Intellect Neurosciences Inc. (fka ILNS)

[nuubie]

TODAY'S NEWS (from an obscure newswire):

Intellect Neurosciences CEO Predicts ‘We are Less than 5 Years from Alzheimer’s Disease-Modifying Drugs,’

Sep. 15, 2010 9:14am ET (Baystreet.ca) --

Dr. Daniel Chain, Chairman and CEO of development-stage biopharmaceutical company Intellect Neurosciences Inc. and inventor of an antibody-based technology platform for the treatment of Alzheimer’s disease, predicts despite recent Big Pharma failures (New York Times: Lilly Halts Alzheimer’s Drug Trial), we are less than five years from an Alzheimer’s drug that treats the disease, not just the symptoms. “I am confident that the first disease-modifying drugs will be on the market within the next five years with follow-on generation improved drugs with increased safety and efficacy also on the way. My confidence is based on the progress that has been made over two decades of intensive research resulting in our current understanding of the underlying root cause of Alzheimer’s disease and the preliminary, but so far encouraging, data starting to emerge from clinical trials regarding products currently in advanced development,” said Chain. Chain is the inventor and patent holder for the ANTISENILIN® technology platform already licensed by Intellect to several major pharmaceutical companies with antibody products in late stage clinical trials. Notable examples of antibodies that possess the key features of the ANTISENILIN® approach are Ponezumab being developed by Pfizer and Bapineuzumab being co-developed by Pfizer and Johnson & Johnson, currently being tested in Alzheimer's Phase II and Phase III clinical trials, respectively.Chain envisions his team at Intellect will play a key role in developing an optimized product with improved efficacy and safety features compared to first generation antibodies for Alzheimer’s. In addition, Chain predicts Intellect will develop a prophylactic vaccine, the holy grail of Alzheimer’s research, with the potential to delay or prevent onset of the disease. In contrast to most other small biopharmaceutical companies that are focused on single technologies, Chain’s approach is to develop a diversified technology and product pipeline which includes a number of products based on different mechanisms giving the company the strongest chance of success. Indeed, the company’s most advanced internally developed product – a copper-binding molecule which was so far tested in Phase I trials –works by a completely different mechanism of action than the antibody approach. Drug development takes more than a dozen years to get to FDA approval and requires at minimum a billion dollars of investment. Most drugs fail due to safety issues or lack of efficacy, which usually manifest in large-scale, late-stage trials. When a major drug trial fails, everyone questions the hypothesis, in this case the amyloid approach, but Chain says it’s not a mistake in amyloid theory that contributed to the most recent setback, but the safety features of the drug in the trial, which made the patients worse and in some cases even increased the risk of skin cancer. In an exclusive to BioMedReports.com after the Lilly announcement, Chain said, “An understanding of the background and the drug’s mechanism of action affecting the function of a physiologically important protein may be helpful to avoid casting the baby out with the bathwater.”





The Amyloid Hypothesis – ILNS Leading the Way In 1906, Dr. Alois Alzheimer first noticed an “unusual disease of the cerebral cortex” during the autopsy of Auguste Deter, a woman in her 50s he was treating for behavioral symptoms and memory loss (today that would be called early onset Alzheimer’s). Her brain showed various abnormalities – a thinner than normal cerebral cortex and senile plaque, which had previously only been found in older people, as well as neurofibrillary tangles. Senile plaques, of which beta amyloid protein is the chief constituent, are considered the hallmark pathological feature of Alzheimer’s disease, although it is now known that more toxic forms of amyloid exist in the cerebrospinal fluid which carries nutrients to the brain and debris away. The amyloid hypothesis is built around the theory that when the beta amyloid protein accumulates in the brain, it becomes toxic, damaging nerve cells. Being able to eliminate the toxic protein without disturbing the delicate ecosystem of the brain can slow the disease, stop progression or even prevent it if treatment begins early. Chain was first to identify a method of achieving this using highly specific monoclonal antibodies that bind only amyloid protein. Alzheimer’s changes the whole brain – nerve cell death, tissue loss and over time, dramatic shrinkage which affects nearly all its functions – and there is no cure. Alzheimer’s disease hallmarks are loss of memory and other brain functions, like the ability to learn, communicate with language and behave appropriately. At only three pounds, the brain is our most powerful organ. The brain is surrounded by a continuous flow of cerebral spinal fluid, which is responsible for carrying nutrients to the brain and debris away from it. In people 65 and over, an accumulation of beta amyloid in the brain is thought to result from the slowing of the cerebral spinal fluid flow, disrupting the delicate in-out balance of nutrients and toxins which can result in beta amyloid plaques, tangles and ultimately Alzheimer’s. Once the brain’s nerve cells are damaged by these plaques, the destruction is irreversible, so researchers are working to stop beta amyloid from accumulating before damage begins. Most current Alzheimer’s research is based around reducing amyloid, clearing it away from the brain and/or blocking its neurotoxicity. Chain’s light bulb moment for him in 1996 was to pinpoint unique molecular signatures of beta amyloid that could be used by antibodies to latch on to the target without interfering with the metabolism or functions of the amyloid precursor protein (APP) which produces beta amyloid. The Intellect Neurosciences ANTISENILIN® technology platform is


designed to promote the safe clearance of the toxic beta amyloid protein away from the damaged sites of the brain while minimizing potential for adverse effects that may result from less specific binding. Chain believes that the use of secretase inhibitors such as Eli Lilly’s Semagacestat – a gamma secretase inhibitor meant to block metabolism of APP – was flawed because gamma secretase also acts on additional proteins to APP thus interfering with important unrelated physiological processes. “Intellect’s overriding philosophy and approach to Alzheimer’s treatments aim to develop efficacious methods to prevent beta amyloid accumulation and block neurotoxicity without compromising safety,” he commented.