R, and such uses as the treatment of anemia by stimulating red blood cell production, the treatment of canine distemper, the treatment of human parvovirus infection, the treatment of basal cell carcinoma, and the topical treatment of skin and eye infections. From the ADVR news release: Mar 24, 2003 |
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MS Research: Component of a Virus (Synctin)
Linked to Multiple Sclerosis In yet another volley for the recently reinvigorated infectious model of Multiple Sclerosis, a new study has found a component of an ancient virus is found in MS brains at a 3 times higher rate than that of controls. Furthermore, this virus protein is known to antagonize the immune system... "Syncytin, a virus protein that has been around for millions of years, may play a role in the nerve damage that occurs with multiple sclerosis (MS), scientists report in the journal Nature Neuroscience... Syncytin is present in the brain tissue of patients with MS at levels about three times higher than in healthy brain tissue. They also found that syncytin stimulates the production of various inflammatory chemicals. Ferulic acid, a readily-available supplement, counters synctin. Interestingly enough, ferulic acid is said to weakly mimic curcumin, which has been shown to be beneficial to MS but is difficult to absorb. However, before you rush out to buy Ferulic acid, remember the golden rule: Every supplement or medicine has its own side effects, and to date there has been no research proving ferulic acid is safe in HUMAN forms of MS. Always consult your doctor! In any case, research on treatments that are readily available is always promising. Full Article Text Ancient Virus Protein Linked to Multiple Sclerosis Mon Sep 27, 2004 06:21 PM ET By Karla Gale NEW YORK (Reuters Health) - Syncytin, a virus protein that has been around for millions of years, may play a role in the nerve damage that occurs with multiple sclerosis (MS), scientists report in the journal Nature Neuroscience. This finding could lead to new treatments for the devastating neurologic disease. Syncytin "can activate immune mechanisms, which can ultimately damage cells that make myelin," an important nerve covering that gradually disappears in patients with MS, senior author Dr. Christopher Power, at the University of Calgary in Alberta, Canada, told Reuters Health. Power and his international research team found that syncytin is present in the brain tissue of patients with MS at levels about three times higher than in healthy brain tissue. They also found that syncytin stimulates the production of various inflammatory chemicals. By introducing the gene for syncytin into mice, the researchers were able to create animals that had symptoms commonly seen in humans with MS, such as weakness and unsteady gait. The symptoms and tissue changes were reversed when the mice were treated with a chemical called ferulic acid. Power noted that ferulic acid was well tolerated by the animals, and said he hopes to further explore its potential as a therapeutic agent in patients with MS. Other drugs currently being tested may be found to have an effect on syncytin, Dr. Mark P. Mattson and Dr. Dennis D. Taub of the National Institute on Aging Intramural Research Program, Baltimore, remark in a related editorial. But it will be important to know what other tissues are affected by syncytin, they add, because critical functions could be compromised by treatments aimed at syncytin. SOURCE: Nature Neuroscience, 2004. Source: http://www.reuters.com/newsArticle.jhtml?type=healthNews&storyID=6346673 |
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T-Cell Costimulatory Immunotherapy
Effective in Rheumatoid Arthritis Model By Will Boggs, MD NEW YORK (Reuters Health) Sept 27 - Immunotherapy mediated by a T-cell costimulatory receptor suppresses rheumatoid arthritis in a mouse model, according to a report in the September 26th advance online publication of Nature Medicine. The receptor, 4-1BB, has been associated with suppression of CD4+ T-cell responses and improved autoimmune diseases by unknown mechanisms, the authors explain. "Autoimmune diseases can be treated by selectively deleting autoreactive pathogenic CD4 T cells by triggering 4-1BB," Dr. Byoung S. Kwon, from Louisiana State University Health Sciences Center, New Orleans, Louisiana, told Reuters Health. "This implies that a therapeutic modality against autoimmune diseases can be developed in which deleterious side effects are minimized or avoided." Dr. Kwon and colleagues used the collagen-induced arthritis (CIA) mouse model to examine the role of 4-1BB in the progression of arthritis. Anti-4-1BB, an agonistic antibody, strongly suppressed CIA, the authors report, and anti-4-1BBL, an antibody that blocks the interaction between the receptor and its ligand, resulted in milder disease. "These results suggest that triggering 4-1BB with anti-4-1BB induces an active suppression mechanism that differs from the effect of blocking [receptor-ligand] interactions," the investigators write. Anti-4-1BB also improved established arthritis in this model, the report indicates. Further experiments suggested the mechanism behind 4-1BB's effects. "Triggering of 4-1BB on CD8 T cells leads to the expansion of CD11cCD8 T cells that produce interferon-gamma, the paracrine effects of which, in turn, regulate transcription of the IDO [indoleamine 2,3-dioxygenase] gene in dendritic cells," Dr. Kwon said. "Expression of IDO in dendritic cells causes selective deletion of antigen-specific CD4 T cells. As a result, CD4 T cell-mediated arthritis can be treated." Moreover, adoptive transfer of CD11cCD8 T cells resulting from 4-1BB immunotherapy effectively treated CIA in other mice, the researchers note in the study. "We have developed an agonistic humanized anti-human 4-1BB and plan to conduct preclinical trials in nonhuman primates," Dr. Kwon added. Nat Med 2004. |
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T-Cell Costimulatory Pathways Upcoming Biologic Agents for the Treatment of Rheumatic Diseases from Current Opinion in Rheumatology Inhibition of T-Cell Costimulatory Pathways T-cell costimulatory molecules are cell surface proteins that play important roles in the activation of T cells. Binding of a T-cell surface costimulatory molecule with its ligand expressed on the surface of an antigen-presenting cell (APC) provides a second signal to the T cell in addition to the signal generated from T cell receptor (TCR) recognition of antigen-MHC complex. The second, costimulatory signal promotes T cell activation in response to antigen recognition. In the absence of costimulatory signals, T-cell responsiveness is impaired. There are several sets of costimulatory molecules, including the CD40-CD40 ligand (CD-40L), CD28-CTLA4-B7, CD11a/CD18 (LFA-1)-intracellular adhesion molecule-1, OX40 (CD134)-OX40L, 4-1BB-4-1BBL, and CD2-LFA3 pathways. The possible roles of these various costimulatory pathways in autoimmune disease and transplantation has been reviewed.[63**, 64 65**, 66] Clinical efforts to treat various inflammatory and immune diseases by inhibiting costimulatory signals with monoclonal antibodies (anti-CD40 ligand) and recombinant naturally occurring inhibitory molecules (CTLA4) are ongoing. CTLA4 Immunoglobulin The B7 family of cell surface molecules delivers stimulatory signals to T cells through interaction with a common ligand, CD28, present on T-cell surfaces and suppressive signals through binding with T-cell surface-expressed CTLA4 (CD154). A soluble chimeric molecule, CTLA4 immunoglobulin has been developed to inhibit T-cell costimulation by B7-family molecules. CTLA4 immunoglobulin consists of the extracellular component of CTLA4 fused to human IgG Fc. The affinity of CTLA4 for B7 molecules is greater than the affinity of CD28, permitting CTLA4 immunoglobulin to prevent B7-mediated CD28 signaling. Administration of this molecule to humans with chronic plaque psoriasis significantly reduces cutaneous inflammation.[67, 68] In a phase I dose-finding study, 214 subjects with RA were given four doses of CTLA4 immunoglobulin, LEA29Y (a second-generation CTLA4 preparation), or placebo. At the end of the study, ACR20 responses were noted to increase in a dose-dependent fashion with both active treatments.[69**] A phase IIb study of CTLA4 immunoglobulin in subjects with RA on concurrent methotrexate found that subjects receiving the higher dose of CTLA4 immunoglobulin (10 mg/kg every 2 weeks) were more likely to achieve an ACR20 response than those receiving placebo and methotrexate (60% vs 35.3%, P > 0.001).[70] Phase III studies of CTLA4 immunoglobulin in methotrexate partial responders and in subjects who have failed to respond to anti-TNF agents are currently in progress. Costimulatory blockade has also been considered in the management of systemic lupus erythematosus (SLE). Preclinical studies have shown that CTLA4-Fc fusion protein effectively reduces disease activity in animal models.[71] In addition, combination costimulatory blockade in lupus-prone New Zealand black and white mice using CTLA4 immunoglobulin and anti-CD40L monoclonal antibody led to sustained suppression of pathogenic anti-dsDNA antibodies and prolonged survival; however treatment with either agent alone failed to reduce disease activity.