In December I wrote a post about a promising treatment for SLE, belimumab (Benlysta/LymphoStatB). This drug decreases the proliferation of B cells by removing the anti-apoptotic effect of BLyS, and Human Genome Sciences has used it to come up with one of the first successful drug trials in SLE. I was curious though as to why the drug was being tested in SLE when the huge rheumatoid arthritis market beckoned. After all, rituximab, another anti-B cell biologic has been shown to be successful in this population, and even though the RA market is becoming saturated, it still seems likely that 10% of the RA market would still be more profitable than the entire SLE market. Well it turns out that the people at Human Genome did think of this but the one smallish study that I did find was not very encouraging. Of 283 patients, only 35% reached the ACR 20 response, and oddly, higher doses did even less well. In this day and age, if you're talking ACR 20, you're not in the game. Most biologics can produce ACR 20 responses of 60% or more, and we quickly move along to check out the ACR 50 and even the ACR70 responses.
So belimumab seems to work in SLE but not in RA, while the other anti-B cell molecule, rituximab, works in RA but not in SLE. (Actually, most people believe that rituximab works in SLE but are having a heck of a time proving it). It goes to show how different these two diseases are and how little we really know about the immune dysfuntion that causes them.