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YM BioSciences Announces Preclinical Data Confirming Nimotuzumab,Binds to the EGF Receptor and Potentiates Radiotherapy

MISSISSAUGA, ON, July 09, 2007 /PRNewswire-FirstCall/ - YM BioSciences Inc. , an oncology company that identifies, develops and commercializes differentiated products for patients worldwide, today announced that a study presented by investigators from Kinki University School of Medicine and Kyoto University at the 11th meeting of The Japanese Association for Molecular Target Therapy of Cancer held on July 5-6, 2007 demonstrated the increased radiosensitivity of human NSCLC cell lines in the presence of nimotuzumab both in vitro and in vivo. The study also confirms previous observations that nimotuzumab inhibits ligand-dependent EGF receptor downstream signaling. Daiichi Sankyo Co., Ltd is the licensee for nimotuzumab in Japan.

In addition, YM BioSciences announced that a paper on the structure of nimotuzumab entitled 'Modeling the interaction between the anti-tumor antibody h-R3 and its target, the epidermal growth factor receptor' was presented at the 11th annual meeting of the SBNet (Structural Biology Network), held on June 15-18, 2007 in Tallberg, Sweden. The paper demonstrated that nimotuzumab specifically competes with cetuximab for binding to the EGF receptor. The authors noted that, "According to our models, nimotuzumab inhibits the EGFr signaling both by inhibiting the binding of EGF to domain III of EGFr and by a conformational change of EGFr that is necessary to shape the EGF binding site."

"These two studies provide independent confirmation of earlier research indicating that nimotuzumab directly binds to the EGF receptor," said Dr. Igor Sherman, Director of Clinical Research at YM BioSciences. "The very rare incidence, in patients treated with nimotuzumab, of the commonly seen side-effects of EGFr-targeting therapy, such as rash and diarrhea, has raised questions about whether nimotuzumab is truly interacting with the EGF receptor. The data presented at SBNet provides further evidence
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