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化學(xué)性質(zhì):
規(guī)格 | 1mg |
CAS | 135598-68-4 |
別名 | N/A |
化學(xué)名 | N/A |
分子式 | C10H12N4O4 |
分子量 | 252.23 |
溶解度 | Soluble in DMSO |
儲(chǔ)存條件 | Store at -20°C |
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
Shipping Condition | Evaluation sample solution : ship with blue ice |
產(chǎn)品描述:
CNDAC is a major metabolite of oral drug sapacitabine, and a nucleoside analog.
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 (IC50=0.006 µM) compared to 51D1.3, the Rad51D-repleted line (IC50=0.32 µM)[1]. CNDAC shows inhibitory activity against HL-60 and THP-1 cells with IC50s 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[2]. 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 IC50s of 0.01 μM and 0.3 μM, respectively. CNDAC-induced DNA damage is repaired through the homologous recombination pathway[3].
[1]. Liu XJ, et al. Sapacitabine, the prodrug of CNDAC, is a nucleoside analog with a unique action mechanism of inducing DNA strand breaks. hin J Cancer. 2012 Aug;31(8):373-80. [2]. Jagan S, et al. Bone Marrow and Peripheral Blood AML Cells Are Highly Sensitive to CNDAC, the Active Form of Sapacitabine. Adv Hematol. 2012;2012:727683. [3]. Liu X, et al. Homologous recombination as a resistance mechanism to replication-induced double-strand breaks caused by the antileukemia agent CNDAC. Blood. 2010 Sep 9;116(10):1737-46.
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原創(chuàng)作者:上海莼試生物技術(shù)有限公司
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普票匯款信息
賬 戶 名:上海生物
開(kāi) 戶 行:中國(guó)銀行山東省分行營(yíng)業(yè)部
賬 號(hào):2169 2341 6278