While the NMSS says they funded the research that lead to Tysabri, I think they may be overstating the case a bit such that they wouldn't have any claim on the returns from the drug. I've asked the scientist in charge of Tysabri at Biogen Idec what research they funded and he wasn't aware of what it was. (Similarly with Interferons). His guess is that it was some very early work 10 years ago or something. You won't get any IP from that. The drug was developed by Elan and Biogen Idec, they'll get the profits.
Ok, this is an example that with under 5 minutes of looking it up, can be cleared up (and another example of how information can be twisted and rumors run rampant). Besides, the NMSS would not be able to directly
accept any "profits" from the marketing of ANY drug. Art, you know that. That's illegal. Why imply in any way, shape or form that they could, even if they were more "directly" involved?
First, if you will go back to what the NMSS really said
, which was (and I highlight), you will see that they never said they were DIRECTLY involved with the creation of the actual drug Tysabri:
To give you but one example, the new drug Tysabri was developed from research done to try to understand the how immune cells leave the blood stream and get into particular organs (the nervous system in the case of MS). When the researchers (one of whom was in fact funded in part by NMSS) were looking at the question, they weren’t really thinking about creating a new drug for MS. They were trying to study how these immune cells move from one place to another and the rules governing that process in the context of MS. At that time scientists had great difficulties answering that very important question. These researchers came up with some molecules which helped them answer their question, and in the course of doing that someone came up with the idea that these sorts of molecules might be another possible way to help treat MS. Looking back one can say that that initial work was a true advancement, even though at the time they didn’t appreciate just how big an advancement that would be. I am optimistic that there are lots so similar examples out there.
The above statement by the NMSS is true. This next article is an example of what the NMSS is referring to. Please note that part of the original research into adhesion molecules WAS done by this gentleman with the support of the NMSS. His initial work (with some others) DID lead to Biogen picking up and running with the ball. Please Note (again I will highlight):
From Bench to Bedside: Dr. Lawrence Steinman receives the 2004 John Dystel Prize for MS Research by Gary Sullivan
Professor Lawrence Steinman, MD, of Stanford Medical Center, has been chosen by a committee of his peers to receive the 2004 John Dystel Prize for Multiple Sclerosis Research. Dr. Steinman is being honored for his major contributions to scientific understanding of MS-like disease models, and for translating these findings to the development of novel therapeutic strategies for people with MS.
In MS, myelin (the fatty tissue that protects nerve fibers in the brain and spinal cord) is lost, resulting in a disruption of communication from the brain to other areas of the body. This “disconnect” causes the many symptoms that people with MS know only too well—blurred vision, weakness, pain, numbness, and so on.
“MS starts in a few trees and then starts burning the whole forest,” said Lawrence Steinman, MD, a professor in Stanford University's departments of Neurology and Neurological Sciences, Pediatrics, and Genetics, and chair of the Stanford University Program in Immunology. Dr. Steinman has spent his life working on ways to put the MS fire out.
As Patricia O'Looney, PhD, director of Biomedical Research at the National MS Society, put it, “Dr. Steinman is an innovator who uses the most current technological advances in other areas of medicine and adapts them for MS research. His work is among the most exciting and innovative in the field.”
In addition to his advances in MS research, Dr. Steinman has published nearly 325 papers or book chapters related to basic and clinical neuroimmunology. He has served as a scientific and medical advisor to the National MS Society and as a member of the Immunological Sciences Study Section of the National Institutes of Health. He was the associate editor of the Journal of Immunology from 1991 to 1995, and is currently associate editor of Neurobiology of Disease.
T cells and the creation of an MS model
In the 1980s, fresh out of Harvard University and internships and fellowships at Stanford University Hospital and Weizmann Institute in Israel, respectively, Dr. Steinman was among the first MS investigators to focus on T cells. T cells, which are white blood cells, are considered the master cells of the immune system. They make the chemical messengers that prompt the system to work. Dr. Steinman investigated T cells that were specifically targeted against one of the major proteins in myelin.
Dr. Steinman and colleagues used these myelin-aggressive T cells to induce an MS-like disease in mice: experimental autoimmune encephalomyelitis, or EAE. The study, published in the September 1985 issue of Nature, led Dr. Steinman to test experimental therapies on mice with EAE designed to block T cells from attacking the protein in myelin.
