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Archive - 03 - 2006
SAN DIEGO, March 27, 2006, (BUSINESS WIRE) -DexCom, Inc. (NASDAQ:DXCM) today announced that it has received Food and Drug Administration (FDA) approval for its STS(TM) Continuous Glucose Monitoring System, a first generation device designed to help people with diabetes more conveniently and effectively manage their blood sugar levels. Widely recognized as one of the leading causes of death and disability in the United States, diabetes is a chronic disease with no known cure that afflicts approximately 20 million people in the U.S., according to the Center for Disease Control (CDC). In the U.S., diabetes is the leading cause of adult blindness, end stage kidney failure and lower limb amputations. People suffering from diabetes are also more significantly at risk for cardiovascular disease and stroke."We are very pleased the FDA has approved the DexCom STS Continuous Glucose Monitoring Product and are hopeful this novel technology will improve the quality of life for people living with diabetes," said Andrew P. Rasdal, DexCom President and Chief Executive Officer.The DexCom STS consists of a tiny wire-like sensor that is inserted by the patient just under the skin. The sensor continuously measures glucose levels which are transmitted wirelessly to the cell phone-like STS Receiver. With the push of a button, the handheld Receiver conveniently provides the patient with real-time glucose measurements and trends, as well as providing alerts to warn of high and low glucose levels. The results of a study on the DexCom STS published in the January 2006 edition of Diabetes Care, a publication of the American Diabetes Association, demonstrated patients could achieve better control of glucose levels when using the information from the DexCom STS."We are appreciative of the efforts by the FDA and FCC to help make this technology available to people with diabetes," said Rasdal. "Further, we are especially thankful for the support of the patients, physicians, nurses, and diabetes educators who have participated in our clinical studies supporting this approval."DexCom management will hold a conference call starting at 4:30 PM (Eastern Time) on Monday, March 27, 2006 to discuss this important development. The conference call will be concurrently webcast. The link to the webcast will be available on the DexCom Inc. website www.dexcom.com under the investor webcast section and will be archived for future reference. To listen to the conference call, please dial (800) 811-0667 (U.S./Canada) or (913) 981-4901 (International) and use the participant code "6796471" approximately five minutes prior to the start time.We have not sold any of our products to date. Successful commercialization of our products is subject to various risks and uncertainties, including possible delays in our development program, the inability of patients to receive reimbursements from third-party payers, a lack of acceptance in the marketplace by physicians and patients, inadequate financial and other resources, and the inability to manufacture products in commercial quantities at an acceptable cost.
BOSTON, March 24, 2006 (Joslin) - Researchers from Joslin Diabetes Center have published in the March 24, 2006, issue of the journal Science a significant study about islet cell recovery and reversal of type 1 diabetes in mice. It is generally believed that an effective cure for type 1 diabetes will require two substantial scientific advances. First, in order to restore the pancreas' ability to produce insulin, new islet beta cells must be provided, either by transplanting cells from a healthy donor or by encouraging the growth and/or function of the diabetic patient's own cells. Second, to protect the new beta cells, no matter what their origin, it is necessary to repair the breakdown in immunological tolerance that precipitated the anti-islet attack in the first place.In a widely discussed paper that appeared in Science in 2003, Dr. Denise Faustman and her colleagues reported successful achievement of both of these advances, resulting in the "cure" of a substantial fraction of severely diabetic NOD mice, the most popular animal model of human type 1 diabetes. Their method entailed giving diabetic mice a temporary islet transplant from a genetically identical mouse, administering a single injection of an immuno-stimulatory compound called Complete Freund's Adjuvant (CFA), and repeatedly injecting a large number of spleen cells taken from genetically different mice. It was thought that the islets served to keep the animals with diabetes healthy long enough for the other treatments to have their effects, that the CFA eliminated the autoimmune attack on the islets, and that the spleen cells somehow gave rise to insulin-producing cells, presumably beta-cells, ultimately leading to islet regeneration."The compound CFA has been used to modulate diabetes in NOD mice for a number of years in a variety of experimental contexts, so its effect was not very surprising. However, the notion that adult spleen cells from one mouse could give rise to new islets in the pancreas of another mouse was a novel and exciting one," said Diane Mathis, Ph.D., who led the Joslin study along with Christophe Benoist, M.D., Ph.D. Drs. Benoist and Mathis head Joslin's Section on Immunology and Immunogenetics, hold the William T. Young Chair in Diabetes Research, and are Professors of Medicine at Harvard Medical School.Therefore, many research teams were interested in extending the potentially important findings of Dr. Faustman and her colleagues by defining the precise cellular and molecular mechanisms involved. As a necessary first step, the researchers needed to reproduce the results published in the 2003 Science paper. Unfortunately, this did not prove possible, as reported in three papers appearing in the March 24, 2006, issue of Science from groups based at Joslin Diabetes Center in Boston, Washington University in St. Louis and the University of Chicago, working entirely independently. For example, the Joslin team was not able to replicate the original findings even though it strove to match as closely as possible the published methods, and also incorporated supplementary details from more extensive protocols provided by the authors. In short, like the study of Dr. Faustman and colleagues, the three new studies resulted in a substantial fraction of severely diabetic NOD mice being "cured" of their hyperglycemia as well as their autoimmunity against beta cells. However, none of the teams found any evidence that new islet cells emanating from donor spleen cells were the source of the insulin responsible for the reversal of diabetes. Rather, even though severely diabetic, the host mice kept a substantial number of residual beta cells, and the recovered islets were all of host, rather than donor spleen cell, origin."Given recent reports from several groups that beta cells in adult mice can undergo active cell division, the most likely explanation for islet recovery in the 'cured' mice is that when the autoimmunity was suppressed, beta-cell growth was permitted -- or even promoted -- exceeding death of the beta cells," said Dr. Benoist. "An additional possibility is that eliminating the inflammation improved the function of the residual beta cells.""The obvious implication from these new results, given that CFA is a reagent that can potentially alter the immune system, is that the donor spleen cells might not be an essential element of the Faustman protocol," Dr. Mathis said. "The original study did not report a control group in which spleen cells were left out of the treatment protocol. Both the Joslin and Washington University groups did include this important control, and found that CFA alone (plus the temporary islets) was as effective as the full protocol with its multiple injections of spleen cells. This finding again argues that the 'cure' of diabetes afforded by the Faustman protocol did not involve donor spleen cells giving rise to host islet beta cells."Should the effectiveness of CFA alone demonstrated in these new studies prompt a reconsideration of the analogous reagent Bacille Calmette-Guerin (BCG), in isolation, to treat people with diabetes? BCG is a component of some human vaccines, like the vaccine agent used against tuberculosis, and the Faustman group has proposed using it as a treatment for type 1 diabetes. Three BCG trials large enough to be informative have previously been performed and failed to show any positive effect. "A likely explanation for the difference in results is that the injection of CFA into the footpad of mice and the injection of BCG under the skin of humans are actually radically different interventions, the former provoking a massive inflammatory response throughout the body, a procedure that is difficult to contemplate in a patient context," Dr. Benoist explained. "It should also be kept in mind that the mice were also treated with an islet transplant, the precise role of which has not really been explored. Lastly, it might be relevant that BCG has been reported to increase the incidence or accentuate the course of diabetes in humans in certain contexts."
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