Pipeline
ART0380 – (ATR Inhibitor)
Our orally dosed ataxia telangiectasia and Rad3-related protein (ATR) inhibitor, ART0380, has the potential to induce DNA damage in sensitive cancer tissue while preserving DNA integrity in healthy tissue. ART0380 is being developed as an oral anticancer agent as both a monotherapy and in combination with established as well as novel agents that cause DNA damage or suppress a cancer cell’s ability to repair DNA damage.
ART4215 – POL THETA (POLΘ inhibitor)
Our Polθ inhibitor offers the unprecedented potential to harness the power of DDR inhibition to specifically target tumor cells while sparing normal tissue from toxicity. It may allow for effective and widespread use across multiple tumor types including PARP inhibitor resistant cancers, as a combination treatment with other DDR inhibitors, or in combination with DNA damaging agents.
RLT SENSITIZERS
In March 2021, Artios entered into a research collaboration and license agreement with Novartis; a global healthcare company based in Switzerland (https://www.novartis.co.uk/) to identify DNA Damage Response (DDR) targets and the agents capable of modulating these targets, for use with Novartis’s proprietary radioligand therapies or as a monotherapy.
DRUG DISCOVERY PLATFORM
(ALT) ALTERNATIVE LENGTHENING OF TELOMERES
The development of our DDR platform has given us the ability to identify novel DDR targets in relevant disease setting where there is unmet medical need.
IMMUNO- ONCOLOGY COMBINATIONS
Medicines that enable the immune system to target and kill cancer cells (immunotherapy) are therapeutics that have proven to be a highly effective means of treating a select group of cancers.
NUCLEASES – MERCK KGaA
In December 2020, Artios entered into a research collaboration and license agreement with Merck KGaA , Pharmaceutical company in Darmstadt, Germany, a leading team of specialists in Healthcare and Life Sciences (https://www.merckgroup.com/en/company.html) for the identification of novel DDR nuclease inhibitors in the oncology field.