[72] Anti-CD40 Ligand Monoclonal Antibody Interaction between CD40 on APC surfaces and its ligand on T-cell surfaces, CD40L, generates c-stimulatory signals for T-cell activation. This ligand-receptor pair also induces B-cell proliferation and formation of germinal centers when CD40L present on activated T cells binds CD40 expressed on B cells. Two monoclonal antibodies against CD40L have been developed and tested in patients but have failed to demonstrate the same success in human subjects with RA and SLE as has been observed in animal models of arthritis and autoimmune disease. The trial of one antibody (IDEC-131) showed limited efficacy.[73] The other (hu5c8, BG9588, Biogen) showed evidence of biologic effect. A recent mechanistic study of B cells obtained from five patients with SLE who participated in an open-label study of this anti-CD40L antibody, found that anti-CD40L treatment induced a persistent reduction in the frequency of anti-dsDNA antibody-producing B cells.[74**] However, studies using this particular agent found an unexpected excess of thrombotic events in the treatment group and were terminated early.[75] Additional studies of CD40/CD40L inhibition are under consideration. Anti-CD11a Monoclonal Antibody The T-cell surface complex CD11a/CD18 (also termed LFA-1) interacts with its ligand, intercellular adhesion molecule-1 (ICAM-1), as part of a costimulatory pathway for T-cell activation. LFA-1-ICAM-1 interaction also serves to form a tight junction adjacent to the TCR that enhances the interaction between the TCR and antigen/MHC complex on APCs. A humanized, monoclonal antibody against CD11a (called efalizumab) has been developed to disrupt this interaction. Efalizumab treatment of psoriasis has resulted in consistent clinical and histologic improvement in several clinical trials.[76, 77] A phase II, randomized, controlled trial of efalizumab for the treatment of subjects with RA on concurrent methotrexate is underway. Curr Opin Rheumatol 15(3):226-236, 2003. |
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Immune system and stress Texas A&M University Stress for newborns could weaken immune system later in life COLLEGE STATION, Sept. 30, 2004 - Intense traumatic events, such as maternal separation, occurring early in the life of an infant may weaken its immune system, making it more susceptible to viral infections later in life that could trigger multiple sclerosis, reveals research at Texas A&M University. The research, by a psychologist Mary Meagher from the College of Liberal Arts and an immunologist Jane Welsh from the College of Veterinary Medicine at Texas A&M, shows that exposure to prolonged maternal separation during the first two weeks of life altered immune, endocrine and behavioral responses to acute "Theiler's virus" infection in mice. Theiler's virus attacks the central nervous system during the first few weeks of infection, which is accompanied by polio-like symptoms. If the virus persists in the central nervous system, a subsequent chronic phase of the disease develops which is similar to multiple sclerosis in humans. Researchers use Theiler's virus to investigate the role of stress in autoimmune diseases, or diseases that cause the body to attack its own cells as if they were foreign pathogens - a similar process occurs in multiple sclerosis, Meagher explains. In this study, infant mice that were subjected to maternal separation and later contracted Theiler's virus as adults demonstrated an increased amount of the virus, altered behavioral signs of infection and had a more difficult time getting over, or "clearing," the infection in its acute stage than did mice that were not separated from their mothers and later contracted the disease. Such results, Meagher explains, suggest that the immune system is undergoing a critical period of development early in an organism's life, and that a considerable stressor can cause significant life-long alterations to the immune system that increase its vulnerability to diseases of the central nervous system later in life. Previous studies have shown stress to play an important role in the contracting of multiple sclerosis in humans, finding that 80 percent of adults who contract the disease reported a stressful life event two years before its onset. Meagher's research takes that exploration a step further, examining how early life stress alters vulnerability to later viral infections of the central nervous system. Her research is being conducted as part of the "Recovery of Function" program, a new interdisciplinary program that enrolls about 30 graduate students and is composed of 14 faculty members from seven departments in four colleges at Texas A&M - the Colleges of Liberal Arts, Veterinary Medicine, Agriculture and Life Sciences, and Medicine. The program focuses on research interests such as the loss and recovery of neural function following injury, infection, aging and neurodegenerative disease in laboratory animal models. In addition, the program is affiliated with several off-campus research centers in Houston, Galveston and Dallas that focus on both laboratory and clinical research. Understanding how early stress affects the developing immune system could lead to interventions that prevent or reverse the harmful effects of newborn stress on disease predisposition, Meagher says. Some treatments could possibly include antidepressants and/or teaching coping mechanisms for individuals who are more likely to be susceptible to the disease, she adds. |
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Antiretroviral Treatment of AIDS
Mothers and High Drug Levels in Nursing Babies 03 Oct 2004 Women who take combination AIDS drugs not only have benefits for their own health but also may pass along high levels of the medication through breast-feeding, potentially protecting their infants from HIV infection, suggests research being presented at the 42nd Annual Meeting of the Infectious Diseases Society of America (IDSA). “It's a really surprising finding and could potentially mean a two-for-one situation,” said Roger Shapiro, MD, research associate for the Harvard School of Public Health and instructor at Harvard Medical School, Boston. As many as one in eight babies born to women with HIV/AIDS acquire the virus during breast-feeding. Because of that risk, HIV-positive women in industrialized nations are advised to formula-feed their infants, rather than nurse them. In developing countries with limited access to infant formula and clean water, breast-feeding often is the most feasible option. Researchers are searching for ways to decrease transmission of the virus during breast-feeding. “Although studies are ongoing, it is believed that putting uninfected babies on antiretroviral medication may prevent them from acquiring the virus from their infected mothers while they are breast-feeding,” said Dr. Shapiro. “Our study suggests that putting mothers on antiretrovirals could provide infants with high enough levels of these medications through breast-feeding, so that the infants may not have to take any medication separately.” He noted, however, that exposure to AIDS medications – known as antiretroviral therapy – through breast milk alone may pose a risk for infants who have already acquired HIV in utero or during birth. In these babies, resistant mutations of the virus may develop from exposure to drug levels that are lower than those needed for treatment, and may potentially compromise future treatment with the drugs. Using antiretroviral therapy to prevent transmission of the virus is standard practice in a number of situations. Women who are HIV-positive are advised to take antiretroviral therapy while pregnant and during childbirth to prevent transmission of the virus to the baby. The babies then typically receive daily doses of an antiretroviral drug such as zidovudine (AZT) for up to a month, sometimes in combination with a single dose at birth of another drug known as nevirapine, said Dr. Shapiro. In the developing world, researchers are now taking the next step and studying the possibility of preventing transmission of HIV during breast-feeding by giving antiretrovirals to babies that are breast-feeding. Conducted in Botswana, the Harvard School of Public Health study included 20 HIV-positive mothers with full-blown AIDS who for their own health were placed on a combination regimen of three antiretrovirals: nevirapine, lamivudine and AZT. All of the infants also received one dose of nevirapine at birth and oral AZT during the course of breast-feeding. Researchers measured drug levels in the breast milk as well as in the blood of mothers and infants either 2 or 5 months after birth. The tests showed high levels of all three drugs in the breast milk. The blood tests showed the infants may have achieved high enough levels of nevirapine (and possibly lamivudine and AZT) through breast-feeding to provide protection against becoming HIV-infected from breast-feeding. In addition to the risk of developing resistance mutations among infants who are already HIV-infected, another potential downside is that babies might develop toxicities to these antiretrovirals. Toxicities to these agents include lowered blood counts, liver problems, or allergic reactions, said Dr. Shapiro. “It is generally believed that maternal antiretroviral therapy will decrease the chances of HIV transmission to breast-feeding infants by lowering the levels of virus in the blood and breast milk of mothers,” said Dr. Shapiro. “This study supports the possibility that maternal antiretroviral therapy may also decrease HIV transmission from breast-feeding by providing the drugs directly to the infants.” Co-authors of a paper based on the topic being presented by Dr. Shapiro at IDSA are Diane Holland, Edmund Capparelli, Shahin Lockman, Ibou Thior, Carolyn Wester, Lisa Stevens, Trevor Peter, Max Essex, James Connor and Mark Mirochnick. IDSA is an organization of physicians, scientists and other health care professionals dedicated to promoting human health through excellence in infectious diseases research, education, prevention and patient care. Housed within IDSA is the HIV Medicine Association (HIVMA), which represents more than 2,600 physicians, scientists and other health professionals dedicated to the field of HIV/AIDS. IDSA, which has 7,500 members, was founded in 1963 and is headquartered in Alexandria, Va. |
