Lpath, Inc in collaboration with researchers at San Diego State University (SDSU), has announced results showing that one of its potential therapeutic antibody products can mitigate excessive fibrosis in the hearts of mice after a heart attack (myocardial infarction or MI).
The results suggest that Lpath's antibody, called Sphingomab, could someday treat a major form of heart failure that is attributed to excessive scarring (fibrosis) due to the over-activity of a cell type in the heart called the cardiac fibroblast. The results of the first cardiac study were presented on November 14th at the Annual Meeting of the American Heart Association, Chicago, Illinois.
According to Dr. Roger A. Sabbadini, biology professor of SDSU and chief scientific officer of Lpath, the company has developed a monoclonal antibody against sphingosine-1-phosphate (S1P) and validated S1P as a therapeutic target for the treatment of heart disease. "The ability of the Sphingomab to target S1P," notes Sabbadini, "validates this bioactive lipid as being responsible, at least in part, for stimulating cardiac fibroblasts to lay down excessive scar tissue. This leads to compromised heart function and decreased diffusion of nutrients to the heart during the first weeks following a heart attack."
In fact, cardiologists have generally recognized the leading cause of post-MI heart failure and death is excessive scarring associated with maladaptive wound healing. The Sphingomab treatment not only blocked the effects of S1P on the isolated fibroblasts in cell culture, but also prevented an important early event called perivascular fibrosis in an animal model. The results were presented in an oral symposium at the AHA meetings by Nicole Gellings Lowe from the SDSU Heart Institute.
Lpath believes that S1P contributes to excessive scarring that exacerbates not only heart disease and cancer, but also various ocular disorders. In fact, three days ago, on November 12, Lpath presented research at the American Academy of Ophthalmologists (www.aao.org) conference in Las Vegas, Nevada, showing Sphingomab can also prevent maladaptive fibrosis in Age-related Macular Degeneration (AMD) as tested in a mouse model.
Sphingomab has previously been tested in several animal models of human cancer and this work was published in a leading cancer journal, Cancer Cell.
Sphingolipids, like S1P, play a primary role in mediating this over-activity. Researchers at Lpath believe interfering with the function of S1P and other sphingolipids can result in clinically relevant therapeutic outcomes in each of these disease states.