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Vadimezan (DMXAA)
僅限科研使用
Vadimezan (DMXAA)
別名: ASA404, NSC 640488 中文名稱：2,5-己酮可可堿
Vadimezan (DMXAA)是一種vascular disrupting agents (VDA)，也是一種DT-diaphorase的競爭性抑制劑，無細胞試驗中Ki為20 μM ，IC50為62.5 μM。DMXAA (Vadimezan) 也是一種STING 激動劑，具有潛在的抗腫瘤活性。DMXAA (Vadimezan) 在體外可有效誘導(dǎo) IFN-β 和 TNF-α 的表達，但對 TNF-α 影響相對較低。DMXAA (Vadimezan)具有抗病毒活性。Phase 3。
Vadimezan (DMXAA) Chemical Structure
CAS: 117570-53-3
產(chǎn)品質(zhì)控
批次：
純度：
99.94%
99.94
Vadimezan (DMXAA)相關(guān)產(chǎn)品
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相關(guān)信號通路圖
細胞實驗數(shù)據(jù)示例
| 細胞系 | 實驗類型 | 給藥濃度 | 孵育時間 | 活性描述 | 文獻信息 |
|---|---|---|---|---|---|
| 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 | ||
| 點擊查看更多細胞系數(shù)據(jù) | |||||
生物活性
| 產(chǎn)品描述 | Vadimezan (DMXAA)是一種vascular disrupting agents (VDA)，也是一種DT-diaphorase的競爭性抑制劑，無細胞試驗中Ki為20 μM ，IC50為62.5 μM。DMXAA (Vadimezan) 也是一種STING 激動劑，具有潛在的抗腫瘤活性。DMXAA (Vadimezan) 在體外可有效誘導(dǎo) IFN-β 和 TNF-α 的表達，但對 TNF-α 影響相對較低。DMXAA (Vadimezan)具有抗病毒活性。Phase 3。 | ||||
|---|---|---|---|---|---|
| 特性 | DMXAA（ASA404)是DT-心肌黃酶競爭性抑制劑。 | ||||
| 靶點 |
|
| 體外研究(In Vitro) | ||||
| 體外研究活性 | 在體外, DMXAA（ASA404)抑制純化的DT-心肌黃酶，IC50為62.5 μM，Ki為20 μM。DMXAA（ASA404)作用于DLD-1人結(jié)腸癌細胞, 抑制DT-心肌黃酶活性，IC50為 49.6 μM，而對細胞色素 b5 還原酶和細胞色素P450還原酶沒有顯著作用效果。[1] DMXAA（ASA404)為抗病毒藥物，作用于RAW 264.7巨噬細胞，抑制VSV-誘導(dǎo)的細胞毒性，也抑制流感病毒復(fù)制。[2] 最新研究顯示DMXAA（ASA404)作用于VEGFR幾種激酶成員,如人人臍靜脈內(nèi)皮細胞中的VEGFR2信號，具有非免疫調(diào)節(jié)的抑制效果。[3] | |||
|---|---|---|---|---|
| 激酶實驗 | DT-心肌黃酶活性和酶抑制動力學(xué)分析 | |||
| 通過在Beckman DU 650分光光度計上檢測細胞色素 c 在 550 nm處減少量而測定純化的DT-心肌黃酶活性。每組實驗含細胞色素c(70 μM), NADH(多種濃度), 純化的DT-心肌黃酶(0.032 μg),及溶于含0.14% BSA終體積為1 mL Tris–HCl buffer(50 mM, pH 7.4)的維生素K(多種濃度)。加入NADH開始反應(yīng)。根據(jù)反應(yīng)曲線初始部分(30秒)計算減少率, 結(jié)果表示為μmol 減少的細胞色素/min/mg 蛋白，使用21 mM?1 cm?1 摩爾消光系數(shù)表示減少的細胞色素c。在室溫下進行酶反應(yīng)，所有反應(yīng)做三次平行。反應(yīng)中含有的DMXAA（ASA404) (不同濃度) 用來表示純化的 DT-心肌黃酶抑制活性,通過改變NADH (維生素K不變)維生素K (NADH不變) 的濃度測定抑制特性。獲得Ki值。通過測量對Dicumarol敏感的DCPIP在 600 nm處的減少量而測定DT-心肌黃酶作用于DLD-1細胞的活性收集處于指數(shù)生長中期的DLD-1細胞，置于冰凍buffer (Tris–HCl, 25 mM, pH 7.4和 250 mM蔗糖)，然后在冰上進行超聲處理。酶反應(yīng)條件為2 mM NADH, 40 μM DCPIP, 溶于含BSA (0.7 mg/mL)終體積為1 mL Tris–HCl (25 mM, pH 7.4) 的 20 μL Dicumarol。使用21 mM?1 cm?1 的摩爾消光系數(shù)表示對Dicumarol敏感的 DCPIP減少量。通過 Bradford檢測測定蛋白水平。 | ||||
