Targeting C-reactive protein for the treatment of cardiovascular disease

Mark B. Pepys (), Gideon M. Hirschfield, Glenys A. Tennent, J. Ruth Gallimore, Melvyn C. Kahan, Vittorio Bellotti, Philip N. Hawkins, Rebecca M. Myers, Martin D. Smith, Alessandra Polara, Alexander J. A. Cobb, Steven V. Ley, J. Andrew Aquilina, Carol V. Robinson, Isam Sharif, Gillian A. Gray, Caroline A. Sabin, Michelle C. Jenvey, Simon E. Kolstoe, Darren Thompson and Stephen P. Wood
Additional contact information
Mark B. Pepys: Royal Free and University College Medical School, University College London
Gideon M. Hirschfield: Royal Free and University College Medical School, University College London
Glenys A. Tennent: Royal Free and University College Medical School, University College London
J. Ruth Gallimore: Royal Free and University College Medical School, University College London
Melvyn C. Kahan: Royal Free and University College Medical School, University College London
Vittorio Bellotti: Royal Free and University College Medical School, University College London
Philip N. Hawkins: Royal Free and University College Medical School, University College London
Rebecca M. Myers: University of Cambridge
Martin D. Smith: University of Cambridge
Alessandra Polara: University of Cambridge
Alexander J. A. Cobb: Royal Free and University College Medical School, University College London
Steven V. Ley: University of Cambridge
J. Andrew Aquilina: University of Cambridge
Carol V. Robinson: University of Cambridge
Isam Sharif: University of Edinburgh
Gillian A. Gray: University of Edinburgh
Caroline A. Sabin: Royal Free and University College Medical School, University College London
Michelle C. Jenvey: University of Southampton
Simon E. Kolstoe: University of Southampton
Darren Thompson: University of Southampton
Stephen P. Wood: University of Southampton

Nature, 2006, vol. 440, issue 7088, 1217-1221

Abstract: Aiming for the heart C-reactive protein (CRP) is a clinical marker for inflammatory disease and infection, but it also binds to damaged cells and activates complement, a host defence and pro-inflammatory system of serum proteins. Complement-mediated inflammation exacerbates tissue injury in heart attacks, and human CRP increases damage in a rat model of acute myocardial infarction via a complement-dependent mechanism. These observations point to CRP as a possible target for drugs intended to protect the heart. Pepys et al. therefore designed a specific small-molecule CRP inhibitor. Five molecules of this palindromic compound are bound by two pentameric CRP molecules arranged face-to-face, as in the X-ray crystal structure of the complex on the cover. The inhibitor blocks the adverse effects of human CRP in rats with acute myocardial infarction, suggesting that early therapeutic inhibition of CRP might be beneficial for heart attack patients.

Date: 2006
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DOI: 10.1038/nature04672

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