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CNDAC

  • 產(chǎn)品貨號(hào):CS-01Y70275
  • 產(chǎn)品價(jià)格:電議
  • 產(chǎn)品產(chǎn)地:進(jìn)口、國(guó)產(chǎn)
  • 包裝類(lèi)型:1mg
  • 采購(gòu)熱度:300
  • 庫(kù)存:100
  • CAS號(hào):135598-68-4
  • 方法:
  • 含量:>98.00%
  • 品牌名稱(chēng):莼試
  • 分子式:C10H12N4O4
  • 分子量:252.23

簡(jiǎn)介內(nèi)容:質(zhì)量保證、價(jià)格優(yōu)惠

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標(biāo)簽:CNDAC 

產(chǎn)品目錄

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聯(lián)系人:高小姐

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商品詳情購(gòu)物流程代測(cè)服務(wù)付款方式常見(jiàn)問(wèn)題

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
All other available size: ship with RT , or blue ice upon request

 

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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