中文名 | CNDAC |
英文名 | CNDAC |
别名 | 化合物 T13621L 4-氨基-1-(2-氰基-2-脱氧-BETA-D-呋喃阿拉伯糖基)-2(1H)-嘧啶酮 |
英文别名 | CNDAC DFP-10917 2'-Cyano-2'-deoxy-1-(b-D-arabinofuranosyl)cytosine 2(1H)-Pyrimidinone, 4-amino-1-(2-cyano-2-deoxy-β-D-arabinofuranosyl)- 4-Amino-1-(2-cyano-2-deoxy-beta-D-arabinofuranosyl)-2(1H)-pyrimidinone |
CAS | 135598-68-4 |
化学式 | C10H12N4O4 |
分子量 | 252.23 |
密度 | 1.75±0.1 g/cm3(Predicted) |
沸点 | 596.9±60.0 °C(Predicted) |
溶解度 | DMSO |
酸度系数 | 12.78±0.70(Predicted) |
存储条件 | -20℃ |
体外研究 | CNDAC-induced SSBs can be repaired by the transcription-coupled nucleotide excision repair pathway, whereas lethal DSBs are mainly repaired through homologous recombination. Deficiency in two Rad51 paralogs, Rad51D and XRCC3, greatly sensitize cells to CNDAC. The Rad51D-null cell line is approximately 50-fold more sensitive to CNDAC (IC 50 =0.006 µM) compared to 51D1.3, the Rad51D-repleted line (IC 50 =0.32 µM). CNDAC shows inhibitory activity against HL-60 and THP-1 cells with IC 50 s of 1.58 µM and 0.84 µM. CNDAC (10 μM) results in a significant drop in cell survival compared to the untreated on days 4, 7, and 14. CNDAC is more effective at reducing viability and inducing apoptosis than ara-C at equivalent concentrations in the THP-1 cell line, which is defined as displaying resistance to ara-C. CNDAC induces DSBs, which are products of replication, rather than a consequence of induction of apoptosis. CNDAC causes DNA damage, and DNA-PK and ATR are dispensable for cell survival. CNDAC exhibits potent activity against human fibroblasts deficient in ATM or transfected with an empty vector, approximately 30-fold more than cells repleted with full-length ATM cDNA, with IC 50 s of 0.01 μM and 0.3 μM, respectively. CNDAC-induced DNA damage is repaired through the homologous recombination pathway. |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 3.965 ml | 19.823 ml | 39.647 ml |
5 mM | 0.793 ml | 3.965 ml | 7.929 ml |
10 mM | 0.396 ml | 1.982 ml | 3.965 ml |
5 mM | 0.079 ml | 0.396 ml | 0.793 ml |
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