Vadimezan (DMXAA)
别名: ASA404, NSC 640488 中文名称：2,5-己酮可可碱
Vadimezan (DMXAA)是一种vascular disrupting agents (VDA)，也是一种DT-diaphorase的竞争性抑制剂，无细胞试验中Ki为20 μM ，IC50为62.5 μM。DMXAA (Vadimezan) 也是一种STING 激动剂，具有潜在的抗肿瘤活性。DMXAA (Vadimezan) 在体外可有效诱导 IFN-β 和 TNF-α 的表达，但对 TNF-α 影响相对较低。DMXAA (Vadimezan)具有抗病毒活性。Phase 3。
Vadimezan (DMXAA) Chemical Structure
CAS: 117570-53-3
产品质控
批次：
纯度：
99.94%
99.94
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相关信号通路图
细胞实验数据示例
| 细胞系 | 实验类型 | 给药浓度 | 孵育时间 | 活性描述 | 文献信息 |
|---|---|---|---|---|---|
| MDA-MB-231 | Apoptosis assay | 24 to 96 uM | 48 hrs | Induction of apoptosis in human MDA-MB-231 cells assessed as increase in cleaved caspase-3 expression at 24 to 96 uM after 48 hrs by Western blot analysis | 28376372 |
| MDA-MB-231 | Apoptosis assay | 24 to 96 uM | 48 hrs | Induction of apoptosis in human MDA-MB-231 cells assessed as increase in cleaved PARP level at 24 to 96 uM after 48 hrs by Western blot analysis | 28376372 |
| MDA-MB-231 | Function assay | 24 to 96 uM | 48 hrs | Decrease in caspase-3 level in human MDA-MB-231 cells at 24 to 96 uM after 48 hrs by Western blot analysis | 28376372 |
| MDA-MB-231 | Function assay | 24 to 96 uM | 48 hrs | Increase in p53 level in human MDA-MB-231 cells at 24 to 96 uM after 48 hrs by Western blot analysis | 28376372 |
| MDA-MB-231 | Function assay | 24 to 96 uM | 48 hrs | Decrease in caspase-9 level in human MDA-MB-231 cells at 24 to 96 uM after 48 hrs by Western blot analysis | 28376372 |
| MDA-MB-231 | Function assay | 24 to 96 uM | 48 hrs | Decrease in MDM2 level in human MDA-MB-231 cells at 24 to 96 uM after 48 hrs by Western blot analysis | 28376372 |
| HepG2 | Cell cycle arrest assay | 0.2 uM | 24 hrs | Cell cycle arrest in human HepG2 cells assessed as accumulation at S phase at 0.2 uM after 24 hrs by propidium iodide staining-based flow cytometric method relative to control | 29129511 |
| HepG2 | Apoptosis assay | 0.2 uM | 24 hrs | Induction of apoptosis in human HepG2 cells assessed as increase in cleaved caspase-3 levels at 0.2 uM after 24 hrs by Western blot method | 29129511 |
| HepG2 | Apoptosis assay | 0.2 uM | 24 hrs | Induction of apoptosis in human HepG2 cells assessed as increase in cleaved caspase-9 levels at 0.2 uM after 24 hrs by Western blot method | 29129511 |
| HepG2 | Apoptosis assay | 0.2 uM | 24 hrs | Induction of apoptosis in human HepG2 cells assessed as increase in cleaved PARP levels at 0.2 uM after 24 hrs by Western blot method | 29129511 |
| HECPP cells | Function assay | 10 ug/mL | Activation of NF-kappaB in HECPP cells at 10 ug/mL | 17616114 | |
