DMXAA (Vadimezan)

Catalog No.S1537 Synonyms: NSC 640488, ASA-404

DMXAA (Vadimezan) Chemical Structure

Molecular Weight(MW): 282.29

DMXAA (Vadimezan) is a vascular disrupting agents (VDA) and competitive inhibitor of DT-diaphorase with Ki of 20 μM and IC50 of 62.5 μM in cell-free assays, respectively. Phase 3.

Size Price Stock Quantity  
In DMSO USD 140 In stock
USD 120 In stock
USD 370 In stock
USD 970 In stock
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1 Customer Review

  • (B and C) sh-scrambled or sh-ck2a–transducted L929 cells (B) and Raw cells (C) were stimulated by DMXAA (100 μg/ml) for various times. Cytosolic and nuclear extracts were prepared as described in Materials and Methods. Five percent of the cytosolic proteins and 20% of the nuclear proteins were resolved by 10% SDS-PAGE. Subsequently, immunoblotting was conducted by indicated Abs. The amounts of Tubulin and Lamin B1 in cytosol versus nuclei detected by respective Abs were used as internal control for fractionation.

    J Immunol, 2015, 194:4477-4488. DMXAA (Vadimezan) purchased from Selleck.

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Biological Activity

Description DMXAA (Vadimezan) is a vascular disrupting agents (VDA) and competitive inhibitor of DT-diaphorase with Ki of 20 μM and IC50 of 62.5 μM in cell-free assays, respectively. Phase 3.
DT-diaphorase [1]
(Cell-free assay)
DT-diaphorase [1]
(Cell-free assay)
20 μM(Ki) 20 μM(Ki)
In vitro

In DLD-1 human colon carcinoma cells, DMXAA inhibits DT-diaphorase activity without significant effects on the activity of cytochrome b5 reductase and cytochrome P450 reductase. Combination of menadione and DMXAA leads to an increase in the antiproliferative activity of DLD-1 cells. [1] DMXAA, as an antiviral agent, inhibits VSV-induced cytotoxicity and influenza virus replication in RAW 264.7 macrophages. [2] A recent study shows that DMXAA has non-immune-mediated inhibitory effects against several kinase members of VEGFR (vascular endothelial growth factor receptor), such as VEGFR2 signalling in human umbilical vein endothelial cells. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human BJ cells M1rzS2N6fG:2b4jpZ:Kh[XO|YYm= M3PHWVI1KGh? NF6wNHJEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBDUiClZXzsd{Bi\nSncjCyOEBpenNiYomgUXRVKGG|c3H5MEBESzVyPUS4Mlkh|ryP NHzt[pEzPDVzOEK5OS=>
HECPP cells MV7GeY5kfGmxbjDhd5NigQ>? MkXtNVAhfWdxbVy= MXPBZ5RqfmG2aX;uJI9nKE6ILXvhdJBiSiCrbjDISWNRWCClZXzsd{BifCBzMDD1[{9uVA>? NV7LR2ZVOTd4MU[xNVQ>

... Click to View More Cell Line Experimental Data

In vivo DMXAA treatment significantly protects C57BL/6J mice infected i.n. with 200 p.f.u. mouse-adapted H1N1 influenza PR8 virus with 60% survival, while the control group only exhibited 20% survival. [2] DMXAA significantly delays tumor growth induced by chemical carcinogen, increases the time to tumor doubling and increases time from treatment to euthanasia. After the treatment of DMXAA, median tumor doubling time, median tumour tripling time and median time from treatment to euthanasia in tumor-bearing animals are increased by approximately 4.4-, 1.8- and 2.7-fold, respectively. [4]


Kinase Assay:[1]
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DT-diaphorase activity and kinetic analysis of enzyme inhibition :

