Human epidermal growth factor receptor bispecific ligand trap RB200: abrogation of collagen-induced arthritis in combination with tumour necrosis factor blockade |
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| Authors: | Luke L Gompels Nasser M Malik Leigh Madden Pei Jin Marc Feldmann H Michael Shepard Ewa M Paleolog |
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| Institution: | (1) Faculty of Medicine, Kennedy Institute of Rheumatology, Imperial College London, 65 Aspenlea Road, London, W6 8LH London, UK;(2) William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Charterhouse Square, London, EC1M 6BQ, UK;(3) Kennedy Institute of Rheumatology, University of Oxford, 65 Aspenlea Road, London, W6 8LH, UK;(4) Receptor BioLogix Inc, 3350 West Bayshore Road, Suite 150, Palo Alto, CA 94303, USA;(5) Novartis Institutes for Biomedical Research, 350 Massachusetts Avenue #1, Cambridge, MA 02139, USA;(6) Halozyme Therapeutics Inc, 11588 Sorrento Valley Road, Suite 17, San Diego, CA 92121, USA |
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| Abstract: | Introduction Rheumatoid arthritis (RA) is a chronic disease associated with inflammation and destruction of bone and cartilage. Although
inhibition of TNFα is widely used to treat RA, a significant number of patients do not respond to TNFα blockade, and therefore
there is a compelling need to continue to identify alternative therapeutic strategies for treating chronic inflammatory diseases
such as RA. The anti-epidermal growth factor (anti-EGF) receptor antibody trastuzumab has revolutionised the treatment of
patients with EGF receptor-positive breast cancer. Expression of EGF ligands and receptors (known as HER) has also been documented
in RA. The highly unique compound RB200 is a bispecific ligand trap that is composed of full-length extracellular domains
of HER1 and HER3 EGF receptors. Because of its pan-HER specificity, RB200 inhibits responses mediated by HER1, HER2 and HER3
in vitro and in vivo. The objective of this study was to assess the effect of RB200 combined with TNF blockade in a murine collagen-induced arthritis
(CIA) model of RA. |
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