Translating cancer biology research into novel oncology treatments

Drug Discovery Pipeline

For futher information on the specific target programs, click on the Pipeline bar.

Hit Discovery
Lead Generation
Lead Optimisation
Commercialisation
 

Tumour Microenvironment

Focal Adhesion Kinase
BrCa, Cancer Stem Cells, Solid Tumours

FAK inhibitors have potential utility in various cancer types to reduce cancer stem cell burden, primary tumour growth and reduction of metastatic disease (alone and in combination with current anti-cancer therapeutic regimens) including cancers of high unmet need known to be enriched for cancer stem cells or merlin-negative cancers. Our partner, CRT-UK, is offering prospective commercial partners global therapeutic rights to the FAK-selective and/or FAK-FLT3-VEGFR3 programmes on an exclusive basis. Download the PDF of Novel oral FAK-selective and FAK-FLT3-VEGFR3 triple kinase inhibitors

FAK/VEGFR3/FLT3
Leukemic Stem Cells, AML, mMelanoma

Triple kinase inhibitor, targeting focal adhesion kinase (FAK), vascular endothelial growth factor receptor 3 (VEGFR3) and FMS-like Tyrosine kinase-3 (FLT3), has potential utility in various cancer types to reduce cancer stem cell burden, primary tumour growth and reduction of metastatic disease (alone and in combination with current anti-cancer therapeutic regimens) including cancers of high unmet need known to be enriched for cancer stem cells or merlin-negative cancers. FAK-FLT3-VEGFR3 inhibitors also have potential utility in FLT3-driven and FAK-positive or FAK splice-variant-positive AML. Our partner, CRT-UK, is offering prospective commercial partners global therapeutic rights to the FAK-FLT3-VEGFR3 programme on an exclusive basis. Download the PDF of Novel oral FAK-selective and FAK-FLT3-VEGFR3 triple kinase inhibitors

VEGFR3
Melanoma, Solid Tumours

Inhibition of vascular endothelial growth factor receptor-3 (VEGFR3) promises to prevent peritumoural lymphangiogenesis, lymph node metastasis and, possibly, proliferation of lymphatic vessels

Undisclosed Target
 

Information about this program is confidential at this time


Hit Discovery
Lead Generation
Lead Optimisation
Commercialisation
 

Tumour Growth–oncogenes, suppressors, epigenetic targets

PRMT5
Haemoglobinopathies, Solid Tumours

PRMT5 is an epigenetic target with cancer and non-cancer clinical potential (e.g. melanoma, mantle cell lymphoma, breast, β-thalassemia, sickle cell disease).  CTx has identified two novel series of PRMT5 small molecule inhibitors with excellent development potential. Biochemical, in vitro and in vivo models are in place and there is an established collaboration with a world leading PRMT5 research group. CTx and our UK partner CRT-UK are seeking a commercial partner for collaborative research for the further development of these novel PRMT5 inhibitors. Download the PDF of Inhibitors of Protein Arginine Methyltransferase 5 (PRMT5)

MOZ
AML

Inhibition of the epigenetic regulator, Monocytic leukaemia zinc finger (MOZ) will be of therapeutic benefit in AML

SIAH
BrCa

Inhibition of seven in absentia homolog (SIAH), a pro-tumourigenic E3 ubiquitin ligase, interferes with several critical aspects of cancer progression. Download summary. Download EACR-22 poster.

E6AP
HPV, Others

Inhibition will stop the E3 ubiquitin ligase E6AP targeting tumour suppressors for destruction. Download summary. Download EACR-22 poster.

USP7
 

Inhibition of the deubiquitination enzyme, USP7, would lead to an increase in the tumour suppressor protein, p53


Note: summary for VEGFR3 currently unavailable

 

 
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