| human BJ cells | Cytotoxic assay | 24 h | Cytotoxicity against human BJ cells after 24 hrs by MTT assay, CC50=48.9 μM | 24518295 | |
| MCF7 | Antiproliferative assay | 24 hrs | Antiproliferative activity against human MCF7 cells co-treated with pyranoxanthone at 1:1 molar ratio after 24 hrs by MTT assay, IC50 = 11.89 μM. | 29129511 | |
| MDA-MB-231 | Antiproliferative assay | 24 hrs | Antiproliferative activity against human MDA-MB-231 cells co-treated with pyranoxanthone at 1:1 molar ratio after 24 hrs by MTT assay, IC50 = 12.12 μM. | 29129511 | |
| K562 | Antiproliferative assay | 24 hrs | Antiproliferative activity against human K562 cells co-treated with pyranoxanthone at 1:1 molar ratio after 24 hrs by MTT assay, IC50 = 19.14 μM. | 29129511 | |
| HepG2 | Antiproliferative assay | 24 hrs | Antiproliferative activity against human HepG2 cells co-treated with pyranoxanthone at 1:1 molar ratio after 24 hrs by MTT assay, IC50 = 21.25 μM. | 29129511 | |
| COLO320 | Antiproliferative assay | 48 hrs | Antiproliferative activity against human COLO320 cells after 48 hrs by CCK8 assay, IC50 = 39.5 μM. | 28376372 | |
| MDA-MB-231 | Antiproliferative assay | 48 hrs | Antiproliferative activity against human MDA-MB-231 cells after 48 hrs by CCK8 assay, IC50 = 48.4 μM. | 28376372 | |
| MDA-MB-231 | Growth inhibition assay | 24 hrs | Growth inhibition of human MDA-MB-231 cells after 24 hrs by MTT assay, IC50 = 48.42 μM. | 29609121 | |
| MDA-MB-231 | Antiproliferative assay | 24 hrs | Antiproliferative activity against human MDA-MB-231 cells after 24 hrs by MTT assay, IC50 = 48.44 μM. | 29129511 | |
| HepG2 | Cell cycle arrest assay | 24 hrs | Cell cycle arrest in human HepG2 cells assessed as accumulation at S phase co-treated with pyranoxanthone at 1:1 molar ratio after 24 hrs by propidium iodide staining-based flow cytometric method | 29129511 | |
| HepG2 | Apoptosis assay | 24 hrs | Induction of apoptosis in human HepG2 cells assessed as increase in cleaved PARP levels co-treated with pyranoxanthone at 1:1 molar ratio after 24 hrs by Western blot method | 29129511 | |
| HepG2 | Apoptosis assay | 24 hrs | Induction of apoptosis in human HepG2 cells assessed as increase in cleaved caspase-3 levels co-treated with pyranoxanthone at 1:1 molar ratio after 24 hrs by Western blot method | 29129511 | |
| HepG2 | Apoptosis assay | 24 hrs | Induction of apoptosis in human HepG2 cells assessed as increase in cleaved caspase-9 levels co-treated with pyranoxanthone at 1:1 molar ratio after 24 hrs by Western blot method | 29129511 | |
| HepG2 | Apoptosis assay | 24 hrs | Induction of apoptosis in human HepG2 cells assessed as downregulation of Bcl-xL expression co-treated with pyranoxanthone at 1:1 molar ratio after 24 hrs by Western blot method | 29129511 | |
| HepG2 | Apoptosis assay | 24 hrs | Induction of apoptosis in human HepG2 cells assessed as upregulation of Bid expression co-treated with pyranoxanthone at 1:1 molar ratio after 24 hrs by Western blot method | 29129511 | |
| A673 | qHTS assay | qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells | 29435139 | ||
| DAOY | qHTS assay | qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells | 29435139 | ||
| RD | qHTS assay | qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells | 29435139 | ||
| SK-N-SH | qHTS assay | qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells | 29435139 | ||
| MG 63 (6-TG R) | qHTS assay | qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells | 29435139 | ||
| NB1643 | qHTS assay | qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells | 29435139 | ||
| Rh41 | qHTS assay | qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells | 29435139 | ||
| SK-N-MC | qHTS assay | qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells | 29435139 | ||
| 点击查看更多细胞系数据 | |||||
生物活性
| 产品描述 | Vadimezan (DMXAA)是一种vascular disrupting agents (VDA)，也是一种DT-diaphorase的竞争性抑制剂，无细胞试验中Ki为20 μM ，IC50为62.5 μM。DMXAA (Vadimezan) 也是一种STING 激动剂，具有潜在的抗肿瘤活性。DMXAA (Vadimezan) 在体外可有效诱导 IFN-β 和 TNF-α 的表达，但对 TNF-α 影响相对较低。DMXAA (Vadimezan)具有抗病毒活性。Phase 3。 | ||||
|---|---|---|---|---|---|
| 特性 | DMXAA（ASA404)是DT-心肌黄酶竞争性抑制剂。 | ||||
| 靶点 |
|
| 体外研究(In Vitro) | ||||
| 体外研究活性 | 在体外, DMXAA（ASA404)抑制纯化的DT-心肌黄酶，IC50为62.5 μM，Ki为20 μM。DMXAA（ASA404)作用于DLD-1人结肠癌细胞, 抑制DT-心肌黄酶活性，IC50为 49.6 μM，而对细胞色素 b5 还原酶和细胞色素P450还原酶没有显著作用效果。[1] DMXAA（ASA404)为抗病毒药物，作用于RAW 264.7巨噬细胞，抑制VSV-诱导的细胞毒性，也抑制流感病毒复制。[2] 最新研究显示DMXAA（ASA404)作用于VEGFR几种激酶成员,如人人脐静脉内皮细胞中的VEGFR2信号，具有非免疫调节的抑制效果。[3] | |||
|---|---|---|---|---|
| 激酶实验 | DT-心肌黄酶活性和酶抑制动力学分析 | |||
| 通过在Beckman DU 650分光光度计上检测细胞色素 c 在 550 nm处减少量而测定纯化的DT-心肌黄酶活性。每组实验含细胞色素c(70 μM), NADH(多种浓度), 纯化的DT-心肌黄酶(0.032 μg),及溶于含0.14% BSA终体积为1 mL Tris–HCl buffer(50 mM, pH 7.4)的维生素K(多种浓度)。加入NADH开始反应。根据反应曲线初始部分(30秒)计算减少率, 结果表示为μmol 减少的细胞色素/min/mg 蛋白，使用21 mM−1 cm−1 摩尔消光系数表示减少的细胞色素c。在室温下进行酶反应，所有反应做三次平行。反应中含有的DMXAA（ASA404) (不同浓度) 用来表示纯化的 DT-心肌黄酶抑制活性,通过改变NADH (维生素K不变)维生素K (NADH不变) 的浓度测定抑制特性。获得Ki值。通过测量对Dicumarol敏感的DCPIP在 600 nm处的减少量而测定DT-心肌黄酶作用于DLD-1细胞的活性收集处于指数生长中期的DLD-1细胞，置于冰冻buffer (Tris–HCl, 25 mM, pH 7.4和 250 mM蔗糖)，然后在冰上进行超声处理。酶反应条件为2 mM NADH, 40 μM DCPIP, 溶于含BSA (0.7 mg/mL)终体积为1 mL Tris–HCl (25 mM, pH 7.4) 的 20 μL Dicumarol。使用21 mM−1 cm−1 的摩尔消光系数表示对Dicumarol敏感的 DCPIP减少量。通过 Bradford检测测定蛋白水平。 | ||||