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Forbes: Companies in Biotechnology
& Drugs industry http://www.forbes.com/finance/mktguideapps/compinfo/CompaniesByIndustry.jhtml?ind=BIOTRX&orderby=coname&sortorder=desc&fullind=Biotechnology+%26+Drugs§or=health+care |
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Girl becomes 11th Thai bird flu
fatality 12 minutes ago Add to My Yahoo! Asia - AFP BANGKOK, (AFP) - An eight-year-old girl has died of bird flu in northern Thailand, becoming the country's 11th confirmed victim of the lethal virus this year, a health ministry official confirmed. http://story.news.yahoo.com/news?tmpl=story&cid=1530&ncid=721&e=10&u=/afp/20041004/wl_asia_afp/health_flu_thailand wonder if the could have used product R for antiviral activity oh thats right thats not what IND is going to be when we eventually get there... darn maybe next time (Voluntary Disclosure: LT Rating- Buy) |
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Cancer in the Crosshairs By Janice Billingsley HealthDay Reporter From HealthDayNews Oct. 1 2004 — The war on cancer in the 21st century is becoming one of guerrilla tactics rather than saturation bombing, with "molecularly targeted" drugs replacing wholesale chemotherapy in many cases. This new approach, experts say, is resulting in patients who can live longer, productive lives despite their diagnoses. "The emphasis in cancer has shifted from broad observation to zeroing in on what we think is important in the biology of tumor cells," said Dr. Owen O'Connor, of Memorial Sloan-Kettering Cancer Center's Department of Medicine in New York City. One tactic — called biologic therapy — helps the body's own immune system fight cancer by using drugs to interfere with uncontrolled cell growth. It can also act indirectly to help healthy immune cells control cancer, or assist in the repair of normal cells damaged by other forms of cancer treatment, O'Connor said. New Toolkit Biologic therapy is the latest cancer-fighting tool, joining such earlier approaches as tumor-removal surgery, chemotherapy and radiation, he said. O'Connor was one of five experts who spoke this week about the state of cancer research and treatments at a conference in New York City. In the past 15 years, scientists have discovered just how complex the biology of cancer can be. And they've been able to develop drugs that target the individual components of cancer growth. The increase in the number of U.S. Food and Drug Administration-approved drugs in the last decade has meant there are more medicines to help manage the disease in a wide variety of patients, O'Connor added. No Magic Bullet This new approach isn't the "magic bullet" cure that doctors used to discuss. But it's a more realistic assessment of how best to deal with the disease, O'Connor said. "Historically, we've held cancer to the standard that all patients with the disease have to be cured, something that we haven't had with other diseases. The objective now is to recognize that treating cancer as a chronic disease — like heart disease, emphysema or asthma — is just as laudable a goal," he said. Along with this recognition of the chronic nature of cancer comes the necessity to help patients and their families adjust to the new paradigm of cancer care, said another speaker, Diane Blum. She is executive director of CancerCare, a non-profit organization in New York City that assists cancer patients. Living Longer More effective cancer treatments have meant that people are spending less time in a hospital, they're living longer with the disease, they have access to far more information about their disease, and they have many more treatment options. All of these are signs of progress, she said. "But with extended survival, people have to know what they can expect in terms of chronic health problems," Blum said, such as fatigue and cognitive impairment. "Further, more information is a wonderful thing. But we need to help people figure out how to use it," she said, particularly in sifting through the available information to know what is relevant to a particular person. Costs and Benefits Then there's the issue of cost, especially for those without insurance. For these patients, the cost of extended medical care can be prohibitive, Blum said. But for those who have faced a cancer diagnosis and have benefited from the new medicines, life is sweet indeed. Gene Grassi, a 50-year-old woman from Long Island, N.Y., was diagnosed seven years ago with multiple myeloma, a cancer of the bone marrow. But she took the drug Velcade from 2001 to 2004 while participating in a clinical trial, and she credits the drug with having kept her alive beyond her expectations. "You know I'm here seven years after my diagnosis," she said. The conference was sponsored by Millennium Pharmaceuticals Inc., the maker of Velcade. The company on Wednesday asked the FDA to approve broader use of Velcade for multiple myeloma based on successful clinical trials of the drug. |
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Jagged Little Pills: Vitamin and
antioxidant supplements By Ed Edelson HealthDay Reporter From HealthDayNews Oct. 1 2004 — People who take vitamin and antioxidant supplements in the hope they're reducing their risk of gastrointestinal cancer are more likely to die of the disease than those who don't take the supplements, a new study finds. The research, which reviewed the results of 14 major trials with more than 170,000 participants, found a small but statistically significant increase in gastrointestinal cancer deaths associated with supplements containing beta carotene and vitamins A, C and E. Four of the trials showed a possible reduction of risk associated with selenium supplements, the report said. In half the trials, there was a 6 percent increased risk of death from cancers of the esophagus, stomach, pancreas, liver, colon and rectum in persons who took supplements, compared to those who took a placebo, the researchers found. Dangerous Combinations But certain combinations of supplements seemed to be more dangerous, the researchers said. A 30 percent higher risk was found for combination supplements containing beta carotene and vitamin A, and a 10 percent risk for supplements combining beta carotene and vitamin E. "The indication that mortality in supplement-taking patients was higher compared to placebo has to be explored extensively in all randomized trials," said study author Dr. Goran Bjelakovic, a professor of internal medicine at the University of Nis in Serbia and Montenegro. "The potential protective effect of selenium should be studied in adequate clinical trials," he added. The study appears in the most recent issue of The Lancet. Popping Apoptosis It's not clear why antioxidant supplements might have a harmful effect, Bjelakovic said. One possible explanation is that they might interfere with apoptosis, the process in which the body destroys cells that turn abnormal. "Someone who takes supplements can suppress apoptosis and thus can influence the growth of different tumors," Bjelakovic said. "But this is only a hypothesis." Neither the American Cancer Society nor the National Cancer Institute recommend vitamin supplements for cancer prevention. A U.S. task force recently reported there is "insufficient evidence" that supplements have any preventive effect. The cancer society recommends getting appropriate amounts of vitamins and minerals by eating a balanced diet. The NCI is conducting a large-scale trial of selenium and vitamin A for prevention of prostate cancer. The trial was started because two earlier studies suggested a possible protective effect. A Work in Progress In an accompanying editorial in the journal, Drs. David Forman of Leeds University in England and Douglas Altman of Cancer Research United Kingdom, said, "The prospect that vitamin pills might not only do no good but also kill their consumers is a scary proposition given the vast quantities used in certain communities." If the findings are correct, "9,000 in every million users of such supplements will die prematurely as a result," the editorial said. But it added the review "is a work in progress and does not offer convincing proof of hazard." Eric Jacobs, a senior epidemiologist at the American Cancer Society, said: "There are other things [that] do work in preventing gastrointestinal cancer. One way to prevent colon cancer is to get screened for it. Quitting smoking helps prevent colon cancer as well as lung cancer, and maintaining proper weight can reduce the risk of gastrointestinal cancer." |
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another week of nothing! posted
before friday so i can move on to other things good luck longs we need it!
