| Stereochemistry | ACHIRAL |
| Molecular Formula | C15H12F2N6O3S |
| Molecular Weight | 394.356 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
NC1=NC(NC2=CC=C(C=C2)S(N)(=O)=O)=NN1C(=O)C3=C(F)C=CC=C3F
InChI
InChIKey=KDKUVYLMPJIGKA-UHFFFAOYSA-N
InChI=1S/C15H12F2N6O3S/c16-10-2-1-3-11(17)12(10)13(24)23-14(18)21-15(22-23)20-8-4-6-9(7-5-8)27(19,25)26/h1-7H,(H2,19,25,26)(H3,18,20,21,22)
| Molecular Formula | C15H12F2N6O3S |
| Molecular Weight | 394.356 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
JNJ-7706621, developed by Johnson & Johnson Pharmaceutical, is pan-CDK inhibitor with the highest potency on cyclin-dependent kinases: CDK1/2. Inhibition of CDK1 kinase activity, altered CDK1 phosphorylation status, and interference with downstream substrates such as retinoblastoma was also shown in human tumor cells following drug treatment. It also potently inhibits Aurora A/B and has no activity on Plk1 and Wee1. In human cancer cells, treatment with JNJ-7706621 inhibited cell growth independent of p53, retinoblastoma, or P-glycoprotein status; activated apoptosis; and reduced colony formation. At low concentrations, JNJ-7706621 slowed the growth of cells and at higher concentrations induced cytotoxicity. JNJ-7706621 is a unique inhibitor regulating cell cycle progression at multiple points, suggesting that it could be useful for cell cycle analysis and therapy of various cancers, including Ewing's sarcoma.
Approval Year
Sample Use Guides
JNJ-7706621 shows inhibitory effect on a panel of human cancer cell types, including HeLa, HCT-116, SK-OV-3, PC3, DU145, MES-SA, and MES-SA/Dx5, with IC50 of 112-514 nM. JNJ-7706621 is several-fold less potent at inhibiting growth of normal cell types, including MRC-5, HASMC, HUVEC, and HMVEC, with IC50 of 3.67-5.42 μM. In HeLa or U937 cells, JNJ-7706621 (0.5-3 μM) delays exit from G1, arrests cells in G2-M, induces endoreduplication, activates apoptosis, and reduces colony formation.