How do you block a T cell? Dr. Steinman and colleagues designed monoclonal antibodies to adhere to the myelin-aggressive T cells—specifically to their “adhesion” molecules, sticky Velcro-like molecules on T cell surfaces. Adhesion molecules enable T cells to pass from the blood–stream into the central nervous system. By blocking them, the T cells could not stick to and pass through the blood-brain barrier. Dr. Steinman's research ultimately led to the development of Antegren, which is now in early clinical trials as an MS therapy. (See “Promising results in early Antegren trial” in the Winter 2002 InsideMS.)
Altered peptide ligands
But there's more than one way to block a T cell.
In the January 1996 issue of Nature, Dr. Steinman and colleagues published a study involving mice wherein the T cells were blocked another way. Specifically, Dr. Steinman found a way to alter the myelin “docking sites” found on the surface of myelin-aggressive T cells and change the way these T cells behave in the mice. Again, this innovative research has led to a possible therapy called “altered peptide ligands” that is now in early clinical trials in people with MS.
Using the latest technology
Some of Dr. Steinman's recent research employs a new and very sophisticated lab tool: DNA microarrays, which can sort through hundreds of genes in tissues at once, sensing whether a gene is switched “on” or “off” in a given cell. Using DNA microarrays, his research team is delving into the human genetic structure. Using brain tissue from people who had MS and comparing it with tissue from people who did not have the disease, Dr. Steinman and colleagues found an unexpectedly high expression of a proinflammatory molecule called osteopontin in the people with MS.
In studies with mice, a similar link between osteopontin and EAE was discovered.
“The activity of the gene controlling osteopontin was totally unexpected,” Dr. Steinman said. “Osteopontin sounds like something to do with bones, but it plays a key role in the immune response. This finding is taking us into some very interesting directions.”
Will the cure for MS be a vaccine?
Dr. Steinman's early research suggests that the initial immune attack in MS is directed against one specific protein. But the attack then spreads to other segments of that protein or to other proteins in myelin. This kind of escalating attack is called “epitope spreading”.
Dr. Steinman and his researchers studied epitope spreading by tracking another kind of immune cell, called the B cell, which produces antibodies. Antibodies “tag” substances for destruction by other immune components. In MS, B cells present fragments of myelin proteins to the T cells, which can then initiate the immune attack against myelin. The study on epitope spreading, published in Nature Biotechnology (2003 Sep; 21: 1033–1039), showed that the mice with the most diverse B-cell responses—meaning that their B cells reacted to many different myelin protein molecules—had the largest number of relapses of EAE. Using this information, Dr. Steinman and colleagues designed customized “cocktails” of the DNA that instruct several of the relevant myelin proteins involved in such B cell responses to the disease. The goal was to induce the immune system to tolerate—instead of attack—all of the proteins in myelin. In studies with mice, the DNA “vaccines” reduced both relapse rates and epitope spreading. Now, early safety and pilot clinical trials involving people with MS are planned.
The next 60 yards
When describing the progress of MS research, Dr. Steinman switches from the forest-fire metaphor to football, admitting that he and other researchers have made gains with “one or two first downs. We have about 60 more yards in the field before we score a touchdown. Until we get the disease cured, it's presumptuous to call any step a big one,” Dr. Steinman said. “They're all small steps.”
The John Dystel Prize for MS Research is given jointly by the National MS Society and the American Academy of Neurology and is funded through the Society's John Dystel Multiple Sclerosis Research Fund. Society National Board member Oscar Dystel and his late wife, Marion, established this fund in 1994 in honor of their son John Jay Dystel, a lawyer whose promising career was cut short by progressive disability from MS. (John died of complications of the disease in June 2003.) The Dystel Prize is the only professional award given annually to honor outstanding contributions to MS research.
Ok, that settles THAT matter, before rumors again go rampant.
