**1. Introduction**

There are no drugs approved to treat cancer cachexia in the US. This is unfortunate and a flaw, I believe, in the FDAs criteria for cancer cachexia drug approval in the United States [1]. Their criterion measure has been an improvement in function. This variable depends on the nervous system in addition to skeletal muscle because they are functional in nature. Cachexia, by definition is the loss of skeletal muscle and adipose tissue. Drugs designed to affect skeletal muscle have little and probably no effect on the nervous system. As such, the FDA should remove the functional requirement or make functional training along with drug administration a requirement in phase I, II and III studies. As it is, all drugs anabolic to skeletal muscle will likely fail a functional test since they have no effect, without functional exercise, on the nervous system.

With this short coming of the approval process in mind, other measures must be taken to attenuate cachexia with the intent of allowing more time for chemotherapeutic agents and radiation therapy to exert their tumor killing activity. It is indeed a matter of time for cachectic cancer patients; the more time they have, the better the outcome with the goal to be to cure cancer for those individuals suffering from cancer cachexia and save lives. Off-label use of drugs that are approved for other conditions would appear to be a very important action to take for clinicians to this end. For example, the use of monoclonal antibodies for IL-6 and TNF-α which are approved for other indications would appear beneficial in treating many cancers as these proinflammatory cytokines are secreted during cancerinflammation mediated by these cytokines wreaks havoc on the patient. In addition, IL-6 and TNF-α are directly related to muscle catabolism in models of cancer cachexia [2, 3]. Hypermetabolism is another manifestation of cancer cachexia [4]. Drugs that block the action of epinephrine (a catecholamine) would act to reduce metabolic rate and slow the rate of muscle wasting [5]. The drug propranolol blocks both beta 1 and beta 2 receptors metabolic rate. This is just one example of a drug that could reduce hypermetabolism of cachexia. A third factor, although taboo especially in the sporting world, is the use of anabolic agents to stimulate muscle protein synthesis [6–8] in the face of reduced muscle protein synthesis, and elevated muscle protein breakdown. Thus, the off-label use of anabolic steroids, testosterone, and growth hormone secretagogues should be explored although some these agents are not FDA approved. For example, anamorelin was found to be safe and effective in increasing lean body mass through phase III trials but did not increase grip strength [9].
