CNDAC 是可口服试剂 Sapacitabine (HY-16445) 的代谢物，为核苷酸类似物。CNDAC 诱导DNA损伤和凋亡 (apoptosis)。
| 生物活性 | CNDAC is a metabolite of the orally active agentSapacitabine(HY-16445), and a nucleoside analog. CNDAC inducesDNA damageandapoptosis[1][2]. |
体外研究
(In Vitro) | CNDAC 有一个独特的作用机制: 进入 DNA 后，它诱导单链断裂 (SSBs)，当细胞经历第二个 S 期时，单链断裂 (SSBs) 转化为双链断裂 (DSBs)[1]。
缺乏 Rad51D 和 XRCC3 可使细胞对 CNDAC (0-1 μM; 24 h) 敏感[1]。
CNDAC (0-100 μM; 3 days) 抑制 HL-60 和 THP-1 细胞的增殖[2]。
CNDAC (0-10 μM; 3-6 days) 诱导 HL-60 和 THP-1 细胞的凋亡[2]。
CNDAC (6 μM; 48 h) 诱导 HCT116 细胞在延迟 S 期后的 G2 期停止细胞周期[3]。
Cell Viability Assay[1] | Cell Line: | Rad51D-deficient 51D1, Rad51D-complemented 51D1.3, wild-type AA8 and XRCC3-deficient irs1SF CHO cells | | Concentration: | 0-1 μM | | Incubation Time: | 24 h | | Result: | Inhibited cell survival with IC50s of 0.006, 0.32, 0.48 and 0.0053 μM against Rad51D-deficient 51D1, Rad51D-complemented 51D1.3, wild-type AA8 and XRCC3-deficient irs1SF cell lines, respectively. |
Cell Proliferation Assay[2] | Cell Line: | HL-60 and THP-1 cells | | Concentration: | 0-100 μM | | Incubation Time: | 3 days | | Result: | Inhibited proliferation with IC50s of 1.5832 μM and 0.84 μM against HL-60 and THP-1 cells, respectively. |
Apoptosis Analysis[2] | Cell Line: | HL-60 and THP-1 cells | | Concentration: | 0, 0.5, 1, 2, 3, 4, 5 and 10 μM | | Incubation Time: | 3, 4, 5, and 6 days | | Result: | Induced apoptosis in both cells. |
Cell Cycle Analysis[3] | Cell Line: | HCT116 | | Concentration: | 6 μM | | Incubation Time: | 48 h | | Result: | 36 and 36% of cells were arrested in late-S and G2/M phases, respectively. |
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体内研究
(In Vivo) | CNDAC (20mg/kg; i.p.; daily for 10 days) 显示小鼠抗肿瘤活性[4]。
| Animal Model: | CDF1 mice, P388 tumor model[4] | | Dosage: | 20 mg/kg | | Administration: | Intraperitoneal injection, daily for 10 days | | Result: | Greatly increased the survival time and survival rate. |
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| 运输条件 | Room temperature in continental US; may vary elsewhere. |
| 储存方式 | Please store the product under the recommended conditions in the Certificate of Analysis. |
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