Compounds > 4-(n-(s-glutathionylacetyl)amino)phenylarsenoxide

4-(n-(s-glutathionylacetyl)amino)phenylarsenoxide and dithiol

4-(n-(s-glutathionylacetyl)amino)phenylarsenoxide has been researched along with dithiol* in 2 studies

Other Studies

2 other study(ies) available for 4-(n-(s-glutathionylacetyl)amino)phenylarsenoxide and dithiol

Article	Year
Preparation of a Dithiol-Reactive Probe for PET Imaging of Cell Death. Methods in molecular biology (Clifton, N.J.), 2019, Volume: 1967 Conjugates of 4-(N-(S-glutathionylacetyl)amino)phenylarsonous acid (GSAO) with optical or radionuclide probes are able to image cell death in vivo. GSAO conjugates are retained in the cytosol of dying and dead cells via the formation of covalent bonds between the As(III) ion and the thiol groups of proximal cysteine residues. Here we describe the method for preparing a NODAGA-GSAO conjugate and its radiolabeling with gallium-68 ( Topics: Acetates; Animals; Arsenicals; Cell Death; Gallium Radioisotopes; Glutathione; Heterocyclic Compounds, 1-Ring; Humans; Positron-Emission Tomography; Radioisotopes; Radiopharmaceuticals; Toluene	2019
Para to ortho repositioning of the arsenical moiety of the angiogenesis inhibitor 4-(N-(S-glutathionylacetyl)amino)phenylarsenoxide results in a markedly increased cellular accumulation and antiproliferative activity. Cancer research, 2005, Dec-15, Volume: 65, Issue:24 The synthetic tripeptide arsenical 4-(N-(S-glutathionylacetyl)amino)p-phenylarsenoxide (p-GSAO) is an angiogenesis inhibitor that inactivates mitochondrial adenine nucleotide translocase (ANT) by cross-linking a pair of matrix-facing cysteine residues. This causes an increase in superoxide levels and proliferation arrest of endothelial cells followed by mitochondrial depolarization and apoptosis. p-GSAO induces proliferation arrest in endothelial cells and is a selective inhibitor of endothelial cells compared with tumor cells. An analogue of p-GSAO has been made in which the arsenical moiety is at the ortho instead of the para position on the phenyl ring. o-GSAO, like p-GSAO, bound to ANT in a dithiol-dependent manner but was approximately 8-fold more efficient than p-GSAO at triggering the mitochondria permeability transition in isolated mitochondria. o-GSAO was an approximately 50-fold more potent inhibitor of endothelial and tumor cell proliferation than p-GSAO. The mechanism of this effect was a consequence of approximately 300-fold faster rate of accumulation of o-GSAO in the cells, which is due, at least in part, to impaired export by the multidrug resistance-associated protein 1. Administration of o-GSAO to tumor-bearing mice delayed tumor growth by inhibiting tumor angiogenesis but there were side effects not observed with p-GSAO administration. Topics: Angiogenesis Inhibitors; Animals; Aorta; Arsenicals; Cattle; Cell Proliferation; Endothelium, Vascular; Female; Glutathione; Mice; Mice, Inbred BALB C; Mice, Nude; Mitochondria; Mitochondrial ADP, ATP Translocases; Multidrug Resistance-Associated Proteins; Neovascularization, Pathologic; Pancreatic Neoplasms; Stereoisomerism; Superoxides; Toluene	2005

Article

Year

Preparation of a Dithiol-Reactive Probe for PET Imaging of Cell Death.

Methods in molecular biology (Clifton, N.J.), 2019, Volume: 1967

Conjugates of 4-(N-(S-glutathionylacetyl)amino)phenylarsonous acid (GSAO) with optical or radionuclide probes are able to image cell death in vivo. GSAO conjugates are retained in the cytosol of dying and dead cells via the formation of covalent bonds between the As(III) ion and the thiol groups of proximal cysteine residues. Here we describe the method for preparing a NODAGA-GSAO conjugate and its radiolabeling with gallium-68 (

Topics: Acetates; Animals; Arsenicals; Cell Death; Gallium Radioisotopes; Glutathione; Heterocyclic Compounds, 1-Ring; Humans; Positron-Emission Tomography; Radioisotopes; Radiopharmaceuticals; Toluene

2019

Para to ortho repositioning of the arsenical moiety of the angiogenesis inhibitor 4-(N-(S-glutathionylacetyl)amino)phenylarsenoxide results in a markedly increased cellular accumulation and antiproliferative activity.

Cancer research, 2005, Dec-15, Volume: 65, Issue:24

The synthetic tripeptide arsenical 4-(N-(S-glutathionylacetyl)amino)p-phenylarsenoxide (p-GSAO) is an angiogenesis inhibitor that inactivates mitochondrial adenine nucleotide translocase (ANT) by cross-linking a pair of matrix-facing cysteine residues. This causes an increase in superoxide levels and proliferation arrest of endothelial cells followed by mitochondrial depolarization and apoptosis. p-GSAO induces proliferation arrest in endothelial cells and is a selective inhibitor of endothelial cells compared with tumor cells. An analogue of p-GSAO has been made in which the arsenical moiety is at the ortho instead of the para position on the phenyl ring. o-GSAO, like p-GSAO, bound to ANT in a dithiol-dependent manner but was approximately 8-fold more efficient than p-GSAO at triggering the mitochondria permeability transition in isolated mitochondria. o-GSAO was an approximately 50-fold more potent inhibitor of endothelial and tumor cell proliferation than p-GSAO. The mechanism of this effect was a consequence of approximately 300-fold faster rate of accumulation of o-GSAO in the cells, which is due, at least in part, to impaired export by the multidrug resistance-associated protein 1. Administration of o-GSAO to tumor-bearing mice delayed tumor growth by inhibiting tumor angiogenesis but there were side effects not observed with p-GSAO administration.

Topics: Angiogenesis Inhibitors; Animals; Aorta; Arsenicals; Cattle; Cell Proliferation; Endothelium, Vascular; Female; Glutathione; Mice; Mice, Inbred BALB C; Mice, Nude; Mitochondria; Mitochondrial ADP, ATP Translocases; Multidrug Resistance-Associated Proteins; Neovascularization, Pathologic; Pancreatic Neoplasms; Stereoisomerism; Superoxides; Toluene

2005