Now, as for Biogen ever receiving some "assistance", indirectly
from MS Societies (this is just an example, but will show again how little informed employees of pharma companies even are regarding their own company's "background" and involvements, shall we say kindly)........I QUICKLY found the following. Again, I will highlight in RED this time. Please Note:
Wednesday, September 18, 2002
Young Scientific Investigator Session
....The Blood Brain Barrier as a Target for
ADHESION MOLECULES AND THEIR ROLE IN PATHOGENESIS
Antel JP, Biernacki K, Seguin R, Prat A
Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada
Abstract Body: Cellular immune trafficking across the blood brain barrier(BBB) involves a series of molecular interactions between such cells and the cells and extra cellular matrix (ECM) that comprise the BBB. These interactions include the processes of cell-cell adhesion; chemoattraction, and ECM degradation by matrix metalloproteinases (MMPs). With specific regard to adhesion molecules, expression of these molecules is up-regulated on lymphocytes and monocytes when such cells are activated, as is observed to occur in concert with active phases of multiple sclerosis (MS). In situ studies of central nervous system (CNS) microvessels derived from MS cases, demonstrate upregulation of the ligands for a number of adhesion molecules on endothelial cells (ECs) when compared to ECs from non-inflammatory control cases. To model the role of cell-cell adhesion in cell trafficking across the BBB, we have examined the interaction of lymphocytes and monocytes derived from the peripheral blood of MS patients and controls with human brain (HB)ECs derived from non-inflammatory surgical tissue specimens. These HBECs constitutively
express moderate levels of ICAM-1 but only very low levels of VCAM-1. Expression of both of these adhesion molecules is up-regulated when the HBECs are exposed to supernatants from Th1 cytokine producing CD4 T cell lines. Th2 cytokine producing cell lines neither up-regulate nor inhibit adhesion molecule expression. Using a Boyden chamber assay system,
we can demonstrate that both lymphocyte and monocyte migration across a barrier of HBECs grown on a fibronectin matrix can be inhibited by antibodies directed at ICAM-1 but not VCAM-1. Antibodies directed at the VCAM-1 ligand VLA-4 do inhibit migration, implicating VLA-4 binding to an alternate ligand (Connecting Segment (CS-1) fragment of fibronectin) as the functional event. Adhesion molecules remain targets for therapeutic intervention in MS (eg anti-VLA-4 antibodies). Neither Copaxone nor intereferon (IFN) directly modulate adhesion molecule expression on HBECs. However, IFN treated lymphocytes induce VCAM on the HBECs with a subsequent release of soluble VCAM-1 (sVCAM) ( Calabrese et al 2001). sVCAM binding to its ligand VLA-4 would provide a means to down-regulate trans-endothelial migration.
Disclosure: J Antel has received honoraria from TEVA Marion, Schering,
Biogen and Serona
Funding: Supported by Multiple Sclerosis Society of Canada
CLINICAL TRIALS OF AGENTS TARGETING THE BLOOD BRAIN
BARRIER: SUCCESSES AND FAILURES
NMR Research Unit, Institute of Neurology, London, United Kingdom
Abstract Body: Several lines of evidence implicate blood brain barrier
(BBB) abnormality as an important component in the development of
multiple sclerosis lesions. New lesions exhibit BBB breakdown and
perivascular lymphocytic infiltrates. The location of lesions around cerebral
venules suggests that BBB breakdown may have a key role in lesion
genesis. Serial MRI studies using gadolinium-chelate contrast agents
have demonstrated BBB breakdown as a consistent feature of new lesions
in relapse onset MS. However, new or enlarging lesions may develop without BBB breakdown in primary progressive MS and possibly in other
forms of the disease. Diffuse abnormalities of the normal appearing white
matter also occur, and the relationship of these to BBB breakdown is
uncertain. It is however, likely that BBB breakdown is more extensive than the regions of gadolinium enhancement that are detectable to the eye.
There is good evidence for low grade leakage in chronic lesions, and it may also exist in normal appearing white matter. Using gadolinium
enhanced MIR, there is a relationship of BBB leakage with relapses, but
not with progressive MS. Many immunosuppressive and immunomodulatory treatments have been shown to suppress new areas of focal BBB leakage.
High dose intravenous steroids have a similar but transient effect on
pre-existing and new enhancing lesions. Recently, the monoclonal antiadhesion molecule antibody, anti-VLA4 (natalizumab), has shown dramatic effects in reducing by 90% the frequency of new areas of BBB leakage, but unlike intravenous steroids, does not effect the existing areas of leakage. Natalizumab treated patients also experienced a reduced relapse rate by 50% in the 6 month placebo controlled exploratory trial, and exhibited increased well being compared to those on placebo. Two year studies of this agent are now underway to evaluate its long term safety and efficacy, and in particular the effect on disability. Such long term studies are important, in view of the uncertain relationship between focal BBB changes and progressive disability.
Disclosure: D Miller has received grants from Elan and Biogen for MRI analysis in clinical trials of Natalizumab
Funding: MS Society of Great Britain and Northern Ireland.
My point in this short exercise is only to provide evidence of how "word of mouth" things can become distorted, and how you can't always believe everything you hear
. Especially when things can be so easily confirmed.