| 细胞实验 | 细胞系 | DLD-1和 H460 | ||
| 浓度 | 0 到2 mM | |||
| 孵育时间 | 96 小时 | |||
| 方法 | DLD-1人结肠癌和H460人非小细胞肺癌细胞单层培养在RPMI 1640培养基中，培养基中补充胎牛血清 (10%), 丙酮酸钠(2 mM), 青霉素/链霉亲和素 (50 IU mL−1/50 μg mL-1) 及l-谷氨酰胺(2 mM)。在有氧条件下进行MTT 实验和所有其他实验，检测药物敏感性。细胞接种在96孔板上，然后在含5% CO2的环境下温育过夜。完全移除培养基，使用含多种药物浓度的培养基替代。在只有维生素K时，药物处理时间为1小时,然后细胞在Hanks’平衡盐溶液中冲洗两次，然后在每孔中加入200 μL 新鲜RPMI 1640培养基。 在只有DMXAA（ASA404) 存在时，药物处理时间为3小时。 随后温育4天，使用MTT检测测定细胞存活情况。为了DMXAA（ASA404)和维生素K联用，初步建立细胞 ，选择非毒性(细胞存活率>95%)浓度的DMXAA（ASA404)。细胞使用DMXAA（ASA404) (2 mM)先处理2小时，随后移除培养基，使用含抑制剂 (DMXAA（ASA404)，持续浓度为2 mM)和维生素K(多种浓度)的培养基更换。再温育7小时，使用Hanks’平衡盐溶液冲洗细胞，再加入生长培养基。 | |||
| 实验图片 | 检测方法 | 检测指标 | 实验图片 | PMID |
| Western blot | p-p38 / p38 p-MK2 / pERK / p-JNK |
|
21819972 | |
| Growth inhibition assay | Cell proliferation |
|
30138430 | |
| 体内研究(In Vivo) | ||
| 体内研究活性 | DMXAA（ASA404)显著延迟化学致癌物诱导的细胞生长, 提高肿瘤倍增时间，且提高从治疗到安乐死的时间。DMXAA（ASA404)处理携带肿瘤的动物后, 平均肿瘤倍增时间,平均肿瘤变三倍时间，及从治疗到安乐死的平均时间分别提高4.4-, 1.8- 2.7-倍。[4] DMXAA（ASA404)处理显著保护感染200 p.f.u.小鼠适应的H1N1流感 PR8病毒的C57BL/6J小鼠，使存活率达60%, 而对照组存活率只为20%。[2] | |
|---|---|---|
| 动物实验 | Animal Models | 注射化学致癌物 (NMU)的雌性 Wistar大鼠 |
| Dosages | ≤300 mg/kg | |
| Administration | 腹腔注射 | |
| NCT Number | Recruitment | Conditions | Sponsor/Collaborators | Start Date | Phases |
|---|---|---|---|---|---|
| NCT00856336 | Completed | Refractory Tumors |
Antisoma Research |
May 2003 | Phase 1 |
| NCT00863733 | Completed | Solid Tumors |
Cancer Research UK|Cancer Society Auckland |
May 1996 | Phase 1 |
化学信息&溶解度
| 分子量 | 282.29 | 分子式 | C17H14O4 |
| CAS号 | 117570-53-3 | SDF | Download Vadimezan (DMXAA) SDF |
| Smiles | CC1=C(C2=C(C=C1)C(=O)C3=CC=CC(=C3O2)CC(=O)O)C | ||
| 储存条件(自收到货起) | |||
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体外溶解度 |
7.5%Sodium bicarbonate : 10 mg/mL (35.42 mM) DMSO : 7 mg/mL ( (24.79 mM) ；DMSO吸湿会降低化合物溶解度，请使用新开封DMSO) Water : Insoluble |
摩尔浓度计算器 |
|
体内溶解度 现配现用，请按从左到右的顺序依次添加，澄清后再加入下一溶剂 |
动物体内配方计算器 | ||||
实验计算
动物体内配方计算器（澄清溶液）
第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量）
mg/kg
g
μL
只
第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系Selleck为您提供正确的澄清溶液配方）
% DMSO
%
% Tween 80
% ddH2O
%DMSO
%
计算结果：
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于μL DMSO溶液（母液浓度mg/mL，注：如该浓度超过该批次药物DMSO溶解度，请先联系Selleck）；
体内配方配制方法：取μL DMSO母液，加入μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入μL ddH2O，混匀澄清。
体内配方配制方法：取μL DMSO母液，加入μL Corn oil，混匀澄清。
注意：1. 首先保证母液是澄清的；
2.一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
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