The use of melanocortin antagonists in cachexia of chronic disease

Jarrad M. Scarlett, Daniel Marks

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Cachexia is a wasting syndrome that frequently develops in the setting of chronic diseases including cancer, congestive heart failure, chronic obstructive pulmonary disease, AIDS, renal failure and liver failure. Loss of lean body mass is believed to be a significant factor contributing to morbidity and mortality in these chronic diseases; however, there are currently no treatments available that have proven to be effective in reversing the progressive loss of lean body mass in cachectic patients. Evidence from animal models suggests a compelling link between inflammation, the central melanocortin system and cachexia. This review summarises the current evidence supporting the role of the melanocortin 4 (MC4) receptor subtype in cachexia, and discusses the development and use of small-molecule MC4 antagonists, which have proved to be effective in preventing the loss of lean body mass in animal models of cachexia. MC4 antagonists represent an attractive therapeutic approach for cachexia that may attenuate the loss of lean body mass in cachectic patients.

Original languageEnglish (US)
Pages (from-to)1233-1240
Number of pages8
JournalExpert Opinion on Investigational Drugs
Volume14
Issue number10
DOIs
StatePublished - Oct 2005

Fingerprint

Melanocortins
Cachexia
Chronic Disease
Animal Models
Receptor, Melanocortin, Type 4
Wasting Syndrome
Liver Failure
Chronic Obstructive Pulmonary Disease
Renal Insufficiency
Acquired Immunodeficiency Syndrome
Heart Failure
Inflammation
Morbidity
Mortality
Therapeutics
Neoplasms

Keywords

  • Cachexia
  • Cytokine
  • MC4 receptor
  • Melanocortins
  • Weight regulation

ASJC Scopus subject areas

  • Pharmacology

Cite this

The use of melanocortin antagonists in cachexia of chronic disease. / Scarlett, Jarrad M.; Marks, Daniel.

In: Expert Opinion on Investigational Drugs, Vol. 14, No. 10, 10.2005, p. 1233-1240.

Research output: Contribution to journalArticle

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