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News

Israeli scientists block the progression of type I diabetes

Washington University In St Louis : 26 November, 2001  (Company News)
A team of researchers led by Prof. Irun Cohen of the Weizmann Institute of Science has developed a unique approach for halting the progression of Type I (juvenile or insulin-dependent) diabetes. Cohen and Dr. Dana Elias (then a postdoctoral fellow at the Institute) discovered that injecting mice with a small peptide fragment known as p277 prevents the progression of Type I diabetes. Based on the results of his research, Peptor, a biopharmaceutical company from Rehovot, Israel, developed DiaPep277, an experimental drug designed to prevent or treat Type I diabetes.
A team of researchers led by Prof. Irun Cohen of the Weizmann Institute of Science has developed a unique approach for halting the progression of Type I (juvenile or insulin-dependent) diabetes.

Cohen and Dr. Dana Elias (then a postdoctoral fellow at the Institute) discovered that injecting mice with a small peptide fragment known as p277 prevents the progression of Type I diabetes. Based on the results of his research, Peptor, a biopharmaceutical company from Rehovot, Israel, developed DiaPep277, an experimental drug designed to prevent or treat Type I diabetes.

A recent clinical study performed by researchers at Hadassah-Hebrew University Medical School, Peptor Ltd., and Prof. Cohen proved that DiaPep277 is successful in arresting the progression of Type I diabetes in newly diagnosed patients. The research findings are published in the November 24, issue of The Lancet.

The study was of 35 patients newly diagnosed with Type I diabetes. Eighteen patients received injections of DiaPep277 at the beginning of the study, at one month, and at six months; 17 patients received three injections of an inert substance (placebo). Patients in the treatment group (those receiving DiaPep277) showed a halt or delay in the attack upon, or destruction of their pancreatic insulin-producing cells by the immune system. These results were evident in the level of the body's own insulin production and in a decreased need for insulin injections. The researchers were able to trace the mechanism of this improvement to changes in the patients' immune lymphocytes called T-cells. In contrast, patients receiving the placebo showed a significant decline in their natural insulin production and a persistent rise in the need for insulin injections. No significant side effects as a result of injecting DiaPep277 were found.

Diabetes is a chronic disease associated with elevated blood sugar levels, in which the body does not produce or properly use insuli, a hormone needed to convert sugar, starches and other foods into energy. Recent data show that between 120 and 140 million people suffer from diabetes worldwide.

Type I (insulin-dependent) diabetes usually results from an autoimmune disorder in which the immune system mistakenly attacks the body's own insulin-producing pancreatic cells, reducing and ultimately eliminating all insulin production. In contrast, Type II diabetes is a metabolic disorder resulting from the body's inability to properly use insulin. All Type I diabetes patients (and the more severe Type II cases) must supplement their natural insulin production with insulin injections.

For the past several years, researchers at the Weizmann Institute's Department of Immunology led by Professor Cohen have been studying the mechanism by which the immune system destroys the insulin-producing pancreatic cells. Working with mice, the scientists discovered that a particular protein called HSP60 was closely linked to this destructive process. The protein acts like an antigen, prompting the immune cells to attack. Further investigation revealed that injecting sick mice with p27, a small peptide fragment of the HSP60 protei, shut down the immune response, preventing the progression of Type I diabetes. 'The peptide essentially acts to 'reeducate' the immune cells, switching off their destructive activity,' Cohen explains. 'The idea for using p277 stemmed from the discovery that the immune system has different options to choose from in responding to an antigen. It can act to destroy the antigen or alternatively protect it from destruction. In this case it indirectly prevents the pancreatic cells from being destroyed.'

The scientists participating in this study are: Professor Itamar Raz and Dr. Muriel Metzger from Hadassah-Hebrew University Medical School, Dr. Dana Elias (now VP R&D at Peptor Ltd.), Dr. Ann Avron, and Dr. Merana Tamir from Peptor Ltd.
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