| 包装 | 价格(元) |
| 250mg | 电议 |
| 500mg | 电议 |
Cell lines | HCT 116 wild-type (WT) colon cancer cells, HCT 116 p53–/– colon carcinoma cells, LS-180 colon cancer cells |
Preparation Method | HCT 116 WT and p53–/– cells were cultured in McCoy's medium supplemented with 10% Newborn Calf Serum, 2 mM glutamine, penicillin (10 U/ml) and streptomycin (10 μg/ml). LS-180 colon cancer cells were cultured in DMEM Medium supplemented with 10% Newborn Calf Serum, 2 mM glutamine, penicillin (10 U/mL) and streptomycin (10 μg/mL). |
Reaction Conditions | 1×106were incubated in 6 well plates in McCoy's 5A medium 1 day before treatment and then treated with 50 μg/mL Cl-amidine. The cells were harvested and fixed with ice cold ethanol. After washing with 1x PBS containing 0.5% BSA twice, the cells were incubated with DNA staining solution consisting of Propidium Iodide (PI; 10 μg/mL) and RNase (0.1 mg/mL) for 30 min at room temperature in the dark. |
Applications | Cl-amidine could lead to a cell cycle arrest at the G1 phase through a p53-mediated mechanism. Cl-amidine could cause miRNA-16 induction in a p53-dependent manner. |
Animal models | Male C57BL/6J mice (18–26 g) |
Preparation Method | Mice were injected with intra-peritoneal Cl-amidine dissolved in DMSO, or vehicle DMSO 1 h after cecal ligation and puncture (CLP). DMSO was also injected into mice that were not subjected to CLP (n = 12/group). Mortality was monitored for 10 days after surgeries. |
Dosage form | 40 mg/kg |
Applications | Cl-amidine protects mice from sepsis-induced lethality. The inhibition of PAD by Cl-amidine significantly suppresses the CitH3 production, while the CitH3 neutralization markedly improves the survival in septic mice. |
| 产品描述 | Cl-amidine (N-α-benzoyl-N5-(2-chloro-1-iminoethyl)-l-ornithine amide), is a PAD4 inactivator with enhanced potency. PAD Inhibitor was proved to exhibit enhanced cell killing in PAD-expressing osteosarcoma cells and block the formation of neutrophil extracellular traps. Cl-amidine, as a PAD inhibitor, could reduce the clinical signs and symptoms of colitis, and induced apoptosis of inflammatory cells. The inhibition of PAD by Cl-amidine markedly suppresses the production of CitH3, and neutralization of CitH3 improves survival markedly in septic mice.[1][2] Cl-amidine is a more potent inhibitor of PAD which has the IC50 of 5.9 ± 0.3 μM. In vitro experiment indicated that Cl-amidine caused a cell cycle arrest at the G1 phase and miRNA-16 induction through a p53-mediated mechanism. In vivo experiment demonstrated that the enhancement of the p300GBD–GRIP1 interaction mediated by PAD4 was antagonized by Cl-amidine in a dose-dependent manner, and that Cl-amidine treatment caused only a minimal reduction in the efficiency of the interaction, indicating that the inhibitory effect of this compound targeted at the active PAD4 enzyme.[1][3] References: |
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