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The wasting syndrome that kills up to a third of cancer patients: tumours send hormonal signals (GDF-15, IL-6) that switch off appetite and burn muscle and fat. The first drug to reverse it, ponsegromab, showed weight gain in 2024.
Tumour- and host-derived GDF-15 acts on the brainstem GFRAL receptor to suppress appetite; IL-6/STAT3, TNF, activin/myostatin, and glucocorticoids drive muscle proteolysis (ubiquitin-proteasome, autophagy) and adipose lipolysis/browning. Cachexia worsens treatment tolerance and is largely irreversible late. Ponsegromab (anti-GDF-15, Pfizer) increased weight and activity in a phase 2 trial (NEJM 2024) and is in phase 3; anamorelin (ghrelin agonist) is approved in Japan; nutrition and exercise remain foundational. Cachexia is now treated as a target in its own right rather than an inevitability.
A thermostat hijacked by the tumour: it tells the body it is full when it is starving and orders the furnace to burn muscle for fuel. Ponsegromab cuts the wire to the thermostat.
Shares Cold Spring Harbor Laboratory, Cancer metabolism, Pancreatic ductal adenocarcinoma and the tag mechanism.
Shares Cancer metabolism, MD Anderson Cancer Center, Non-small-cell lung cancer and the tag mechanism.
Shares Inflammation & NF-κB, MD Anderson Cancer Center, Pancreatic ductal adenocarcinoma and the tag mechanism.
Shares Cold Spring Harbor Laboratory, Inflammation & NF-κB and the tag mechanism.
Shares MD Anderson Cancer Center, Pancreatic ductal adenocarcinoma and the tag mechanism.
Shares Cold Spring Harbor Laboratory, Inflammation & NF-κB, MD Anderson Cancer Center, Pancreatic ductal adenocarcinoma and the tag mechanism.
Shares Cold Spring Harbor Laboratory, Cancer metabolism, Pancreatic ductal adenocarcinoma, Non-small-cell lung cancer and the tag mechanism.
Shares Cancer metabolism and the tag mechanism.