Multimodal action of MAS activation for systemic cancer cachexia therapy

Cancer cachexia remains a largely intractable, deadly condition for patients with no approved, effective therapies. However, research progress over the past few decades demonstrates that cachexia is a disease with specific, targetable mechanisms. New work by Murphy and colleagues in this issue of Cancer Research suggests that activation of the alternative renin–angiotensin system with the nonpeptide Mas receptor agonist AVE 0991 holds promise for reducing muscle wasting in cancer. Their cell studies demonstrate on-target activity in skeletal muscle cells, whereas their mouse results suggest potentially more important systemic effects.