RPI-78M Decreases Progression of Multiple Sclerosis by Altering Gene Expression
Mar 3, 2005 - 4:23:38 PM
Nutra Pharma Corp.,a biotechnology holding company that owns rights to intellectual property related to the development of drugs for HIV and Multiple Sclerosis has announced that its contract researchers, Eno Research and Development, Inc. (ERDI) have completed their analysis of a series of microarray studies with RPI-78M in the gene expression of cells from Multiple Sclerosis (MS) patients.
RPI-78M is the lead drug candidate of Nutra Pharma's minority holding, ReceptoPharm, Inc. and is being studied in preclinical assays for its efficacy in treating MS. ERDI measured the effect of RPI-78M on gene expression using cDNA microarray technology to identify any potentially unique changes in gene expression that may be caused by the therapy.
ERDI was contracted by Nutra Pharma to analyze immune cells and brain lesions of Multiple Sclerosis patients with and without the addition of RPI-78M. They measured the changes in gene expression that occurred with treatment.
After statistical evaluation of the data, ERDI found more than sixty genes with significant changes in expression as compared to the control. In analyzing the affected genes, at least thirty of them may have a specific role in the progression of the disease and symptoms of MS.
"RPI-78M had a significant affect on the genes in the cytokine pathway as well as the myelination pathway," commented James Flowers, President and Chief Scientific Officer of Eno Research and Development, Inc. (ERDI).
"The cytokine pathway genes play a role in marshaling the attack on the nervous system by immune cells. Since this is one of the principle pathways that lead to the forward progression of MS, it is notable that if these results were replicated in the patient population it may greatly reduce the severity of the disease" he continued.
"Additionally, genes responsible for repair and maintenance of the myelin sheathes of neurons were upregulated. MS patients have a loss of myelin, the insulating material that surrounds the nerve fibers in the brain, spinal cord, and optic nerves. This damage or loss of myelin can prevent nerve signals from being conducted, or can cause those signals to be conducted too slowly. The data from this study suggests that RPI-78M may aid the patient in reversing some of the damage caused to the myelin by their disease." ERDI will continue to study RPI-78M and its effects on gene expression as well as the drug's effects in histoculture experiments that may further elucidate its mechanism of action.
There has been a great deal of interest surrounding research in Multiple Sclerosis therapies. There are currently four drugs on the market for the treatment of the disease. A fifth drug, Tysabri, was voluntarily pulled from the marketplace earlier this week by the drug's manufacturers, Biogen-Idec and Elan.
"We are working diligently with ERDI to bring this information to the scientific community," commented Rik J Deitsch, Chief Executive Officer of Nutra Pharma. "We expect to present the data at related conferences and to seek publication of the finished work. These studies, when coupled with the positive results in the recently-completed animal model, create substantial evidence of the drug's effects against MS. We are currently seeking potential partners that should allow us to move into sanctioned human trials," he added.
Multiple sclerosis (MS) is an autoimmune disease in which the immune system, the body's principal defense against foreign substances such as bacteria, mistakenly attacks normal tissues of the central nervous system. It afflicts approximately 400,000 people in the United States and more than 2.5 million worldwide. Specifically, the disease results in damage to a fatty tissue called myelin that surrounds and protects nerve fibers, creating scarring (sclerosis) that interferes with the normal transmission of nerve impulses. This damage, in turn, leads to a variety of chronic and highly individual and unpredictable neurological symptoms, ranging from movement and balance problems to vision impairment.
The disease is largely caused by activation of a specific subset of the patient's own white blood cells, T-cells that then attack the myelin and are largely responsible for disease progression.
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