Idera Pharmaceuticals, Inc. announced today that it is presenting data on IMO-3100, an antagonist of TLR7 and TLR9, in a preclinical model of lupus showing that treatment with IMO-3100 suppressed several key disease progression parameters. The presentation, entitled “Treatment with IMO-3100, a novel TLR7 and TLR9 antagonist, inhibits disease development in lupus prone NZBW/F1 mice,” is being made at the Keystone Symposia: Dendritic Cells and the Initiation of Adaptive Immunity being held February 12-17, 2011 in Santa Fe, New Mexico.
“In this study, IMO-3100, Idera’s proprietary dual antagonist of TLR7 and TLR9, was shown to suppress multiple key markers of lupus,” commented Nicola La Monica, Ph.D., Vice President, Biology of Idera Pharmaceuticals. “These results are consistent with the extensive body of scientific literature suggesting the important role of TLR7 and TLR9 in the progression of lupus.”
In the study presented today, IMO-3100 was evaluated at increasing dose levels in NZBW/F1 mice, a strain of mice which are prone to develop a lupus-like autoimmune disease. Treatment was initiated in a therapeutic setting at 21 weeks of age, after detection of anti-DNA antibodies in these mice. Weekly doses of IMO-3100 were administered subcutaneously for 13 weeks. Disease progression was assessed on a weekly basis by monitoring serum anti-DNA antibody levels, blood urea nitrogen (BUN) levels and urine protein levels. Histopathology analysis of selected organs was performed at least two weeks after the last dose of IMO-3100.
IMO-3100 treatment led to a dose-dependent reduction in serum anti-DNA antibody levels, BUN levels and urine protein levels. Histological evaluation of the kidneys showed IMO-3100 treatment led to dose-dependent reduction in disease-associated kidney damage. Histopathology of organs of IMO-3100-treated mice showed reduction in lymphoid hyperplasia. IMO-3100 treatment also led to dose-dependent reduction in serum cholesterol levels.
Source: Idera Pharmaceuticals