| 細胞實驗 | 細胞系 | DLD-1和 H460 | ||
| 濃度 | 0 到2 mM | |||
| 孵育時間 | 96 小時 | |||
| 方法 | DLD-1人結(jié)腸癌和H460人非小細胞肺癌細胞單層培養(yǎng)在RPMI 1640培養(yǎng)基中，培養(yǎng)基中補充胎牛血清 (10%), 丙酮酸鈉(2 mM), 青霉素/鏈霉親和素 (50 IU mL?1/50 μg mL-1) 及l(fā)-谷氨酰胺(2 mM)。在有氧條件下進行MTT 實驗和所有其他實驗，檢測藥物敏感性。細胞接種在96孔板上，然后在含5% CO2的環(huán)境下溫育過夜。完全移除培養(yǎng)基，使用含多種藥物濃度的培養(yǎng)基替代。在只有維生素K時，藥物處理時間為1小時,然后細胞在Hanks’平衡鹽溶液中沖洗兩次，然后在每孔中加入200 μL 新鮮RPMI 1640培養(yǎng)基。 在只有DMXAA（ASA404) 存在時，藥物處理時間為3小時。 隨后溫育4天，使用MTT檢測測定細胞存活情況。為了DMXAA（ASA404)和維生素K聯(lián)用，初步建立細胞 ，選擇非毒性(細胞存活率>95%)濃度的DMXAA（ASA404)。細胞使用DMXAA（ASA404) (2 mM)先處理2小時，隨后移除培養(yǎng)基，使用含抑制劑 (DMXAA（ASA404)，持續(xù)濃度為2 mM)和維生素K(多種濃度)的培養(yǎng)基更換。再溫育7小時，使用Hanks’平衡鹽溶液沖洗細胞，再加入生長培養(yǎng)基。 | |||
| 實驗圖片 | 檢測方法 | 檢測指標 | 實驗圖片 | PMID |
| Western blot | p-p38 / p38 p-MK2 / pERK / p-JNK |
|
21819972 | |
| Growth inhibition assay | Cell proliferation |
|
30138430 | |
| 體內(nèi)研究(In Vivo) | ||
| 體內(nèi)研究活性 | DMXAA（ASA404)顯著延遲化學(xué)致癌物誘導(dǎo)的細胞生長, 提高腫瘤倍增時間，且提高從治療到安樂死的時間。DMXAA（ASA404)處理攜帶腫瘤的動物后, 平均腫瘤倍增時間,平均腫瘤變?nèi)稌r間，及從治療到安樂死的平均時間分別提高4.4-, 1.8- 2.7-倍。[4] DMXAA（ASA404)處理顯著保護感染200 p.f.u.小鼠適應(yīng)的H1N1流感 PR8病毒的C57BL/6J小鼠，使存活率達60%, 而對照組存活率只為20%。[2] | |
|---|---|---|
| 動物實驗 | Animal Models | 注射化學(xué)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 |
化學(xué)信息&溶解度
| 分子量 | 282.29 | 分子式 | C17H14O4 |
| CAS號 | 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 | ||
| 儲存條件(自收到貨起) | |||
|
體外溶解度 |
7.5%Sodium bicarbonate : 10 mg/mL (35.42 mM) DMSO : 7 mg/mL ( (24.79 mM) ；DMSO吸濕會降低化合物溶解度，請使用新開封DMSO) Water : Insoluble |
摩爾濃度計算器 |
|
體內(nèi)溶解度 現(xiàn)配現(xiàn)用，請按從左到右的順序依次添加，澄清后再加入下一溶劑 |
動物體內(nèi)配方計算器 | ||||
實驗計算
動物體內(nèi)配方計算器（澄清溶液）
第一步：請輸入基本實驗信息（考慮到實驗過程中的損耗，建議多配一只動物的藥量）
mg/kg
g
μL
只
第二步：請輸入動物體內(nèi)配方組成（配方適用于不溶于水的藥物；不同批次藥物配方比例不同，請聯(lián)系Selleck為您提供正確的澄清溶液配方）
% DMSO
%
% Tween 80
% ddH2O
%DMSO
%
計算結(jié)果：
工作液濃度： mg/ml；
DMSO母液配制方法： mg 藥物溶于μL DMSO溶液（母液濃度mg/mL，注：如該濃度超過該批次藥物DMSO溶解度，請先聯(lián)系Selleck）；
體內(nèi)配方配制方法：取μL DMSO母液，加入μL PEG300，混勻澄清后加入μL Tween 80，混勻澄清后加入μL ddH2O，混勻澄清。
體內(nèi)配方配制方法：取μL DMSO母液，加入μL Corn oil，混勻澄清。
注意：1. 首先保證母液是澄清的；
2.一定要按照順序依次將溶劑加入，進行下一步操作之前必須保證上一步操作得到的是澄清的溶液，可采用渦旋、超聲或水浴加熱等物理方法助溶。
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