| Stereochemistry | ABSOLUTE |
| Molecular Formula | C18H18FN5O2S |
| Molecular Weight | 387.431 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 1 / 1 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
COC1=CC(F)=CC=C1C2=NC=NC(NC3=CC=CC(C[S@](C)(=N)=O)=C3)=N2
InChI
InChIKey=ACWKGTGIJRCOOM-HHHXNRCGSA-N
InChI=1S/C18H18FN5O2S/c1-26-16-9-13(19)6-7-15(16)17-21-11-22-18(24-17)23-14-5-3-4-12(8-14)10-27(2,20)25/h3-9,11,20H,10H2,1-2H3,(H,21,22,23,24)/t27-/m1/s1
Atuveciclib (previously known as BAY 1143572) was developed as a highly selective inhibitor of positive transcription elongation factor b (PTEFb) /CDK9 for the treatment of cancer. PTEFb is a heterodimer of CDK9 and one of four cyclin partners, cyclin T1, cyclin K, cyclin T2a or cyclin T2b. Atuveciclib also inhibits RNA polymerase II (Ser2) phosphorylation and downregulate MYC protein expression in hematologic malignancies. The drug participated in phase I clinical trials in subjects with advanced acute leukemia and for patients with advanced malignancies. Information about further studies for these types of cancer is not available. Recently published article has shown that atuveciclib enhanced the antineoplastic effects of cisplatin and promoted inhibitory effects on breast cancer stem-like cells grown as mammospheres. In addition, was suggested that CDK9 could be a potential therapeutic target in aggressive forms of CDK9-high triple-negative breast cancer (TNBC).
Originator
Approval Year
Targets
| Primary Target | Pharmacology | Condition | Potency |
|---|---|---|---|
| 13.0 nM [IC50] |
PubMed
ACTIVE MOIETY
