CANCER cachexia is a syndrome of progressive wasting which has been suggested to be mediated by tumour-necrosis factor-α (ref. 1), interleukins 1 and 6 (ref. 2), interferon-γ (ref. 3) and leukaemia-inhibitory factor⁴. It has proved difficult to correlate levels of tumour-necrosis factor-α and interleukin-6 with cancer cachexia^5,6, and the weight loss induced by leukaemia-inhibitory factor may be due to toxicity⁷. In the murine adenocarcinoma MAC 16, cachexia is mediated by circulatory catabolic factors^8,9, which we have now isolated using an antibody cloned from splenocytes of mice transplanted with the MAC16 tumour, with a delayed cachexia¹⁰. The material is a proteoglycan of relative molecular mass 24K which produces cachexia in vivo by inducing catabolism of skeletal muscle. The 24K material was also present in urine of cachectic cancer patients, but was absent from normal subjects, patients with weight loss due to trauma, and cancer patients with little or no weight loss. This suggests that cachexia in mice and humans may be produced by the same material.