What is a PIM inhibitor?
Pan-PIM kinase inhibitor AZD1208 inhibits the activities of PIM1, PIM2 and PIM3 serine/threonine kinases, which may result in the interruption of the G1/S phase cell cycle transition, thereby causing cell cycle arrest and inducing apoptosis in cells that overexpress PIMs.
What is Pim in biology?
Pim-1 is a proto-oncogene which encodes for the serine/threonine kinase of the same name. The pim-1 oncogene was first described in relation to murine T-cell lymphomas, as it was the locus most frequently activated by the Moloney murine leukemia virus.
What is Pan kinase?
An orally bioavailable pan-HER tyrosine kinase inhibitor with potential antineoplastic activity. BMS-599626 inhibits human epidermal growth factor receptors (HER) HER1, HER2 and HER4, thereby inhibiting the proliferation of tumor cells that overexpress these receptors. Code name: AC480.
What are PIM kinase inhibitors?
PIM kinase inhibitors: Structural and pharmacological perspectives The PIM kinase, also known as serine/threonine kinase plays an important role in cancer biology and is found in three different isoforms namely PIM-1, PIM-2, and PIM-3.
What is the function of Pim-1 protein kinase?
The Pim-1 protein kinase is an important regulator of MET receptor tyrosine kinase levels and signaling MET, the receptor for hepatocyte growth factor (HGF), plays an important role in signaling normal and tumor cell migration and invasion.
Are there any inhibitors of PIM1?
Inhibitors. A large number of small molecule inhibitors of PIM1 have been developed. Clinical trial results so far have showed promising anti-cancer activity, but side effects due to insufficient selectivity have proved problematic and research continues to find more potent and selective inhibitors for this target.
Do PIM1 kinase inhibitors induce radiosensitization in non-small cell lung cancer?
Kim W, et al. PIM1 kinase inhibitors induce radiosensitization in non-small cell lung cancer cells. Pharm. Res. 2013;70:90–101. doi: 10.1016/j.phrs.2013.01.005. [ PubMed] [ CrossRef] [ Google Scholar] 11.