CRT to license CTx’s FAK inhibitor programmes bringing treatment hope for triple-negative breast cancer
Tuesday 14 August 2012
Cancer Research Technology Press Release
Cancer Research Technology, (CRT), the commercial arm of Cancer Research UK, is entering into two licences with Cancer Therapeutics CRC (CTx), an Australian cancer drug and development company, to commercialise CTx’s pre-clinical focal adhesion kinase (FAK) inhibitor programmes.
CRT, as global commercial partner of CTx, has exercised its options to take forward these two programmes, which were developed by CTx, to in vivo proof-of-concept stage in mice.
The FAK inhibitor portfolio includes CTx-0294945, a highly-selective small molecule inhibitor, and CTx-0294886, a potent small molecule inhibitor of three proteins: FAK; vascular growth factor receptor 3 (VEGFR3); and FMS-like tyrosine kinase 3 (FLT3).
FAK is a non-receptor tyrosine kinase involved in controlling the growth, development and spread of different solid tumours. These include triple-negative breast cancer and merlin-negative mesothelioma, diseases which have urgent need for new treatments – and for which these molecules have potential use.
Both CTx-0294945 and CTx-0294886 separately boost the effectiveness and response length of anti-angiogenic antibody cancer drug Avastin to treat triple-negative breast cancer in mice.
FAK also has an important role in controlling cancer stem cell survival, suggesting these molecules may also be able to destroy cancer stem cells.
CTx-0294886 could also be used for the treatment other cancers, including a subset of acute myeloid leukaemia (AML) patients with mutations in FLT3. FLT3 is a receptor tyrosine kinase involved in controlling the growth and development of several blood cancers, including AML.
CRT is seeking to exclusively license these two programmes.
Dr Phil L’Huillier, CRT’s director of business management, said: “This important partnership combines CRT’s unique global commercialisation expertise in cancer with CTx’s translational expertise, to further develop these exciting programmes of potent, highly-selective and triple kinase small molecule inhibitors. These molecules have already shown promise in preclinical research to treat triple-negative breast cancer – for which there is no standard chemotherapy treatment.
“We hope that commercialisation of this project will pave the way for entry into early clinical trials – leading to new adjuvant treatment options for this disease and other cancers.”
Dr Warwick Tong, CTx’s CEO, said: “We are excited that our two lead programmes have reached the stage of being actively commercialised for further development with the potential to bring significant benefits to cancer patients. That these two drug candidates could contribute in the battle to reduce tumour recurrence and spread through activity on cancer stem cells is an added bonus.
“This success recognises the benefits of a highly-focused collaborative research effort led by CTx under the Australian Government CRC program. The level of expertise and the capabilities available within our group of research partners is of the highest level; these two programmes and the depth of our pipeline reflects the strength of the partnership.
“We will continue with our work translating great Australian cancer biology into new drugs for cancer patients and look forward to working with CRT to advance our programmes down the development path.”
For media enquiries please contact the CRT press office on 020 3469 8300 or, out-of-hours, the duty press officer on 07050 264 059.
Notes to editors
CRT has options to commercialise certain therapeutic projects from CTx.
Research presented on April 3 2012 at the AACR: Combination of CTX-0294945 a highly selective inhibitor of focal adhesion kinase with bevacizumab in pre-clinical models of breast cancer.
Research presented on July 8 2012 at the EACR: Inhibition of focal adhesion kinase in combination with Bevacizumab reduces the rate of tumour revascularisation and increases survival in a pre-clinical model of basal breast cancer.
The prognosis for AML patients that have activating FLT3 mutations is significantly worse than that for patients with forms of FLT3 that have not been mutated (wild type FLT3). While FLT3 inhibitors have shown promising activity in AML patients, there is also evidence of patients with AML becoming resistant to FLT3 inhibitors after developing additional mutations. CTx-0294886 has been shown to block wild type FLT3 and key FLT3 mutations in the laboratory.
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