Inflammation – one of the body’s earliest responses to infection or injury – can help the healing process when it’s closely controlled by the immune system. Mismanaged inflammation, however, can contribute to a variety of disorders, such as autoimmune diseases or allergic reactions. The immune system maintains this careful balance in part through the activity of a protein known as NF-κB. When triggered by cellular damage, infectious bacteria or some other molecular signal, NF-κB binds to DNA and turns on genes that activate inflammation. Since NF-κB acts like a master inflammation regulator, it makes an attractive target for researchers hoping to manipulate the immune response in patients suffering from either too much or too little inflammation.

A bi-coastal Sanford-Burnham research team led by Dr. Greg Roth in Lake Nona, Orlando, Fla. and Dr. John Reed in La Jolla, Calif. recently used the robotic technology in the Conrad Prebys Center for Chemical Genomics (Prebys Center) to screen a collection of more than 100,000 chemical compounds to find that one needle-in-a-haystack (or handful of needles) capable of blocking NF-κB. In a pair of studies published in ACS Chemical Biology (March 19, 2010) and the Journal of Medicinal Chemistry (May 18, 2010), they discovered a chemical compound that selectively impairs NF-κB activity under certain conditions. By inhibiting NF-κB this way, the compound has the potential to dampen potentially harmful inflammation without shutting down the whole immune system.

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