Vadimezan

Description

DMXAA (117570-53-3) is a STING (Stimulator of Interferon Genes) agonist selective for mouse STING.1,2 Intratumoral administration of DMXAA resulted in tumor regression and complete rejection in mouse xenografts.3 Tumor regression induced by DMXAA results from a cascade of cellular events which include disruption of tumor vasculature followed by the release of chemokines which trigger the recruitment of immune cells.4 DMXAA induced expression of IFN-β resulting in a striking expansion of leukemia-specific T cells extending survival in two acute myeloid leukemia models.5

The Uses of Vadimezan

Vadimezan is a drug that displayed vascular-disrupting activity and induced haemorrhagic necrosis and tumour regression in pre-clinical animal models.

The Uses of Vadimezan

Vadimezan is a drug that displayed vascular-disrupting activity and induced haemorrhagic necrosis and tumour regression in pre-clinical animal models. It is a substrate for the immune adaptor protein STING in mice.

What are the applications of Application

DMXAA is an apoptosis inducer for proteomics research

Definition

ChEBI: A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is replaced by a 5,6-dimethyl-9-oxoxanthen-4-yl group.

General Description

5,6-dimethylxanthenone-4-acetic acid (DMXAA) is a flavone acetic acid derivative. It acts as a vascular disrupting agent (VDA), which damages tumor vasculature and stimulates an anti-tumor immune response. It stimulates hemorrhagic necrosis.

Biochem/physiol Actions

DMXAA is an apoptosis inducer; anti-vascular.

Storage

Store at +4°C

References

1) Prantner et al. (2012), 5,6-Dimethylzanthenone-4-acetic acid (DMXAA) activates stimulator of interferon gene (STING)-dependent innate immune pathways and is regulated by mitochondrial membrane potential; J. Biol. Chem., 287 39776 2) Conlon et al. (2013), Mouse, but not human STING, binds and signals in response to the vascular disrupting agent 5,6-dimethylxanthenone-4-acetic acid; J. Immunol., 190 5216 3) Corrales et al. (2015), Direct Activation of STING in the Tumor Microenvironment Leads to Potent and Systemic Tumor Regression and immunity; Cell Rep., 11 1018 4) Weiss et al. (2017), The STING agonist DMXAA triggers a cooperation between T lymphocytes and myeloid cells that leads to tumor regression; Oncoimmunology, 6 e1346765 5) Curran et al. (2016), STING Pathway Activation Stimulates Potent Immunity Against Acute Myeloid Leukemia; Cell Rep., 15 2357