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ADVR
and AVR118: Exposure, Exposure, Exposure: The press clip below was seen in 11 newsletters. Cancer Therapy; Successful pre-IND meeting for AVR118 with FDA reported 285 words 10 October 2004 25 English (c) Copyright 2004 Medical Letter on the CDC & FDA via NewsRx.com 2004 OCT 10 Advanced Viral Research Corp. (ADVR) announced that the company had a successful pre-investigational new drug (IND) meeting with the U.S. Food & Drug Administration (FDA) at the end of August. Based on the results of the meeting, Advanced Viral Research Corp. believes it is well positioned to submit an IND application for the injectable use of AVR118 in patients with cancer by the end of 2004/beginning of 2005. "We were delighted with the outcome of the pre-IND meeting with the agency," said Elma Hawkins, president and CEO of Advanced Viral Research Corp. "We are building on all of the previously acquired clinical and non-clinical data as we move AVR118 through the drug approval process. Our strategy of pursuing oncology as our first therapeutic area affords us many advantages, both currently and in the future." ADVR's AVR118 is a biopolymer that possesses novel immunomodulator activity. This peptide-nucleic acid complex, which to date has demonstrated a very favorable safety profile, appears to stimulate the pro-inflammatory responses required to combat viral infections such as AIDS and human papillomavirus and to dampen aberrant autoimmune-type inflammatory responses, such as occur in patients with rheumatoid arthritis. Data presented at the American Society of Clinical Oncology (ASCO) annual meeting in June 2004, showed that AVR118 appears to have activity against fatigue, loss of appetite, and weight loss in patients with HIV. This article was prepared by Medical Letter on the CDC & FDA editors from staff and other reports. Copyright 2004, Medical Letter on the CDC & FDA . Cancer Therapy; Successful pre-IND meeting for AVR118 with FDA reported Medical Letter on the CDC & FDA, 10 October 2004, 285 words, (English) 2004 OCT 10 -- Advanced Viral Research Corp. (ADVR) announced that the company had a successful pre-investigational new drug (IND) meeting with the U.S. Food & Drug Administration (FDA) at the end of ... More Like This . Cancer Therapy; Successful pre-IND meeting for AVR118 with FDA reported Obesity, Fitness & Wellness Week, 9 October 2004, 281 words, (English) 2004 OCT 9 - Advanced Viral Research Corp. (ADVR) announced that the company had a successful pre-investigational new drug (IND) meeting with the U.S. Food & Drug Administration (FDA) at the end of ... More Like This . Cancer Therapy; Successful pre-IND meeting for AVR118 with FDA reported Drug Week, 8 October 2004, 275 words, (English) 2004 OCT 8 - Advanced Viral Research Corp. (ADVR) announced that the company had a successful pre-investigational new drug (IND) meeting with the U.S. Food & Drug Administration (FDA) at the end of ... More Like This . Advanced Viral Research Corp. Successful pre-IND meeting for AVR118 with FDA reported Biotech Week, 6 October 2004, 277 words, (English) 2004 OCT 6 - Advanced Viral Research Corp. (ADVR) announced that the company had a successful pre-investigational new drug (IND) meeting with the U.S. Food & Drug Administration (FDA) at the end of ... More Like This . Cancer Therapy; Successful pre-IND meeting for AVR118 with FDA reported Science Letter, 5 October 2004, 275 words, (English) 2004 OCT 5 - Advanced Viral Research Corp. (ADVR) announced that the company had a successful pre-investigational new drug (IND) meeting with the U.S. Food & Drug Administration (FDA) at the end of ... More Like This . Cancer Therapy; Successful pre-IND meeting for AVR118 with FDA reported Life Science Weekly, 5 October 2004, 277 words, (English) 2004 OCT 5 - Advanced Viral Research Corp. (ADVR) announced that the company had a successful pre-investigational new drug (IND) meeting with the U.S. Food & Drug Administration (FDA) at the end of ... More Like This . Cancer Therapy; Successful pre-IND meeting for AVR118 with FDA reported Cancer Weekly, 5 October 2004, 275 words, (English) 2004 OCT 5 - Advanced Viral Research Corp. (ADVR) announced that the company had a successful pre-investigational new drug (IND) meeting with the U.S. Food & Drug Administration (FDA) at the end of ... More Like This . Cancer Therapy; Successful pre-IND meeting for AVR118 with FDA reported Pharma Business Week, 4 October 2004, 277 words, (English) 2004 OCT 4 - Advanced Viral Research Corp. (ADVR) announced that the company had a successful pre-investigational new drug (IND) meeting with the U.S. Food & Drug Administration (FDA) at the end of ... More Like This . Cancer Therapy; Successful pre-IND meeting for AVR118 with FDA reported Health & Medicine Week, 4 October 2004, 279 words, (English) 2004 OCT 4 - Advanced Viral Research Corp. (ADVR) announced that the company had a successful pre-investigational new drug (IND) meeting with the U.S. Food & Drug Administration (FDA) at the end of ... More Like This . Cancer Therapy; Successful pre-IND meeting for AVR118 with FDA reported Biotech Business Week, 4 October 2004, 277 words, (English) 2004 OCT 4 - Advanced Viral Research Corp. (ADVR) announced that the company had a successful pre-investigational new drug (IND) meeting with the U.S. Food & Drug Administration (FDA) at the end of ... More Like This . Cancer Therapy; Successful pre-IND meeting for AVR118 with FDA reported AIDS Weekly, 4 October 2004, 275 words, (English) 2004 OCT 4 - Advanced Viral Research Corp. (ADVR) announced that the company had a successful pre-investigational new drug (IND) meeting with the U.S. Food & Drug Administration (FDA) at the end of ... # # # Veronica Welch Principal CWR & Partners, LLP Office: 508-222-4802 Fax: 508-222-4804 - - - - - View Replies » |
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Luv, Don't you realize that no company even talks about pre status mtgs with the FDA!!!!, except this one. |
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New Scrutiny of Drugs in Vioxx's
Family NYTimes, October 4, 2004 By ANDREW POLLACK Now that Merck has removed its arthritis painkiller Vioxx from the market after tests found that it increased the risk of heart attacks and strokes, its rival Pfizer is taking a surprising stance. Pfizer says it is looking into whether its somewhat similar drug, Celebrex, may actually help prevent heart attacks. "We're not running away from cardiology,'' Dr. Mitch Gandelman, a Pfizer vice president, said in an interview on Friday, adding that a couple of studies on a very small scale by university scientists suggested that Celebrex could be good for cardiovascular health. "We are actually looking into cardiology.'' Dr. Gandelman acknowledged that evidence for this is scant and inconclusive. But it is part of Pfizer's effort to distance itself from Merck's problems and provide an answer to what has become a central question: Is it a class effect? Do all the drugs in the widely prescribed group known as COX-2 inhibitors carry the same risk as Vioxx? Millions of patients and billions of dollars in sales could be affected by the answer. Spurred by heavy advertising, COX-2 inhibitors took off faster than any other group of drugs after Celebrex and Vioxx went on sale in 1999. Sales of the two medications, plus those of the newer Bextra, exceeded $6 billion worldwide last year. Patients discontinuing Vioxx can now decide whether to switch to one of the other COX-2 inhibitors on the market - Celebrex or Bextra, another Pfizer product. And it is possible that safety concerns could delay approval of two other drugs that are in advanced stages of development - Merck's Arcoxia and Prexige from Novartis - as well as several further behind. Merck said last week that it would no longer sell Vioxx because a study showed a higher risk of heart attacks and strokes among patients who had taken it for longer than 18 months. The reason for the greater risk is not known. Many experts say that Celebrex, the oldest and biggest seller in the category, is somewhat different chemically from Vioxx and has not shown signs of increasing cardiovascular risk in clinical trials or in studies examining medical records of people who have taken the drug. Dr. Daniel Solomon, a rheumatologist and epidemiologist at Brigham and Women's Hospital in Boston, said, "I feel comfortable as a clinician, as someone prescribing these drugs, that it has a clean bill of health." By contrast, he and others said, several studies dating to 2000 pointed to a risk for Vioxx. But Dr. Eric J. Topol, chairman of the cardiovascular medicine department at the Cleveland Clinic, said that the drugs had not been tested adequately in people with heart disease, even though such people use them. "The real answer is we don't know,'' he said. There have been at least a couple of studies on animals suggesting that Celebrex could be harmful to the cardiovascular system. And a Food and Drug Administration reviewer expressed concern over cases of elevated blood pressure and edema, or swelling, in a clinical trial of Bextra as a painkiller in patients undergoing coronary bypass surgery, according to agency files obtained in a lawsuit by the advocacy group Public Citizen. Dr. Gandelman said that the results of animal studies using Celebrex varied and that, in any case, such studies did not always reflect what happens with people. As for the Bextra study, he said, "It's a finding in a narrow type of surgery, and it's a use we would not recommend.'' Pfizer issued a statement on Friday saying that three trials involving a total of 6,000 patients that have been under way for several years had not shown any significant safety issues. The tests are trying to determine whether Celebrex can help prevent colon cancer or prevent or slow Alzheimer's disease. For the moment, investors seem to think that Pfizer's sales will rise as a result of the withdrawal of Vioxx. Pfizer's shares, which had recently been battered, rose 42 cents on Thursday, the day Merck said it would withdraw its drug, and 37 cents more on Friday, closing at $30.97. Still, fears of a class effect could slow sales of Pfizer's drugs in the long run and could increase focus on the COX-2 inhibitors, which cost many times as much as drugs like aspirin but are not more effective in relieving pain. Their main benefit is that they are supposed to lower the rate of ulcers and gastrointestinal bleeding, though that has not been established to the F.D.A.'s satisfaction with Celebrex and Bextra. And some doctors say the COX-2 drugs are being used by many people with no real risk of ulcers. "This is an opportunity for people to re-evaluate the need for these more expensive options in general,'' Dr. Solomon of Brigham and Women's Hospital said. The cause of the Vioxx recall - the discovery of new risks five years after it went on the market - may also re-energize those who have criticized the way pharmaceutical companies market their treatments directly to consumers. Such critics say industry ads do not sufficiently emphasize drugs' potential risks. The industry argues that the ads help consumers recognize conditions they have and encourage them to seek help from doctors. The effect of advertising on prescription drug sales can be unpredictable. After a steep ascent, sales of Vioxx and Celebrex have barely grown recently, said Steve Scala, an analyst with SG Cowen. "In this class,'' he said, "drugs tend to get off to very quick starts followed by a quick leveling off'' as people try each new pain remedy that comes out. He predicted that sales of Bextra and Celebrex would get a short-term lift from the withdrawal of Vioxx from the market and then return to slower growth. Both the COX-2 inhibitors and the older painkillers like aspirin, ibuprofen (sold under the brand names Motrin and Advil) and naproxen (Aleve) block an enzyme in the body called cyclooxygenase, or COX, that contributes to pain and inflammation. (Tylenol, a brand-name version of acetaminophen, works by a different mechanism to block pain, but not inflammation.) There are two forms of COX, and one of them, COX-1, helps protect the stomach lining from acids. The older drugs block both forms, which is why they cause ulcers and gastrointestinal complications that have been estimated to result in 7,500 to 16,500 deaths a year in the United States. The COX-2 inhibitors, as their name implies, block COX-2 much more than the stomach-protecting COX-1. But the role of the COX enzymes in the body is not completely understood. There is evidence that COX-1 helps promote blood clotting and COX-2 helps retard it. So blocking COX-2 but not COX-1 could tip the balance in favor of clotting, thereby increasing the risk of heart attacks. But inflammation is also an important contributor to heart attacks and strokes. So controlling inflammation, as the newer drugs do, could conceivably have a helpful effect. With the withdrawal of Vioxx, the F.D.A. is considering whether longer studies will be needed for COX-2 inhibitors - both those on the market and those still under development. Dr. Sidney M. Wolfe, director of health research at Public Citizen, sharply criticized the agency for not requiring such studies after the initial evidence of a risk with Vioxx in 2000. "It is very likely that there is some kind of class effect,'' Dr. Wolfe said. "You start demanding of all the companies that they do studies that are large enough and last long enough to prove if this is a problem.'' He also called for the F.D.A. to be extremely cautious about Merck's Arcoxia and Novartis's Prexige, saying, "No one can argue that these other two are needed rapidly because there's nothing like them around.'' Dr. John Jenkins, who directs the agency's Office of New Drugs, said, "The danger is if this is not a class effect, if this is unique to Vioxx, if you start asking for much longer data prior to approval, then you can blunt the product development pipeline.'' Drugs, he noted, can have benefits and not just risks. The F.D.A.'s thinking should become clear soon. It is scheduled to decide by the end of the month whether to approve Arcoxia, which is already on the market in many countries. Mr. Scala, the SG Cowen analyst, predicts that the F.D.A. will tell Merck that the drug is "approvable'' pending the outcome of an additional trial that should be completed in 2006. Prexige is already approved for use in Britain and Novartis hopes for approval for use in the rest of Europe by the end of the year. The F.D.A. rejected Novartis's application last year, saying that more data would be needed on the drug's effectiveness, according to Jörg Reinhardt, head of pharmaceutical development for the company. He said Novartis hoped to reapply in 2006. The results of an 18,000-patient trial sponsored by Novartis, the largest ever for a COX-2 inhibitor, showed that the drug reduced the risk of gastrointestinal side effects without increasing the risk of heart attacks, when compared with ibuprofen and naproxen. Still, in a commentary that accompanied publication of the results in the journal The Lancet in August, Dr. Topol of the Cleveland Clinic said they did "not clearly exonerate'' Prexige because the trial excluded many people with coronary artery disease. The trial also pointed out potential liver toxicity problems. Dr. Reinhardt said that Dr. Topol's view was not shared "by the totality of the medical community'' and that the results show Prexige does not have the risks of Vioxx. "It cannot be the whole class that has the issue here,'' he said. "It seems to be this one compound." Nat Ives contributed reporting for this article. |
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The Israeli Trial results should be
in sometime this year or next year. I wonder if they will beat the Weismann release. Don't forget that Dr.Jim may be dusting off the ole Royal or Remington for his paper. So many things to look forrrrrrrrrrward to. 'mxcited! Of course it goes without saying the standard safe harbour disclaimer applies here. Shouldn't get overly optimistic. Random thoughts; I guess Dr.H I is considered a short timer now. Did Bill put the check in the mail yet? Who is the Chairman of the Bored? How's the property in Barbados? What do the Bored talk about? About cryogenics, many are "called" but few are frozen. (Voluntary Disclosure: Position- Long) |
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Adenovirus: Flu-Like Virus Sickens
Military Recruits Flu-Like Virus Kills Four U.S. Military Recruits in Past Year and Sickens Some 2,500 Each Month The Associated Press SEATTLE Oct. 3, 2004 — Four military recruits died in the past year and thousands others were sickened by a flu-like virus that the military once had a vaccine program for but abandoned to save money. The respiratory virus now infects up to 2,500 service members each month 1 in 10 recruits at the nation's eight basic-training centers, according to a Seattle Times' analysis of military health-care records. More than three decades ago, the Pentagon commissioned two pills to ward off the adenovirus, but defense officials abandoned the program in 1996 as too expensive, the paper reported. The vaccine's original manufacturer, Wyeth Laboratories, warned as early as 1984 that it would stop churning out pills costing $1 each unless defense officials allocated $5 million to repair a deteriorating production plant. Wyeth executives shuttered the facility in 1996. A military health budget later stated the program had been stopped "to pay higher priority items." Military foot-dragging and high turnover of procurement officers have caused the replacement vaccine to fall behind schedule, making pills unavailable until at least 2007, military health-care records show. Dr. Margaret Ryan, a commander at the Naval Health Research Center in San Diego and an expert on the virus, calls the vaccine lapse "indefensible." Since vaccines stopped, the virus has been associated with six deaths, including four within the past year, according to military records and internal reports obtained by The Times. A top Pentagon official called it "a major screw-up," hobbling U.S. efforts to rapidly deploy troops abroad. The virus is expected to kill an additional six to 10 recruits before a vaccine is again available, according to a classified Defense Department briefing this year. Six children of service members in the Puget Sound area also were diagnosed with the virus last winter, doctors at Madigan Army Medical Center near Tacoma said. Adenovirus can be spread through contact and thrives in confined places such as overcrowded barracks. Overstressed recruits, trying to get in shape and adapt to the military, are ideal incubators for the virus. Most people rebound from the infection within days, but if untreated, fever, sore throat and labored breathing can quickly develop and lead to severe respiratory problems such as pneumonia and perhaps death. Nationally, the virus has killed more than two dozen civilian children and adults in outbreaks in medical facilities in Illinois, Louisiana, Iowa, Tennessee and New York, the federal Centers for Disease Control and Prevention reports. The Pentagon's unwillingness to spend $5 million on health care is now costing taxpayers tens of millions of dollars to remedy, The Times said. In September 2001, plagued by boot-camp outbreaks, defense officials finally agreed to spend $35.4 million to develop a new vaccine through Barr Laboratories of Forest, Va. Shortly afterward, Assistant Secretary of Defense William Winkenwerder Jr. ordered vaccine efforts accelerated, according to transcripts of a Feb. 19, 2002, meeting at North Island Naval Air Station in San Diego. "This is one of the most disappointing facts and stories that I've learned upon coming into my position," he said. "I don't want to cast aspersions on anybody who had responsibility in the past, but to be blunt this is a major screw-up." Information from: The Seattle Times, |
