Seliciclib
An orally available small molecule and cyclin-dependent kinase (CDK) inhibitor with potential apoptotic and antineoplastic activity. CDKs, serine/threonine kinases that play an important role in cell cycle regulation, are overexpressed in various malignancies. Seliciclib primarily inhibits CDK 2, 7, and 9 by competing for the ATP binding sites on these kinases, leading to a disruption of cell cycle progression. In addition, this agent seems to interfere with CDK-mediated phosphorylation of the carboxy-terminal domain of RNA polymerase II, thereby inhibiting RNA polymerase II-dependent transcription. This may lead to the down-regulation of anti-apoptotic factors, such as myeloid cell leukemia sequence 1 (Mcl-1), a protein crucial for the survival of a range of tumor cell types. The down-regulation of anti-apoptotic factors may lead to an induction of apoptosis, thereby further contributing to seliciclib's antiproliferative effects. [ ]
Term info
Seliciclib
- CYC202
- R-roscovitine
- SELICICLIB
- Seliciclib
NCIT_C116978, NCIT_C63923, NCIT_C128784, NCIT_C116977, NCIT_C157711, NCIT_C157712
186692-46-6
C19H26N6O
CTRP, FDA
Seliciclib
0ES1C2KQ94
http://purl.obolibrary.org/obo/NCIT_C17767
Seliciclib
511023
511023
Seliciclib
Pharmacologic Substance, Organic Chemical
C1436187
C62783
Term relations
- Antineoplastic Enzyme Inhibitor
- Cyclin-Dependent Kinase Inhibitor
- Chemical_Or_Drug_Has_Physiologic_Effect some Gene Regulation Process
- Chemical_Or_Drug_Has_Mechanism_Of_Action some Enzyme Inhibition
- Chemical_Or_Drug_Has_Physiologic_Effect some Positive Regulation of Apoptosis
- Chemical_Or_Drug_Has_Physiologic_Effect some Protein Phosphorylation Inhibition
- Chemical_Or_Drug_Has_Physiologic_Effect some Negative Regulation of G1 Phase
- Chemical_Or_Drug_Affects_Gene_Product some Cyclin-Dependent Kinase
- Chemical_Or_Drug_Has_Physiologic_Effect some Negative Regulation of G2 to M Transition