Technical Report abstract


Nature Medicine 13, 1108 - 1113 (2007)
Published online: 26 August 2007 | doi:10.1038/nm1610

A ligand-receptor fusion of growth hormone forms a dimer and is a potent long-acting agonist

Ian R Wilkinson1,7, Eric Ferrandis2,7, Peter J Artymiuk3,7, Marc Teillot2, Chantal Soulard2, Caroline Touvay2, Sarbendra L Pradhananga1, Sue Justice1, Zida Wu4, Kin C Leung5, Christian J Strasburger4, Jon R Sayers6 & Richard J Ross1


Cytokine hormones have a short plasma half-life and require frequent administration. For example, growth hormone replacement involves daily injections. In common with other cytokines, the extracellular domain of the growth hormone receptor circulates as a binding protein, which naturally prolongs the biological half-life of growth hormone. Here we have studied the biological actions of a ligand-receptor fusion of growth hormone and the extracellular domain of its receptor. The genetically engineered ligand-receptor fusion protein was purified from mammalian cell culture. In rats, the ligand-receptor fusion had a 300-times reduced clearance as compared to native growth hormone, and a single injection promoted growth for 10 d, far exceeding the growth seen after administration of native growth hormone. The ligand-receptor fusion forms a reciprocal, head-to-tail dimer that provides a reservoir of inactive hormone similar to the natural reservoir of growth hormone and its binding protein. In conclusion, a ligand-receptor fusion of cytokine to its extracellular receptor generates a potent, long-acting agonist with exceptionally slow absorption and elimination. This approach could be easily applied to other cytokines.

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  1. School of Medicine and Biomedical Sciences, Royal Hallamshire Hospital, University of Sheffield, Sheffield S10 2JF, UK.
  2. Institut Henri Beaufour, Ipsen, 5 Avenue du Canada, 91966 Les Ulis Cedex, France.
  3. Department of Molecular Biology and Biotechnology, University of Sheffield, Sheffield S10 2JF, UK.
  4. Department of Medicine, Campus Mitte Charite-Universitatsmedizim, 10117 Berlin, Germany.
  5. Pituitary Research Unit, Garvan Institute of Medical Research, Sydney, New South Wales 2010, Australia.
  6. Unit of Infection and Immunity, Royal Hallamshire Hospital, University of Sheffield, Sheffield S10 2JF, UK.
  7. These authors contributed equally to this work.

Correspondence to: Richard J Ross1 e-mail: r.j.ross@sheffield.ac.uk




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