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Stress, depression, the immune
system, and cancer Edna Maria Vissoci Reiche, Sandra Odebrecht Vargas Nunes, and Helena Kaminami Morimoto "Evidence mainly from animal models and human studies suggests that stress and depression result in an impairment of the immune response and might promote the initiation and progression of some types of cancer, mainly associated with a DNA tumour virus, retrovirus insertion near a cellular oncogene, and other viruses such as EBV. Through HPA activation, the mediators released during chronic stress suppress some non-specific and specific parts of the immune response, including NK-cell activity, phagocytosis, production of inflammatory cytokines (ie, interleukin 2, interferon Y, and TNF a by Th1 cells), and cytotoxic T-cell activity, compromising the most important effectors of the immune response against tumours. Furthermore, other relevant biological processes affected by stress, such as the increases in DNA damage, accumulation of somatic mutations, alterations in DNA repair, and inhibition of apoptosis might be involved in the onset and outcome of some types of cancer. Future research in psychoneuroimmunology will be needed to learn what pathways and circuits are involved in the relation of stressors with the HPA and the immune systems with respect to cancer onset and progression. Our growing understanding of immunomodulation and the links between the CNS, and endocrine and immune systems might improve the chances for successful psychoneuroimmunoendocrine interventions." For complete review: http://oncology.thelancet.com/journal/vol5/iss10/full/lonc.5.10.review_and_opinion.30858.1 |
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Sure, it DOES happen: FDA Grants
Fast Track Status to Squalamine in Macular Degeneration PLYMOUTH MEETING, Pa., Oct. 4 /PRNewswire-FirstCall/ -- Genaera Corporation today announced that the U.S. Food and Drug Administration (FDA) has granted Fast Track designation to squalamine, an intravenously administered, first in class, small molecule anti-angiogenic drug for the treatment of "wet" age-related macular degeneration (AMD). Under the FDA Modernization Act of 1997, Fast Track drug development programs are designed to expedite the review and facilitate the development of a new drug that demonstrates the potential to address unmet medical needs for the treatment of a serious or life-threatening condition. "Fast Track status will help accelerate the development and commercialization of squalamine," commented Roy C. Levitt, MD, President and Chief Executive Officer. "This FDA designation recognizes the serious unmet medical need of patients with AMD and the potential of squalamine to affect this disease. All of our Phase II trials for squalamine in AMD are up and running. We anticipate reporting early data from our first Phase II study later this year with additional Phase II data expected, starting in the first half of 2005. We intend to begin Phase III in the first half of 2005 to run concurrently with our largest Phase II trial." Squalamine is currently being evaluated in three Phase II clinical trials. MSI-1256F-209 is the cornerstone of Genaera's Phase II studies and is designed to evaluate the safety and efficacy of squalamine in 100 patients with AMD over a two-year period. This Phase II multi-center, randomized, double masked, controlled study will evaluate two dose levels of squalamine (20 mg or 40 mg) given once weekly for four weeks, followed by maintenance doses once every four weeks until week 48. At the end of 48 weeks of therapy, each patient will be followed for 12 months. Genaera anticipates using data analyses from this study in coordinating Phase III activities. MSI-1256F-208 is the second Phase II trial designed to evaluate the effects of three different doses of squalamine in combination with an initial Visudyne® treatment in 45 patients with AMD. Specifically, this study will evaluate the safety and effects of systemically administered squalamine before and after photodynamic therapy with Visudyne®. Based on its mechanism of action, this squalamine pretreatment has the potential to improve the effect of Visudyne®, and squalamine follow up treatment may inhibit the detrimental effects of the VEGF 'burst' that commonly occurs after Visudyne® treatment. The multi-center, randomized, controlled, masked study also includes monthly squalamine maintenance therapy through six months, along with an additional twelve months follow-up for each patient. MSI-1256F-207 is a Phase II pharmacokinetic and safety trial that will evaluate 18 patients with AMD at three different doses of squalamine over four months. In this open-label, parallel group study, squalamine is administered intravenously at three doses, once weekly for four weeks. Squalamine Mechanism of Action Squalamine directly interrupts and reverses multiple facets of the angiogenic process. Working within activated endothelial cells, squalamine inhibits growth factor signaling including VEGF, integrin expression, and reverses cytoskeletal formation, thereby resulting in endothelial cell inactivation and apoptosis. Systemically administered squalamine inhibits abnormal angiogenesis in rodent models of retinopathy of prematurity, and the development of choroidal neovascular membranes in rat models of AMD. Additional preclinical studies have demonstrated that systemic squalamine administration is effective in reaching abnormal ocular blood vessels in primates, and leads to partial regression and inhibition of new abnormal vessels in the eye. These results support that squalamine may have a role in the treatment of human choroidal neovascular membrane formation that underlies the pathology of wet AMD. About AMD Wet AMD resulting from angiogenesis is the leading cause of legal blindness among adults age 50 or older in the Western world. About 25 to 30 million people are affected globally and is expected to triple over the next 25 years. AMD occurs in two types: the "dry" form and the more severe "wet" form. Wet AMD is caused by the growth of abnormal blood vessels, or choroidal neovascularization, under the central part of the retina, the macula. Dry AMD, or the avascular form is the more common and milder form of AMD, accounting for 85% to 90% of all cases. Dry AMD results in varying forms of sight loss and may or may not eventually develop into the wet form. Although the wet form of AMD accounts for only 10% to 15% of all AMD, the chance for severe sight loss is much greater. It is responsible for 90% of severe vision loss associated with AMD. Approximately 500,000 new cases of wet AMD are diagnosed annually worldwide. In North America alone, approximately 200,000 new cases of wet AMD are diagnosed each year. Source: Genaera Corporation |
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Shaggy says....On September 1, 1960
a symposium covering results from clinical case studies involving the use of
the drug Reticulose [pre AVR118] was held in Miami, Florida. The Proceedings
from that Symposium reported that Reticulose had HIGH EFFICACY AGAINST
INFLUENZA ‘A’ WHILE AT THE SAME TIME BEING NON TOXIC." ------------------------------------- I say --- 44 years ago -- worthless study! ------------------------------------- In 1989 the US Department of Heath conducted an ‘in vitro’ study showing that Reticulose inhibited the growth of three different Influenza A viruses. Christopher Tseng, Phd, a scientist employed by the NIH in 1989, conducted the ‘in vitro’ studies on Reticulose and showed it to be effective against all three type A virus. [NIH report ARB No. 89-048 of 12 October 1989.] ------------------------------------- I say --- STILL no drug on the market 15 years after the NIH study? (Test tube talk) -- Worthless, as well! IMO!!! |
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ot: Most Promising Clinical Uses
