Burn results in a substantial release of inflammatory mediators, which leads to significant metabolic derangements and the introduction of a post-injury stress environment, hypermetabolic response. This hypermetabolic response is characterized by vast catabolism, and if untreated, it leads to substantial physiological exhaustion, organ failure, and even death. Particularly, an important feature of the post-burn hypermetabolic response is generalized catabolism. Hypercatabolism can be attributed to a shift in the production of anabolic to catabolic factors. Increased levels of proinflammatory cytokines occur immediately after injury and are intimately associated with augmented catabolic hormones, principally cortisol and catecholamines. Furthermore, hypermetabolism is associated with a suppression of the endocrine axis, which can result in a substantial decrease in serum levels of endogenous anabolic hormones. Indeed, burn patients exhibit diminished levels of hormones such as human growth hormone (hGH), IGF-I, and testosterone post-trauma. Non-pharmacologic interventions such as exercise, appropriate nutrition, and heating the environment have been employed to manage post-trauma hypermetabolism. While they improve hypermetabolic catabolism, pharmacologic interventions appear critical for clinical efficacy. Various pharmacological strategies have been used to prevent catabolism and promote anabolism in thermally injured patients. This chapter analyzes the anticatabolic and anabolic pharmacologic interventions currently utilized. It will cover propranolol, growth hormone (GH), insulin growth factor 1 (IGF-1), insulin growth factor binding protein 3 (IGFBP-3), insulin, metformin, testosterone, oxandrolone, and thyroid hormones. Furthermore, novel therapeutics utilized in other conditions, such as cancer-related cachexia, are discussed.