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當前位置: 首頁> 産品中心> 信号轉導研究相(xiàng)關 > DNA損傷/修複 > Veliparib (ABT-888) 維利帕尼
Veliparib (ABT-888) 維利帕尼
目錄号 MZ3701-100MG 售價 4188.00元
規格 100mg 運輸溫度 室溫
其他名稱 Veliparib free base; ABT-888; A-861695; NSC 737664; 保存溫度 -20ºC幹燥保存
CAS号 912444-00-9 有效期 3年(nián)
應用 PARP1/ PARP2抑制劑 訂購數量
産品簡介:

Veliparib (ABT-888) 維利帕尼

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産品标簽

Veliparib 維利帕尼;ABT-888;PARP1/ PARP2抑制劑;Temozolomide 替莫唑胺;Radiopotentiation輻射增強;chemopotentiation化療增強;CAS:912444-00-9;


産品信息

産品名稱

産品編号

規格              

價格(元)     

Veliparib (ABT-888) 維利帕尼

MZ3701-10MG        

10mg

868

Veliparib (ABT-888) 維利帕尼         

MZ3701-50MG

50mg

2428

Veliparib (ABT-888) 維利帕尼

MZ3701-100MG

100mg

4188


産品描述

維利帕尼(Veliparib),又(yòu)稱為(wèi)ABT-888,是一(yī)種有效的PARP1和PARP2抑制劑,Ki值分别是5.2nM和2.9nM,對SIRT2沒有活性。ABT-888具有良好的口服生(shēng)物(wù)活性,能(néng)夠穿透血腦(nǎo)屏障,在同源腫瘤模型和異種移植腫瘤模型中增強替莫唑胺(Temozolomide)、鉑類、環磷酰胺和放(fàng)射效果[1]。ABT-888具有廣譜的化學和放(fàng)射增強效應[1-3]。PARP1抑制劑INO-1001和ABT-888明顯減少肌源性緊張度和改善内皮依賴性舒張,恢複内皮一(yī)氧化氮合酶磷酸化和cGMP,以及降低(dī)切割PARP1表達。PARP1抑制劑可能(néng)用來克服糖尿病微血管功能(néng)障礙[4]。


産品特性

1)   CAS NO:912444-00-9

2)   化學名:1-[3-[4-amino-3-(4-phenoxyphenyl)pyrazolo[3,4-d]pyrimidin-1-yl]piperidin-1-yl]prop-2-en-1-one

3)   同義名:Veliparib free base; ABT-888; A-861695; NSC 737664;

4)   分子式:C13H16N4O

5)   分子量:244.29 g/mol

6)   純度:>98%

7)   外觀:白(bái)色至類白(bái)色結晶性固體或粉末

8)  溶解性:溶于DMSO(≥10mg/ml)【“>”:表明溶于标示濃度,但飽和溶解度未知。】

9)   化學結構式:


保存與運輸方法

保存:-20ºC幹燥保存,3年(nián)有效。

運輸:常溫運輸。


注意事(shì)項

1)   為(wèi)了讓化合物(wù)更好的溶解,可通(tōng)過37℃加熱或(和)超聲波水(shuǐ)浴中震動片刻來處理。若實驗所需濃度過大甚至達産品溶解極限,請添加助溶劑助溶或自(zì)行調整濃度。

2)   本品僅用作科研用途,不得用作臨床診斷或治療,不得用于食品或藥品,絕對禁止用在人身上(shàng)。

3)   為(wèi)了您的安全和健康,請穿實驗服并戴一(yī)次性手套操作。


儲存液制備

         質量        

溶劑體積

濃度

1mg

5mg

10mg

1mM

4.0935 mL       

20.4675 mL       

40.9350 mL      

5mM

0.8187 mL

4.0935 mL

8.1870 mL

10mM

0.4093 mL

2.0467 mL

4.0935 mL


使用方法【源自(zì)文獻,僅作參考】

文獻1,Boerner JL et al. Protein expression of DNA damage repair proteins dictates response to topoisomerase and PARP inhibitors in triple-negative breast cancer. PLoS One. 2015 Mar 16;10(3):e0119614.PMID: 25774912

體外研究(細胞實驗):

細胞類型(Cell type):BRCA mutated TNBC cell lines: SUM149, SUM159 and SUM1315; HCC1937 and MDA-MB-231; MX-1;

藥物(wù)配制(Preparation):ABT-888 was dissolved in dimethylsulphoxide (DMSO) to make a stock concentration of 10mM and stored at -20°C.

實驗方法(Assay):Exponentially growing cells were seeded in 96-well plates (MX-1: 5,000 per well, all others: 2,000 per well) and the single agent drugs (ABT-888 or CPT-11) were addedin concentrations ranging from 0.01 nM to 100 μM the following day. When the drugs were used in combination, CPT-11 was added to media with a constant ABT-888 concentration of 500nM. Cell proliferation was determined 5 days after continuous exposure to drug by addition of MTT.

文獻2,Liu X et al.Potentiation of Temozolomide Cytotoxicity by Poly(ADP)Ribose Polymerase Inhibitor ABT-888 Requires a Conversion of Single-Stranded DNA Damages to Double-Stranded DNA Breaks. Mol Cancer Res. 2008 Oct;6(10):1621-9. PMID: 18922977

體内研究(動物(wù)模型):

動物(wù)模型(Animal Model):B16F10 melanoma syngeneic model

藥物(wù)配制(Preparation):ABT-888 was delivered in a vehicle containing 0.9% NaCl adjusted to pH 4.0.

實驗方法(Assay):B16F10 cells (6×104) were injected s.c. into the flank of female C57BL/6 mice. Mice were injection-order allocated to treatment groups, and therapy was initiated on day 1 following inoculation. ABT-888 was delivered in a vehicle containing 0.9% NaCl adjusted to pH 4.0. Temozolomide was formulated using 0.2% hydroxypropyl methylcellulose.Temozolomide was administered on an oral, qd × 5 schedule on days 6 to 10 at 50 mg/kg/d concurrently with ABT-888 on an oral, bd × 5 schedule at 25, 5, and 1 mg/kg/d.The experiment consists of 10 mice per treatment group;


參考文獻

[1] Donawho CK et al. ABT-888, an orally active poly(ADP-ribose) polymerase inhibitor that potentiates DNA- damaging agents in preclinical tumor models. Clin Cancer Res. 2007 May 1;13(9):2728-37.

[2] Shelton JW et al. In vitro and in vivo enhancement of chemoradiation using the oral PARP inhibitor ABT-888 in colorectal cancer cells. Int J Radiat Oncol Biol Phys. 2013 Jul 1;86(3):469-76.

[3] Shunkwiler L et al. Inhibition of Poly(ADP-Ribose) Polymerase Enhances Radiochemosensitivity in Cancers Proficient in DNA Double-Strand Break Repair. Int J Mol Sci. 2013 Feb 8;14(2):3773-85.

[4] Choi SK et al. Poly(ADP-ribose) polymerase 1 inhibition improves coronary arteriole function in type 2 diabetes mellitus. Hypertension. 2012 May;59(5):1060-8.



— —Written/Edited by V. Shallan【版權歸MKBio懋康所有】



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