Cyclin-dependent kinases (CDKs) regulate the cell cycle, apoptosis, neuronal functions, transcription, and exocytosis. The observation of CDK deregulations in a variety of pathological situations shows that CDK inhibitors could have a therapeutic value. In the following paragraphs, we set of the identification of 6-phenyl[5H]pyrrolo[2,3-b]pyrazines (aloisines) like a novel potent CDK inhibitory scaffold. A selectivity study performed on 26 kinases implies that aloisine A is extremely selective for CDK1/cyclin B, CDK2/cyclin A-E, CDK5/p25, and GSK-3 alpha/beta the 2 latter enzymes happen to be implicated in Alzheimer’s. Kinetic studies, along with the resolution of the CDK2-aloisine cocrystal structure, show aloisines act by competitive inhibition of ATP binding towards the catalytic subunit from the kinase. As observed with all of inhibitors reported to date, aloisine interacts using the ATP-binding pocket through two hydrogen bonds with backbone nitrogen and oxygen atoms of Leu 83. Aloisine inhibits cell proliferation by arresting cells both in G1 and G2.BMS-265246