I have heard a lot about DiaPep277 in the last few days. Could you please explain more about it and also give insight as to if and when this could become a viable, widely available treatment for early type 1 diabetes? Do you know if there are presently any clinical trials in the United States for this new treatment? Are there any potential harmful side effects to the injection? Will this be an option for those who are in the early stages of type 1 right now? Time is certainly of the essence in these cases. Any delays could lead to insulin dependence with no hope of beta cell response recovery for many.

As the extraordinary intricacies of the autoimmune process have been gradually dissected over the last twenty years, it has been possible to think of ways to prevent type�1A diabetes and to avert insulin dependence or prolong the honeymoon. period. There was a meeting in the early part of last year when a number of these possibilities were reviewed.

One of these was DiaPep277 which is a peptide fraction of Heat Shock Protein. Its rational, which has been confirmed in mice, is that it changes the T-cell response to an antigen from a destructive Th1 response to a protective Th2 one.

The copyright to the product is owned by Peptor and the original basic research was carried out at the Weizman Institute in Israel. The product has not been approved so far for clinical trials by the FDA in the US.

Although it had no apparent ill effects, it is reasonable to have some doubts about its long-term efficacy. There have been clinical trials in adults with recent onset type 1A diabetes, and this in itself raises some questions in that in the age group (16-55), many of the subjects would have been deemed to have Late-onset Autoimmune Diabetes of Adulthood (LADA) which is possibly different from conventional autoimmune diabetes. More important is the fact that by the time clinical type�1 diabetes is manifest less than 10% of the beta cell mass is still present. This in turn suggests that while DiaPep277 may indeed have made possible some initial rise of C-peptide in the first months of treatment, there is absolutely no evidence whatsoever that it in any way restores lost beta cell function.

Moreover, Peptor has declined to publish their long term results which raises the possibility that whilst beta cell decay was slowed it was not averted, something that has already been shown for nicotinamide in children in New Zealand. Many similar trials are now underway, but my own expectation is that it will soon be possible to transplant some form of a surrogate beta cell and at the same time to induce permanent tolerance in the host without the need of immunosuppressive medication.

DOB