A synthetic compound originally derived from a sea anemone toxin being investigated as a treatment for multiple sclerosis, lupus, autoimmune nephritis, rheumatoid arthritis, and other autoimmune diseases, may also be of use for the treatment of obesity and insulin resistance.
Researchers at the University of California, Irvine, studying ShK-186—the compound licensed to Seattle biotech Kineta in 2009—have found that in obsese mice fed a high-fat, high-sugar diet, ShK-186 therapy reduced weight gain, white fat deposits, fatty liver, blood cholesterol and blood sugar by activating calorie-burning brown fat, suppressing inflammation of white fat and augmenting liver function.
They also found that the compound had no effect on mice that ate a standard chow diet, suggesting that the obesity-causing diet triggers the expression of ShK-186’s target, Kv1.3.
“Knowing that ShK-186’s unique mechanism of action may have broad utilization across multiple therapeutic disciplines, such as autoimmune diseases and now obesity, further adds to the potential of this compound. This study also shows how medical progress can be made through academic and private sector partnerships,” Charles Magness, Ph.D., Kineta president and CEO, said in a statement.
“These data are quite exciting and strongly support the notion that inhibition of the Kv1.3 channel provides a highly effective method for managing obesity and its associated metabolic abnormalities,” added Yale University’s Gary V. Desir, M.D., who was not a part of this work. “While additional studies are needed, the potential clinical relevance of this work is enormous, since a significant number of people are afflicted with obesity and its associated complications, and no Kv1.3 inhibitor, as a drug candidate for obesity, has reached the clinic until now.”