For Stem Cells From Fat Agreed On By International Society 10/5/2004 Source: University of Pittsburg Medical School While questions still remain about the nature and function of stem cells found in fat, a group of researchers and clinicians convened today in Pittsburgh at the Second Annual Meeting of the International Fat Applied Technology Society (IFATS) agreed that research should move forward with the ultimate goal of performing human clinical trials to test the cells' therapeutic potential for specific indications. Today concludes scientific sessions exploring how adipose tissue, or fat, can be an abundant source of stem cells that could be used for tissue engineering and regenerative medicine. An important outcome of the meeting was the development of a consensus defining key scientific questions for future study and determining the field's most promising clinical applications. More than 300,000 liposuction procedures are performed in the United States each year, producing about 150,000 gallons of fat that is normally discarded. In 2001, researchers first reported that such tissue contained stem cells, and since then, additional studies have suggested they can be coaxed into other cell types, such as nerve, bone, muscle and blood vessels; or it may be that they have properties of these cells. Some research has progressed more rapidly, with animal studies indicating potential for the development of treatments for heart attack or bone injury, for example, while results looking at other uses are still quite preliminary. There are currently no human trials in the United States evaluating the potential of stem cells derived from fat, but in reaching consensus on the most promising clinical applications, those attending the IFATS meeting believe the first clinical attempts in patients should be for repairing or healing bone defects, promoting growth of blood vessels in tissues not receiving sufficient blood supply, and for treating acute or chronic cardiac and peripheral vascular diseases. Moreover, the group felt the best use of the technology should be to develop therapies using patients' own cells, as opposed to cells that might be donated by other individuals. Because adipose is both abundantly available and easily accessible, it offers a practical source of stem cells. A key question the group answered was simply what to call the cells, with the decision in favor of the term adipose-derived stem cells, even though it also was agreed that these cells are most likely comprised of multiple cell populations – some that are capable of proliferation and differentiation and other groups consisting of mature cells. The society aims to develop common scientific methods in order to best compare results between studies, and believes that much of the research effort should be directed toward identifying the protein markers for adipose stem cells in order to better understand how they differentiate into other cell types and what factors they secrete. In developing its consensus, the society focused on three main areas, with separate sessions addressing each. Leading discussions that addressed the biology of the cells was Patricia Zuk, Ph.D., research director, Regenerative Bioengineering and Repair Lab, at the David Geffen School of Medicine, University of California, Los Angeles. The session focusing on scientific methods was led by Jeffrey Gimble, M.D., Ph.D., a professor at the Pennington Biomedical Research Center at Louisiana State University. Discussions on clinical applications and opportunities were moderated by Keith March, M.D., Ph.D., director of the Indiana Center for Vascular Biology and Medicine and professor of medicine at the Indiana University School of Medicine. |
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AVR 118 applications A through Z
(reported in the past in company publications, reports and patents, or
otherwise rumored): AIDS Adenovirus Infections Basal Cell Carcinoma Cachexia Cancers Chicken Pox Crohn's disease Diabetes Distemper Eczema Erythrocyte Count Augmentation Feline Immunodeficiency Virus Infection Flu Genital warts Gout Hepatitis Herpesvirus infections Hives HPV Infection Immune System Stimulation Iritis Jaundice, viral Juvenile Rheumatoid Arthritis Keratitis Leukemias Lymphomas Measles Melanoma Multiple Sclerosis Neoplasms Neutropenia Non-Hodgkin's Lymphoma Nutritional Deficiencies Ocular Viral Infections Papillomavirus Infections Parvovirus infections Psoriasis Q Fever Rashes Red Blood Cell Production Retroviral Infections Rheumatoid Arthritis Skin Infections Suppressed Immune System T-Cell Activation Tumors Undernutrition Urticaria Venereal Papillomavirus infection Warts Weight Gain White Blood Cell Activation Xeroderma Yellow fever virus Zoonoses (Viral infections transmitted by animals to man). I've probably missed a few. My, this drug is much bigger than Aspirin!!! |
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Years decades....centuries...as a stakeholder I don't worry about the $ I have invested here. 1960...1985...2004 as a person with an interest in this Company I want to know what the hel they plan on testing. Test the drug, see if it works, let the pps take care of itself. After all these years I must say I am beginning to believe the management does not believe "it" works. This is not a private or government enterprise. ADVR is public company and therefore the management dang well have a responsibility to their shareholders. Focus on the business decisions, leave out the science, and answer this questions; Has management clearly identified and implemented a good plan? (Voluntary Disclosure: Position- Long) |
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Hey, poppop53! You're one of my
favorites! BUT.... Re: AVR118 We really don't know that it cures anything yet, but it certainly does have a long history of alleviating a lot of pain and suffering. Our clinical trial results have so far been very good as well. No one ever claimed it is was a "piece of cake" even if it is being eaten up and spit out by our vultures here. It looks like it's going nowhere but I still think we've made much progress over the years. Unfortunately our PPS doesn't reflect it and we have many disgruntled shareholders because of this. After all, who can blame them/you/us? I feel the same pain and bleed with the same questions, the same wonder of "why aren't we 'there' yet?, why is our PPS so low? Our investment has dwindled. Everything is taking too long, we need clinical trial results sooner, we need IND approval sooner from the FDA, and for more than one indication",... etc., etc., etc. But after all said and done, I know we're still a small biotech with a great drug, imo, and have the same problems that beset many other small biotechs. And, we're still considered to be a 'new' company with a new Board and a new CEO with great scientists. Will we go anywhere? That has yet to be seen. You and others don't think so. I do. Luv |
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luv nothing personal but ive been
involved since 1986 and have heard the same hopes wishes and will bes for 18
years. i wish everyone well and i still have a few shares but the
frustration of this stock has gotten to me. its like the picture groundhog
day over and over again. everything posted is deja vu and when i see people
falling for the same pipedreams it gets to me. regards mark - - - - - |
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buckaroobanzai, stop making things
complicated. AVR118 simply helps to regulate the immune system. It
up-regulates the immune system to fight viral infections and it
down-regulates the immune system when it goes awry. Now that is not hard to understand, is it? The people from Missouri [or should I say misery] will soon realize this when things are corroborated for them. They just lack faith. Us enlighten ones poses the faith. It is as simple as that. I guess my attitude stems from the fact that I am a Red Sox fan and delighted in belonging to the Red Sox Nation. All we Red Sox Fans have is faith and nothing but faith along with one hel.l of a good time. LOL Fenway Park was half filled with 10-20 thousand fans Monday night just for a pep rally to cheer on the Soxs. There is just no place like Boston’s Fenway Park when it comes to baseball and the Red Sox. It is simply a magical place full of electrifying faith. - - - - - View Replies » |
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Scientists resurrect genes from
1918 flu pandemic Richard Ingham | Paris 06 October 2004 13:03 Scientists working in top-security labs say they have recreated pathogens from the 1918 flu pandemic, the greatest plague of the 20th century, in a bid to find out why this strain was so extraordinarily lethal. Using reverse genetic engineering, the United States team took two key genes from the 1918 virus and slotted them into human flu viruses to which lab mice were known to be immune. The two genes code for a spike-like molecule called haemagglutinin (HA), which binds to specific receptors on the surface of cells in the body, and another protein, neuraminidase (NA). The mice were injected in the nose with the recombinant viruses. Within three days, mice that had been exposed to the HA gene were mortally ill. Post-mortems showed the virus had rampaged through their lungs, producing inflammation and haemorrhaging characteristic of the symptoms induced by the 1918 outbreak. At least 20-million and perhaps as many as 50-million people died in the 1918-1919 pandemic, the highest toll of any disease in the last century. Scientists say that the disease leapt to humans by mutating from bird flu, possibly after passing through pigs, which are able to harbour both human and avian viruses and thus allow them to swap genes as the viruses reproduce. For that reason, experts are deeply concerned that the avian flu that has broken out in poultry flocks in parts of Southeast Asia may acquire genes that will make it highly infectious as well as lethal for humans. The researchers, led by Yoshihiro Kawaoka of the University of Wisconsin at Madison, stress that the experiment is only conclusive for lab mice, not humans. Nevertheless, they say, it adds strongly to suspicions that what made the type A 1918 virus strain so extraordinarily vicious was the unique profile of its HA gene. That finding opens up good avenues for diagnostic tools for spotting emergent viruses with this genetic signature, thus tackling an outbreak in its early stages. "Once the properties of the [1918] HA gene that gave rise to its lethal infectivity are better understood, it should be possible to devise effective control measures and to improve global surveillance networks for influenza viruses that pose the greatest threat to humans as well as other animal species," the authors say. The study is published on Thursday in Nature, the British science weekly. A previous study into the 1918 strain, published in Science in February, also pointed the finger at HA, theorising that only minor changes in its structure were needed for it to start binding with human cells as well as bird cells. The latest research takes this a step forward, for it actually recreated the suspect gene and tested it on animals. In order to prevent their creation from escaping into the open, Kawaoka's team carried out the genetic resurrection at a Biosafety Level Four facility -- the most secure level -- at the National Microbiology Laboratory in Winnipeg, Canada and at an "enhanced" Level Three lab at the University of Wisconsin. By some estimates, the 1918 pandemic, called "Spanish flu" in the probably erroneous belief that it began in Spain, infected up to a billion people, which was half the world's population at the time. The strain was especially lethal for healthy young adults, killing many of the World War I troops who had survived trench warfare, but leaving the very old and the very young -- the more usual victims of flu --unscathed. The reason for this is unclear. One theory is that the immune system reacts differently at various stages of life, and that young people may have been particularly vulnerable to an uncontrolled response by cytokines, the proteins that play a big role in causing inflammation. - Sapa (South African Press Association)-AFP |
