OUR DRUG DEVELOPMENT PIPELINE
All of our compounds are designed to be first-in-class or best-in-class anticancer agents.

- Address unmet clinical needs
- Potent against validated or new cancer targets
- Excellent pharmaceutical characteristics, including:
- oral bioavailability
- blood-brain-barrier permeability
- Effective as single agent and as combination therapies
- Superior efficacy in comparison to current and late stage development drugs
- Highly specific for individual kinase targets
- Unique chemical entities, with strong patentability
AU07
Oral CDK9 inhibitor
Haematological malignancies, high-risk MDS, triple-negative breast cancer, colon cancer, lung cancer, prostate cancer, ovarian cancer and other MCL1 and MYC-dependent cancers
PHASE I: AML

AU3-14
Oral CDK4/6 inhibitor
Breast cancer, colorectal cancer, liver cancer, metastatic brain tumours, other ER+/Rb+ cancers
COMPLETED PRE-CLINICAL

AU2-94
Oral CDK4 inhibitor
Colorectal cancer, glioblastoma, ovarian cancer, haematological malignancies, other ER+/Rb+ cancers
LATE PRE-CLINICAL

AU2-85
Oral CDK8 inhibitor
Haematological malignancies and all STAT1/5 and Wnt/ß-catenin dependent cancers
LATE PRE-CLINICAL

AU14-5
Oral CDK2 inhibitor
Haematological malignancies, breast cancer, colorectal cancer, lung cancer, ovarian cancer, prostate cancer and other hormone dependent cancers
LATE PRE-CLINICAL

AU4-53
Oral CDK9/TRK inhibitor
All MCL1/MYC-dependent haematological malignancies, prostate cancer, ovarian cancer and TRK-positive cancers
LATE PRE-CLINICAL

AU5-5
Oral FLT3 inhibitor
FLT3-ITD+ and all TKD mutant haematological malignancies
LATE PRE-CLINICAL

AU07: A HIGHLY POTENT CDK9 INHIBITOR FOR TREATING HAEMATOLOGICAL AND SOLID TUMOURS
AU07 is one the most potent CDK9 inhibitors identified to date that demonstrates potent anti-tumour efficacy against multiple haematological and solid tumour types including AML, CLL, triple-negative breast cancer, colorectal cancer, lung cancer, prostate cancer, and ovarian cancer by oral administration. AU07 is currently under investigation in patients with AML.
AU2-94: A FIRST-IN-CLASS CDK4 INHIBITOR
We have developed a novel and highly potent inhibitor that exhibits an excellent selectivity for CDK4 over a large panel of protein kinases. Consistent with the CDK4-targeted mechanism this candidate inhibits the growth of Rb-positive cancer cells and demonstrates excellent in vivo anticancer efficacy by oral administration without showing any overt toxicity. Significantly, our CDK4 inhibitor is capable of access into the brain that is far readier than any of the FDA-approved CDK4/6 inhibitors, suggesting its therapeutic potential for treating glioblastoma and the tumours metastasised into the brain.
AU3-14: A HIGHLY POTENT AND SELECTIVE CDK4/6 INHIBITOR
CDK4/6 are fundamental for the initiation and progression of the majority of malignancies. As such, components of the CDK4/6 signalling pathway represent molecular targets for cancer therapy. CDK4/6 inhibitors have been FDA-approved for the treatment of ER+ breast cancer and are demonstrating their success in the market. However, current agents are not specific to CDK4 and CDK6 and also inhibit other kinases, resulting in undesirable toxicity.
We have purposely developed a novel and highly potent inhibitor that exhibits a high selectivity to CDK4 and CDK6 over 370 human kinases. AU3-14 inhibits the growth of Rb-positive cancer cells and demonstrates excellent in vivo anticancer efficacy by oral administration with superior safety profiles. Significantly, AU3-14 is capable of accessing the brain, being readier than the FDA-approved CDK4/6 inhibitors, suggesting therapeutic potential for treating a wide range of human cancers including these metastasised into the brain.
AU2-85: A HIGHLY POTENT AND SELECTIVE CDK8 INHIBITOR
CDK8 plays a vital role in regulating transcription either through its association with the Mediator complex or by phosphorylating transcription factors. We have developed a novel and highly selective CDK8 inhibitor. AU2-85 has demonstrated excellent anti-tumour efficacy against human xenograft models by oral administration, including AML and ovarian cancer, with excellent safety profiles. Significantly, AU2-85 activates natural killer (NK) cells by reducing CDK8-mediated phosphorylation of STAT1. AU2-85 represents a novel therapeutic strategy for stimulating the immune system to fight cancer.
AU14-5: A FIRST-IN-CLASS CDK2 INHIBITOR
CDK2 plays a pivotal role in cell cycle regulation and is known to be important in tumorigenesis. Inhibition of CDK2 has been shown to force MYC or RAS expressing cells into senescence. Thus, CDK2 is a potential target for treatment of tumours driven by MYC or RAS. Another important role for CDK2 is phosphorylation of the receptors of androgen, estrogen and progesterone, increasing their transcription. Estrogen and progesterone contribute to breast and ovarian cancer progression, and androgen receptor phosphorylation is strongly implicated in prostate cancer. This, combined with the fact that CDK2 overexpression is associated with recurrence and metastases, highlights CDK2 as a promising therapeutic target in hormone dependent cancers. Despite decades of development of CDK2 inhibitors, none have yet been approved for the clinic.
We have developed a highly potent inhibitor that exhibits an excellent selectivity for CDK2 over a panel of 360 human protein kinases. AU14-5 inhibits cancer cell proliferation and demonstrates excellent in vivo anticancer efficacy by oral administration without any overt toxicity. AU14-5 is being developed for treating a range of cancers.
AU4-53: A HIGHLY POTENT CDK9/TRK INHIBITOR
CDK9 is a key regulatory enzyme of RNA polymerase II (RNAPII) and as such, enables the excessive production of multiple oncogenes, such as MYC, HOXA9, MCL1, BCL-2 and XIAP. CDK9 inhibitors block the transcription of these oncogenes and induce cancer cell apoptosis.
AU4-53 is one of the most potent and selective CDK9 inhibitors identified to date and is highly cytotoxic against a panel of human cancer cell lines, including leukaemia and cancers of the breast, colon, lung, ovary and prostate. The drug candidate demonstrates anticancer efficacy in vivo xenograft models by oral administration. By simultaneously targeting CDK9 and TRK, AU4-53 has the advantage to treat a broad spectrum of cancers and address resistance associated with current TRK inhibitors.
AU5-5: A HIGHLY POTENT AND SELECTIVE FLT3 INHIBITOR FOR TREATING LEUKAEMIA
FMS-like tyrosine kinase 3 (FLT3) is expressed at high levels in a spectrum of hematologic malignancies including 70-100% of AML of all subtypes, ALL, and CML. Patients with FLT3 mutations have a very poor prognosis, experience higher rates of relapse and subsequent death.
We have developed a selective FLT3 inhibitor (over 360 human kinases) that is highly cytotoxic in human leukaemia (FLT3+) cells. AU5-5 is particularly effective against multiple mutations, including FLT3 (ITD), FLT3 (D835Y), FLT3 (F594_R595insR), FLT3 (F594_R595insREY), FLT3 (ITD)-NPOS, FLT3 (ITD)-W51, FLT3 (R595_E596insEY) and FLT3 (Y591V592insVDFREYEYD) with low picomolar potencies. Thus, it has an advantage of effectively blocking these mutations that have been clinically shown to confer resistance to the current chemotherapies and FLT3 inhibitor treatment.