For research use only. Not for therapeutic Use.
CVT-313（Cat No.:I002535） is a highly potent inhibitor of cyclin-dependent kinase 2 (CDK2), displaying an IC50 value of 0.5 μM in vitro studies. It specifically targets CDK2 and does not significantly affect other unrelated ATP-dependent serine/threonine kinases. CDK2 is a critical regulator of the cell cycle and plays a crucial role in cell proliferation. By inhibiting CDK2, CVT-313 has the potential to interfere with cell cycle progression and proliferation, making it a valuable tool in studying CDK2-dependent cellular processes and a potential therapeutic candidate for diseases associated with dysregulated cell cycle control.
| Catalog Number | I002535 |
| CAS Number | 199986-75-9 |
| Synonyms | 2-[2-hydroxyethyl-[6-[(4-methoxyphenyl)methylamino]-9-propan-2-ylpurin-2-yl]amino]ethanol |
| Molecular Formula | C₂₀H₂₈N₆O₃ |
| Purity | ≥95% |
| Target | Cyclin-Dependent Kinases |
| Solubility | DMSO 10 mg /ml |
| Storage | Store at -20°C |
| IC50 | 0.5 uM(Cdk2/A and Cdk2/E); 4.2 uM(Cdk1/B); 215 uM(Cdk4/D1) |
| IUPAC Name | 2-[2-hydroxyethyl-[6-[(4-methoxyphenyl)methylamino]-9-propan-2-ylpurin-2-yl]amino]ethanol |
| InChI | InChI=1S/C20H28N6O3/c1-14(2)26-13-22-17-18(21-12-15-4-6-16(29-3)7-5-15)23-20(24-19(17)26)25(8-10-27)9-11-28/h4-7,13-14,27-28H,8-12H2,1-3H3,(H,21,23,24) |
| InChIKey | NQVIIUBWMBHLOZ-UHFFFAOYSA-N |
| SMILES | CC(C)N1C=NC2=C(N=C(N=C21)N(CCO)CCO)NCC3=CC=C(C=C3)OC |
| Reference | 1:J Biol Chem. 1997 Nov 14;272(46):29207-11. CVT-313, a specific and potent inhibitor of CDK2 that prevents neointimal proliferation.Brooks EE,Gray NS,Joly A,Kerwar SS,Lum R,Mackman RL,Norman TC,Rosete J,Rowe M,Schow SR,Schultz PG,Wang X,Wick MM,Shiffman D, PMID: 9360999 </br><span>Abstract:</span> The activity of cyclin-dependent kinase 2 (CDK2) is essential for progression of cells from G1 to the S phase of the mammalian cell cycle. CVT-313 is a potent CDK2 inhibitor, which was identified from a purine analog library with an IC50 of 0.5 microM in vitro. Inhibition was competitive with respect to ATP (Ki = 95 nM), and selective CVT-313 had no effect on other, nonrelated ATP-dependent serine/threonine kinases. When added to CDK1 or CDK4, a 8.5- and 430-fold higher concentration of CVT-313 was required for half-maximal inhibition of the enzyme activity. In cells exposed to CVT-313, hyperphosphorylation of the retinoblastoma gene product was inhibited, and progression through the cell cycle was arrested at the G1/S boundary. The growth of mouse, rat, and human cells in culture was also inhibited by CVT-313 with the IC50 for growth arrest ranging from 1.25 to 20 microM. To evaluate the effects of CVT-313 in vivo, we tested this agent in a rat carotid artery model of restenosis. A brief intraluminal exposure of CVT-313 to a denuded rat carotid artery resulted in more than 80% inhibition of neointima formation. These observations suggest that CVT-313 is a promising candidate for evaluation in other disease models related to aberrant cell proliferation. |
