London: Friday, 30 October 2015: Hutchison China MediTech Limited ("Chi‑Med") (AIM: HCM) today announces that Hutchison MediPharma Limited ("HMP"), its drug R&D subsidiary, will present further scientific data on sulfatinib (HMPL‑012), fruquintinib (HMPL‑013) and savolitinib (AZD6094, HMPL‑504) at the International Conference on Molecular Targets and Cancer Therapeutics, which will be held in Boston, Massachusetts, USA from 5 to 9 November 2015. Sulfatinib, fruquintinib and savolitinib were all discovered by HMP and are currently being evaluated in clinical trials for the treatment of various cancers.
Sulfatinib is an oral drug candidate that selectively inhibits the tyrosine kinase activity associated with the vascular endothelial growth factor receptor ("VEGFR") and fibroblast growth receptor ("FGFR"), a receptor for a protein which also plays a role in tumour growth. HMP will present clinical data from its Phase I trial in China, focusing on neuroendocrine tumour ("NET") patients. In this study, sulfatinib's objective response rate among the 18 efficacy-evaluable NET patients was 44.4% and disease control rate was 100%. By comparison, sunitinib and everolimus, the two approved single agent therapies for neuroendocrine tumours, achieve objective response rates of less than 10% in their pivotal clinical trials. Furthermore, neuroendocrine tumour responses to sulfatinib have been observed to improve gradually with time.
Savolitinib is an inhibitor of the c-Met receptor tyrosine kinase, an enzyme which has been shown to function abnormally in many types of solid tumours, and fruquintinib is a highly selective inhibitor of VEGFR1, 2 and 3. In clear cell renal cell carcinoma ("ccRCC"), c-Met activation has emerged as one of the mechanisms for resistance to anti-VEGF/VEGFR therapies, implying that inhibition of the c-Met and VEGFR pathways in a combination therapy could produce additional clinical benefit. HMP will present data from a preclinical study to assess the effect of savolitinib and fruquintinib combined in ccRCC xenograft models. In this study, while single-agent treatment at clinically relevant doses only exhibited mild to moderate tumour growth inhibition, a significantly increased anti-tumour effect was observed for the group receiving combination therapy.
Preclinical data will also be presented regarding savolitinib in non-small cell lung cancer ("NSCLC") and mechanisms of acquired savolitinib resistance.
The following posters will be made available at www.chi‑med.com/news/ after they are presented at the conference:
| 1st Presentation Title: | First-in-human phase I study of a selective VEGFR/FGFR dual inhibitor sulfatinib in patients with advanced solid tumours |
| Authors: | Jian-Ming Xu, et al. |
| Session: | Poster Session A – Angiogenesis and Antiangiogenesis Agents |
| Date & Time: | Friday 6 November 2015, 12:15 PM – 3:15 PM |
| 2nd Presentation Title: | Synergistic effect of c-Met inhibitor Savolitinib in combination with a VEGFR inhibitor Fruquintinib in clear cell renal cell carcinoma xenograft models |
| Authors: | Yongxin Ren, et al. |
| Session: | Poster Session B –Therapeutic Agents: Small Molecule Kinase Inhibitors |
| Date & Time: | Saturday 7 November 2015, 12:30 PM – 3:30 PM |
| 3rd Presentation Title: | Acquired resistance to the cMET inhibitor savolitinib in lung cancer models through EGFR/mTOR/MYC deregulation and adoption of PIM signalling |
| Authors: | Ryan Henry, et al. |
| Session: | Late-Breaking Poster Session – Drug Resistance and Modifiers |
| Date & Time: | Sunday 8 November 2015, 12:30 PM – 3:30 PM |
Hosted by the American Association for Cancer Research ("AACR"), the National Cancer Institute ("NCI"), and the European Organisation for Research and Treatment of Cancer ("EORTC"), the 2015 Molecular Targets and Cancer Therapeutics conference will bring together an estimated 3,000 academics, scientists, and pharmaceutical industry representatives from across the globe to discuss innovations in drug development, target selection, and the impact of new discoveries in molecular biology.