DMXAA

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

血管破坏剂 (VDA) 和 DT-心肌黄酶竞争性抑制剂，Ki 为 20 uM；激活 STING 依赖性先天免疫途径。

A vascular disrupting agent (VDA) and competitive inhibitor of DT-diaphorase with Ki of 20 uM; activates STING dependent innate immune pathways.(In Vitro):Vadimezan (DMXAA), the vascular disrupting agent, is a murine agonist of the stimulator of interferon genes (STING) and also a potent inducer of type I IFNs and other cytokines. Vadimezan (DMXAA) has no detrimental effect on 344SQ-ELuc cell viability. It is found that Vadimezan-mediated up regulation of the NF-κB pathway as shown by increased p65 phosphorylation in M2 macrophages. Results demonstrate that Vadimezan (DMXAA)-treated cells are protected from VSV-induced cytotoxicity at all MOIs in contrast to medium-pretreated macrophages. Vadimezan (DMXAA) effectively inhibits growth of both strains of influenza, demonstrating the potential of Vadimezan for treatment of drug-resistant strains of human influenza. (In Vivo):344SQ-ELuc NSCLC subcutaneous tumors respond dramatically to Vadimezan (DMXAA), with a marked decrease in bioluminescence (BLI) signals post-drug injection. Vadimezan (DMXAA) treatment of 344SQ-ELuc metastases yields no decrease in photon emission rates, with the tumors remaining histologically similar to controls after this treatment. As with the large subcutaneous tumors, Vadimezan (DMXAA) administration to mice with small subcutaneous tumors still leads to ~2-log decreases in photon emission at both 6 and 24 hours. In vivo, Vadimezan (DMXAA) is a more potent inducer of IFN-β mRNA and a relatively poor inducer of TNF-α mRNA. Vadimezan (DMXAA) administration leads to significantly less weight loss in influenza-infected mice.

Vadimezan (DMXAA), the vascular disrupting agent, is a murine agonist of the stimulator of interferon genes (STING) and also a potent inducer of type I IFNs and other cytokines. Vadimezan (DMXAA) has no detrimental effect on 344SQ-ELuc cell viability. It is found that Vadimezan-mediated up regulation of the NF-κB pathway as shown by increased p65 phosphorylation in M2 macrophages. Results demonstrate that Vadimezan (DMXAA)-treated cells are protected from VSV-induced cytotoxicity at all MOIs in contrast to medium-pretreated macrophages. Vadimezan (DMXAA) effectively inhibits growth of both strains of influenza, demonstrating the potential of Vadimezan for treatment of drug-resistant strains of human influenza.

344SQ-ELuc NSCLC subcutaneous tumors respond dramatically to Vadimezan (DMXAA), with a marked decrease in bioluminescence (BLI) signals post-drug injection. Vadimezan (DMXAA) treatment of 344SQ-ELuc metastases yields no decrease in photon emission rates, with the tumors remaining histologically similar to controls after this treatment. As with the large subcutaneous tumors, Vadimezan (DMXAA) administration to mice with small subcutaneous tumors still leads to ~2-log decreases in photon emission at both 6 and 24 hours. In vivo, Vadimezan (DMXAA) is a more potent inducer of IFN-β mRNA and a relatively poor inducer of TNF-α mRNA. Vadimezan (DMXAA) administration leads to significantly less weight loss in influenza-infected mice.

ASA-404 | Vadimezan

Autophagy

Autophagy

DT-diaphorase

Cancer

——

117570-53-3

282.2906

C17H14O4

>98% (HPLC)

DMSO: 6.5 mg/mL

O=C(O)CC1=CC=CC(C2=O)=C1OC3=C2C=CC(C)=C3C

9H-Xanthene-4-acetic acid, 5,6-dimethyl-9-oxo-

(-20℃)

With Ice Pack

≥ 2 years