Purified DT-diaphorase enzyme activity is assayed by measuring the reduction of cytochrome c at 550 nm on a Beckman DU 650 spectrophotometer. Each assay contains cytochrome c (70 μM), NADH (variable concentrations), purified DT-diaphorase (0.032 μg), and menadione (variable concentrations) in a final volume of 1 mL Tris–HCl buffer (50 mM, pH 7.4) containing 0.14% BSA. The reaction is started by the addition of NADH. Rates of reduction are calculated over the initial part of the reaction curve (30 seconds), and results are expressed in terms of μmol cytochrome c reduced/min/mg protein using a molar extinction coefficient of 21.1 mM−1 cm−1 for reduced cytochrome c. Enzyme assays are carried out at room temperature and all reactions are performed in triplicate. Inhibition of purified DT-diaphorase activity is performed by the inclusion of DMXAA (at various concentrations) in the reaction, and inhibition characteristics are determined by varying the concentration of NADH (constant menadione) or menadione (constant NADH) at several concentrations of inhibitor. Ki values are obtained by plotting 1/V against. The activity of DT-diaphorase in DLD-1 cells is determined by measuring the dicumarol-sensitive reduction of DCPIP at 600 nm. Briefly, DLD-1 cells in mid-exponential growth are harvested by scraping into ice-cold buffer (Tris–HCl, 25 mM, pH 7.4 and 250 mM sucrose) and sonicated on ice. Enzyme assay conditions are 2 mM NADH, 40 μM DCPIP, 20 μL of dicumarol (when required) in a final volume of 1 mL Tris–HCl (25 mM, pH 7.4) containing BSA (0.7 mg/mL). Results are expressed as the dicumarol-sensitive reduction of DCPIP using a molar extinction coefficient of 21 mM−1 cm−1. Protein levels are determined using the Bradford assay
Cell Research:[1]
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  • Cell lines: DLD-1 and H460 cells
  • Concentrations: 0-2 mM
  • Incubation Time: 96 hours
  • Method: DLD-1 human colon carcinoma and H460 human non-small cell lung carcinoma cells are routinely maintained as monolayer cultures in RPMI 1640 culture medium supplemented with foetal calf serum (10%), sodium pyruvate (2 mM), penicillin/streptomycin (50 IU mL−1/50 μg mL-1) and l-glutamine (2 mM). Chemosensitivity is assessed using the MTT assay and all assays are performed under aerobic conditions. Briefly, cells are plated into each well of a 96-well culture plate and incubated overnight in an atmosphere containing 5% CO2. Culture medium is completely removed from each well and replaced with medium containing a range of drug concentrations. In the case of menadione alone, the duration of drug exposure is 1 hour, after which the cells are washed twice with Hanks' balanced salt solution prior to the addition of 200 μL fresh RPMI 1640 medium to each well of the plate. In the case of DMXAA alone, the duration of drug exposure is 3 hours. Following a four-day incubation, cell survival is determined using the MTT assay. For combinations of DMXAA with menadione, cells are initially set up and a non-toxic (>95% cell survival) concentration of DMXAA is selected. Cells are then initially exposed to DMXAA (2 mM) for a period of 2 hours, following which the medium is removed and replaced with medium containing the inhibitor (DMXAA at a constant concentration of 2 mM) and menadione (at a range of drug concentrations). Following a further 7-hour incubation, cells are washed twice with Hanks' balanced salt solution prior to the addition of growth medium.
    (Only for Reference)
Animal Research:[4]
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  • Animal Models: Chemical carcinogen (NMU) is injected into female Wistar rats.
  • Formulation: DMXAA is dissolved in 5% sodium bicarbonate.
  • Dosages: ≤300 mg/kg
  • Administration: Administered via i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 7 mg/mL (24.79 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5% NaHCO3 (aq) warmed
For best results, use promptly after mixing.

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 282.29


CAS No. 117570-53-3
Storage powder
in solvent
Synonyms NSC 640488, ASA-404

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01278758 Terminated Metastatic Cancer Novartis Pharmaceuticals|Novartis March 2010 Phase 1
NCT01290380 Terminated Solid Tumor Malignancies Novartis Pharmaceuticals|Novartis February 2010 Phase 1
NCT01057342 Completed Lung Cancer Swiss Group for Clinical Cancer Research January 2010 Phase 2
NCT01299415 Terminated Solid Tumors Novartis Pharmaceuticals|Novartis August 2009 Phase 1
NCT01285453 Completed Advanced or Recurrent Solid Tumors Novartis Pharmaceuticals|Novartis March 2009 Phase 1
NCT00111618 Completed Prostate Cancer Antisoma Research May 2005 Phase 2

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VDA Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID