Inhibition of tumour cell growth by carnosine: some possible mechanisms

Alan R. Hipkiss*, Frank Gaunitz

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


The naturally occurring dipeptide carnosine (β-alanyl-l-histidine) has been shown to inhibit, selectively, growth of transformed cells mediated, at least in part, by depleting glycolytic ATP levels. The mechanism(s) responsible has/have yet to be determined. Here, we discuss a number of probable and/or possible processes which could, theoretically, suppress glycolytic activity which would decrease ATP supply and generation of metabolic intermediates required for continued cell reproduction. Possibilities include effects on (i) glycolytic enzymes, (ii) metabolic regulatory activities, (iii) redox biology, (iv) protein glycation, (v) glyoxalase activity, (vi) apoptosis, (vii) gene expression and (viii) metastasis. It is possible, by acting at various sites that this pluripotent dipeptide may be an example of an endogenous "smart drug".

Original languageEnglish
Pages (from-to)327-337
Number of pages11
JournalAmino Acids
Issue number2
Early online date1 Dec 2013
Publication statusPublished - 1 Feb 2014


  • cancer
  • carnosine
  • glycation
  • glycolysis
  • metastasis
  • NAD
  • Redox biology
  • regulation
  • signalling
  • tumour


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