ETH-155008：Novel PIM3 and CDK4/6 Dual Inhibitor
- Simultaneous inhibition of Pim1/3 and CDK4/6 pathways can act synergistically to arrest tumor cells in G1 phase and induces apoptosis.
- Dual inhibition within the same modality could avoid DDI and increased toxicity caused by the combination of two single drugs and attenuates the drug resistance of CDK4/6 inhibitors
- ETH-155008 also showed potent inhibition of FLT3
Emerging Data suggesting PIM3 as an excellent Co-targeting Target for Endodermal Solid Tumors
- Pim-3 kinase is aberrantly expressed in malignant lesions, but not normal tissues,particularly those of endoderm-derived organs, including the liver, pancreas, colon, and stomach
- A defificiency of the Pim-3 gene does not result in apparent changes in phenotype, suggesting that Pim-3 may be physiologically dispensable. Pim kinases are not localized downstream of the insulin receptor signaling pathway and therefore inhibition of the Pim kinases has few effects on normal metabolism
- Inhibit Pim-3, with chemotherapeutic agents, can aid in decreasing chemoresistance in pancreatic cancer. Treatment of solid tumors having aberrant expression of Pim-3, with Pim-3 inhibitors either as single agents or in combination with traditional chemotherapy may help provide a safe and novel drug regimen
Pim-3 Kinases Expressed in many Solid Tumors
