product name CGK 733
Description: CGK 733 is a potent and selective inhibitor of ATM and ATR with IC50 of ~200 nM. CGK733 significantly enhanced taxol-induced cytotoxicity in HBV-positive HepG2.2.15 cells. The mechanism lies in CGK733 triggers the formation of multinucleated cells thus promotes the premature mitotic exit of taxol-induced mitotic-damaged cells through multinucleation and mitotic catastrophe in HBV-positive HepG2.2.15 cells. These results suggest that CGK733 could potentially reverse the taxol resistance in HBV-positive HCC cells and may suggest a novel strategy to treat HBV-infected HCC patients.
References: Nat Chem Biol. 2006 Jul;2(7):369-74; Clin Cancer Res. 2008 Mar 15;14(6):1877-87.
555.84
Formula
C23H18Cl3FN4O3S
CAS No.
905973-89-9
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (179.9 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
CGK-733
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19395356
| In Vitro |
In vitro activity: CGK733 is able to confer robust growth to senescent cells that have ceased proliferation. Senescence-associated β-galactosidase (SA–β-gal) activity disappears in CGK733-treated cells. CGK733 shows greater potency in inhibiting ATM/ATR than LY294002 (IC50 , ~5 μM for ATM and ATR), a pan-inhibitor of PI3K and PIKKs. CGK733 (30 μM) treated for 24h causes ~60% cell death in senescent MCF-7 cells. CGK733 (20 μM) induces the loss of cyclin D1 via the ubiquitin- dependent proteasomal degradation pathway in MCF-7 and T47D breast cancer cell lines. CGK733 at concentrations ranging from 0.6- 40 μM, inhibits proliferation of MCF-7 and T47D estrogen receptor (ER) positive breast cancer cells, MDA-MB436 ER negative breast cancer cells, LnCap pros-tate cancer cells and HCT116 colon cancer cells. Furthermore, CGK733 also suppresses proliferation of non- transformed mouse BALB/c 3T3 embryonic fibroblast cells. The CGK733-mediated inhibition of proliferation is dose dependent and significant at doses as low as 2.5 μM. Kinase Assay: Cell Assay: Cells are seeded in 96-well plates at a predetermined, optimal cell density to ensure exponential growth for duration of the assay. After a 24 h preincubation, growth medium is replaced with experimental medium containing the appropriate drug concentrations or 0.1% (v/v) vehicle control. After a 48 h incubation, cell proliferation is estimated using the sulforhodamine B colorimetric assay. |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | Nat Chem Biol. 2006 Jul;2(7):369-74; Clin Cancer Res. 2008 Mar 15;14(6):1877-87. |
Related Posts
product name CGK 733
Description: CGK 733 is a potent and selective inhibitor of ATM and ATR with IC50 of ~200 nM. CGK733 significantly enhanced taxol-induced cytotoxicity in HBV-positive HepG2.2.15 cells. The mechanism lies in CGK733 triggers the formation of multinucleated cells thus promotes the premature mitotic exit of taxol-induced mitotic-damaged cells through multinucleation and mitotic catastrophe in HBV-positive HepG2.2.15 cells. These results suggest that CGK733 could potentially reverse the taxol resistance in HBV-positive HCC cells and may suggest a novel strategy to treat HBV-infected HCC patients.
References: Nat Chem Biol. 2006 Jul;2(7):369-74; Clin Cancer Res. 2008 Mar 15;14(6):1877-87.
555.84
Formula
C23H18Cl3FN4O3S
CAS No.
905973-89-9
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (179.9 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
CGK-733
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19395356
| In Vitro |
In vitro activity: CGK733 is able to confer robust growth to senescent cells that have ceased proliferation. Senescence-associated β-galactosidase (SA–β-gal) activity disappears in CGK733-treated cells. CGK733 shows greater potency in inhibiting ATM/ATR than LY294002 (IC50 , ~5 μM for ATM and ATR), a pan-inhibitor of PI3K and PIKKs. CGK733 (30 μM) treated for 24h causes ~60% cell death in senescent MCF-7 cells. CGK733 (20 μM) induces the loss of cyclin D1 via the ubiquitin- dependent proteasomal degradation pathway in MCF-7 and T47D breast cancer cell lines. CGK733 at concentrations ranging from 0.6- 40 μM, inhibits proliferation of MCF-7 and T47D estrogen receptor (ER) positive breast cancer cells, MDA-MB436 ER negative breast cancer cells, LnCap pros-tate cancer cells and HCT116 colon cancer cells. Furthermore, CGK733 also suppresses proliferation of non- transformed mouse BALB/c 3T3 embryonic fibroblast cells. The CGK733-mediated inhibition of proliferation is dose dependent and significant at doses as low as 2.5 μM. Kinase Assay: Cell Assay: Cells are seeded in 96-well plates at a predetermined, optimal cell density to ensure exponential growth for duration of the assay. After a 24 h preincubation, growth medium is replaced with experimental medium containing the appropriate drug concentrations or 0.1% (v/v) vehicle control. After a 48 h incubation, cell proliferation is estimated using the sulforhodamine B colorimetric assay. |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | Nat Chem Biol. 2006 Jul;2(7):369-74; Clin Cancer Res. 2008 Mar 15;14(6):1877-87. |