The majority of patients with advanced cancer suffer from cachexia, a systemic wasting syndrome, which causes a reduction in tolerance to anti-cancer treatment, response to therapy, quality of life, and eventually, duration of survival. Currently, there is no specific remedy available despite the urgent medical need for an effective treatment of cachexia. An important aspect of cachexia is the inexorable loss of skeletal muscle mass leading to progressive functional impairments. It is, therefore, crucial to identify early readouts for the loss of muscle mass and function to initiate appropriate and timely treatments. Here, we describe mouse models of cancer-induced cachexia using readouts such as hind limb muscle mass and volume, as well as evoked force and food intake measurement, to allow the testing of potential therapeutic agents for the treatment of cachexia. We focus on experimental cancer models using a mouse (syngeneic) or a human (xenograft) cancer cell lines with a rapid onset of tumor growth and cachexia, which are easier to establish, monitor and reproduce compared to the genetically engineered mouse models.