Abstract
Type 1 diabetes (T1D) is a chronic autoimmune disease. Manifestation of the disease occurs when most of the insulin producing beta-cells have been destroyed. At onset of the disease, there is still significant residual secretion of endogenous insulin. The American DCCT and other studies showed an evidently lower risk for complications in patients who had still positive C-peptide levels. Long-term maintenance of this residual function is only possible by causally acting drugs which either interfere with the autoimmune process or enhance beta-cell regeneration. DiaPep277® is a biopharmacon developed in the 1990s which does not act as a wide spectrum immunosupressant but is meant to specifically modulate islet autoimmunity. The synthetic peptide consisting of a 24 amino acid sequence (437-460) of the 60 kDA human heat shock protein hsp60 is administered subcutaneously. A cytokine shift from the proinflammatory T helper (Th)1 towards the antiinflammatory Th2 phenotype seems to be responsible for the cessation of the autoimmune process. In a phase II study, in subjects treated with DiaPep277®, C-peptide secretion was similar to baseline levels 10 months after the first injection, whereas it had decreased to less than a third in the placebo group. These results are now to be verified in a double-blind placebo-controlled phase III study. Also four German diabetes centers are involved.
Translated title of the contribution | DiaPep277®: A peptide for the causal treatment of type 1 diabetes? |
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Original language | German |
Pages (from-to) | 83-86 |
Number of pages | 4 |
Journal | Diabetes, Stoffwechsel und Herz |
Volume | 15 |
Issue number | 4 |
State | Published - 20 Jul 2006 |
Externally published | Yes |