alvocidib

Flavopiridol (Alvocidib) (Alvocidib) competes with ATP to inhibit CDKs including CDK1, CDK2, CDK4 and CDK6 with IC50 of ~ 40 nM. It is 7.5-fold more selective for CDK1, 2, 4, 6 versus CDK7. Flavopiridol is initially found to inhibit EGFR and PKA. Phase 1/2.

Flavopiridol hydrochloride (MDL 107826A) is a synthetic N-methylpiperidinyl chlorophenyl flavone compound. As an inhibitor of cyclin-dependent kinase, alvocidib induces cell cycle arrest by preventing phosphorylation of cyclin-dependent kinases (CDKs) and by down-regulating cyclin D1 and D3 expression, resulting in G1 cell cycle arrest and apoptosis. This agent is also a competitive inhibitor of adenosine triphosphate activity.

Zotiraciclib (also known as TG02 and SB1317) is an innovative small-molecule compound with potent inhibitory effects on CDK, JAK2, and FLT3. By inhibiting cyclin-dependent kinase 9 (CDK9) and depleting Myc, it serves as a treatment for cancers that can penetrate the blood-brain barrier. Zotiraciclib is one of the numerous CDK inhibitors under investigation; other compounds targeting CDK9, utilized for treating acute myeloid leukemia, include alvocidib and atuveciclib. Myc overexpression is a known factor in many cancers, with 80% of glioblastomas exhibiting this characteristic.

TP-1287 is an oral phosphate prodrug of the CDK9 inhibitor, alvocidib.

Zotiraciclib, also known as TG02 and SB1317, is a novel small molecule potent CDK/JAK2/FLT3 inhibitor. Zotiraciclib may be useful for the treatment of cancer that crosses the blood brain barrier and acts by depleting Myc through the inhibition of cyclin-dependent kinase 9 (CDK9). It is one of a number of CDK inhibitors under investigation; others targeting CDK9 for the treatment of acute myeloid leukemia include alvocidib and atuveciclib. Myc overexpression is a known factor in many cancers, with 80 percent of glioblastomas characterized by this property.