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Old Drug, New
Hope Used in WWII, immune-system booster is now tested in AIDS fight
by Jamie Talan, Staff Writer AN EXPERIMENTAL MEDICINE injected into U.S. military men during World War II fell into obscurity for decades and now has re-emerged in the battle against AIDS. The drug-Substance R or Reticulose- stimulates the immune system and also interferes with viral replication, making it an important advance in pharmacology, doctors say. After more than 60 years of use, the drug is finally undergoing testing to move it through the Food and Drug Administration process. Meanwhile, people such as Octavio A. Perez, a 32-year-old AIDS patient in Manhattan, report substantial benefit through the current drug trials. Perez spent years on a mix of AIDS drugs that caused such troublesome side effects-distressing nightmares and neuropathies of the hands and legs-that they kept him housebound. Two months ago, he began taking injections of Reticulose. "It's really been unbelievable," said Perez. "I can walk without pain. I can sleep again." It is too early to tell whether Substance R will become a mainstream, federally approved drug for AIDS, or for any of the other conditions that might benefit from enhancing the immune system. But a small pharmaceutical company called Advanced Viral Research Corp. is betting on the drug's 67-year-old anecdotal history and has begun testing it in AIDS patients overseas. The company is planning to file several applications for its use with the Food and Drug Administration, which means that testing could move forward. Whether the drug proves as powerful as the developers' claim, the substance stands as a lesson in endurance. Substance R was created in 1933 by a doctor who wanted to develop a medicine for his patients that would mimic the body's immune system. What Dr. Vincent Lapenta didn't know-and what no one would know for more than 60 years-is that the compound fits into a relatively new class of drugs called protein nucleic acids. "I had never known anything to do this," said Dr. Shalom Z. Hirschman, former director of infectious diseases at Mount Sinai School of Medicine, who has left his tenured position to develop and test Reticulose. "The lure of opening up an entire new field of therapeutics was too much," Hirschman said. It will take years of testing before the FDA has enough data to rule on a drug's effectiveness and grant approval for use in the United States. Ironically, Reticulose had a place in medicine for decades, listed in the Physician's Desk Reference from 1940 to 1960. At the time, Phillips Roxanne Pharmaceutical Co. was manufacturing the drug for Lapenta. In the early '60s, the company sold rights of the drug to Key Pharmaceuticals. Then, it disappeared from the PDR. Scientists at Key Pharmaceuticals were having difficulty figuring out the chemistry of the drug-how it works-in an attempt to comply with new FDA guidelines on drug regulation passed in 1962. Scientists at Phillips Roxanne had made a slight change in the formula in 1959-bovine serum replaced horse serum as a stabilizing compound-and the newly created FDA would not allow the drug to bypass the regulation process as it had done with thousands of other drugs developed before the federal law went into effect. (The change was necessary because horse serum was linked to serum sickness.) Reticulose, now owned by Key, would have to be tested as a new drug. Perplexed by its chemistry, the company abandoned the drug, selling rights to the substance to a Singapore firm. Within a few years, the overseas company began bankruptcy proceedings, and chances that Substance R would ever see the light of day seemed bleak. But Bernard Friedland, a chemist at Key, would not give up on the drug. He'd heard about the bankruptcy proceedings that began in 1972 and ended in 1985. He decided to buy the drug around 1985, and a manufacturing plant in the Bahamas that had been sitting in moth balls for more than a decade. "I felt the drug was too important to lose," said Friedland, now 74. "I couldn't let it die." The mixture created by Lapenta in 1933 was a brew of genetic RNA material and proteins grown at certain temperatures. He used the substance on his own patients for viral infections. Others also talked about its benefits. But like all drugs of its time, the clinical success was anecdotal. There was never a serious drug trial. When the FDA threatened its availability in the early '60s, doctors began to hoard the injectable drug for their patients. Hundreds of thousands of patients were treated for influenza A, encephalitis and other viruses during the pre-FDA decades, Friedland said. Col. Ralph Thompson, a physician of the U.S. Medical Corps and deputy director of the Armed Forces Institute of Pathology in Washington, D.C., witnessed the same benefits in some of his charges during World War II and later: "I shall never forget the miraculous course that followed the treatment with this drug," he told colleagues at a 1960 meeting. " ... and will remember those others of my command who became ill and stricken with influenza who did not receive Reticulose therapy." He said he had also recommended its use in children with virulent encephalitis. The substance was still a chemical mystery to Friedland when he bought the drug from the bankruptcy courts. In 1995, Hirschman was asked to take a look at the drug. Hirschman had studied nucleic acids at the National Institutes of Health in the '60s, and he had just been reading a study on nucleic acids in Science when it hit him. "I was looking at a peptide nucleic acid, a relatively new class of substances that have powerful effects on the inflammatory process," Hirschman said. Peptide nucleic acids were first described in the early '90s. "No one would have appreciated this chemistry," Hirschman said of the early developers of the drug. The first person he called was Friedland, who had set up a company to work on Substance R. Hirschman's wife, Frances E. Newmann-Hirschman, a geneticist and AIDS crisis worker in Westchester, had been given samples of the drug to test. She'd been trying to find substances to fight AIDS, and she learned about Reticulose. Her husband took the formula back to his lab. "I immediately began experimenting with it," he said. He discovered that the drug had potent interactions with the immune system, stimulating cytokines, interferon, tumor necrosis factor and other immune substances. In addition to AIDS, the researchers believe it can also be a treatment for genital warts, human papillomavirus, herpes C virus and certain forms of arthritis. Hirschman said it could even help boost the immune system in cancer patients, a possibility that was first described by Thompson in 1960. There are probably thousands of drugs in development that never make it into the hands of patients. But the protein nucleic acids are a new entity, opening up the possibilities of strengthening the immune system in its fight against infections, said Howard Young, section head of cellular and molecular immunology at the National Cancer Institute. He's done some genetic laboratory work with Reticulose. "There's a reasonable basis for it to work. A lot of people are studying this new class of drugs for their potential to modulate the immune system." In 1996, Hirschman's company launched the first rigorous double-blind control trials of Reticulose. In the study, 43 AIDS patients in Barbados were randomized to receive Reticulose or a placebo injection for 60 days. This was the only treatment these patients received. At the end of the study, patients who received the drug had no signs of opportunistic infections and reported feeling more energetic, Hirschman said. Those on placebo did not report similar benefits. Nine of the patients are still on the drug, which is taken by injection every day. Hirschman hopes that Reticulose might be used in conjunction with conventional AIDS cocktails to strengthen the immune system. "The more we learn about this class of drugs, the better we will be able to tailor them to treat specific diseases," Hirschman said. July 11, 2000, Newsday |
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lovingitall0, this article you
posted makes Col. Ralph Thompson, former deputy director of the Armed Forces
Institute of Pathology in Washington, D.C., look like a genius as to the way
he approached the treatment of the Flu once contracted. Vaccination, of cause, is the preferred approach. Why get the Flu in the first place? - - - - - View Replies » |