Since Hench and his co-workers1demonstrated the action of adrenal corticosteroids and corticotropin in treatment of rheumatoid arthritis six years ago, much experience and data have been accumulated. The consensus of opinion at the present time appears to be that these hormones are of definite, yet limited, value.2These limitations are the result of the balance between the therapeutic response and the occurrence of undesirable side-effects. Furthermore, these hormones have not prevented continued development of the pathological process in the joints. For this reason, biochemical investigations have explored the effects of modification of the steroid molecule aimed at enhancement of its therapeutic ratio. Prednisone, formerly known as metacortandracin, represents an outgrowth of such investigations. This steroid, recently synthesized by Schering, is produced by dehydrogenation at positions one and two of the cortisone nu cleus. It is Δ 1,4-pregnadiene-17α,21-diol-3,11,20-trione. Its structure compared with that of cortisone and hydrocortisone is