Exact Mass: 943.3626
Exact Mass Matches: 943.3626
Found 10 metabolites which its exact mass value is equals to given mass value 943.3626
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within given mass tolerance error 0.05 dalton. Try search metabolite list with more accurate mass tolerance error
0.01 dalton.
10-Deacetyltaxol 7-Xyloside
10-Deacetyl-7-xylosyl paclitaxel is a Paclitaxel (a microtubule stabilizing agent; enhances tubulin polymerization) derivative with improved pharmacological features. IC50 value: Target: Microtubule inhibitor 10-Deacetyl-7-xylosyl paclitaxel induced mitotic cell cycle arrest and apoptosis as measured by flow cytometry, DNA laddering, and transmission electron microscopy. Pro-apoptotic Bax and Bad protein expression was up-regulated and anti-apoptotic Bcl-2 and Bcl-XL expression down-regulated, which lead to a disturbance of the mitochondrial membrane permeability and to the activation of caspase-9. In turn, caspase-9 activated downstream caspases-3 and -6, but not caspase-8. Bid was also activated by caspase-3. Reversely, treatment with a caspase-10-specific inhibitor could not protect PC-3 cells from 7-xylosyl-10-deacetyl-paclitaxel-triggered apoptosis. Moreover, 7-xylosyl-10-deacetylpaclitaxel had no effect on the expression of CD95 and NF-kappaB proteins, indicating that apoptosis was induced through the mitochondrial-dependent pathway in PC-3 cells. 10-Deacetyl-7-xylosyl paclitaxel is a Paclitaxel (a microtubule stabilizing agent; enhances tubulin polymerization) derivative with improved pharmacological features. IC50 value: Target: Microtubule inhibitor 10-Deacetyl-7-xylosyl paclitaxel induced mitotic cell cycle arrest and apoptosis as measured by flow cytometry, DNA laddering, and transmission electron microscopy. Pro-apoptotic Bax and Bad protein expression was up-regulated and anti-apoptotic Bcl-2 and Bcl-XL expression down-regulated, which lead to a disturbance of the mitochondrial membrane permeability and to the activation of caspase-9. In turn, caspase-9 activated downstream caspases-3 and -6, but not caspase-8. Bid was also activated by caspase-3. Reversely, treatment with a caspase-10-specific inhibitor could not protect PC-3 cells from 7-xylosyl-10-deacetyl-paclitaxel-triggered apoptosis. Moreover, 7-xylosyl-10-deacetylpaclitaxel had no effect on the expression of CD95 and NF-kappaB proteins, indicating that apoptosis was induced through the mitochondrial-dependent pathway in PC-3 cells.
10-Deacetyl-7-xylosyl Paclitaxel
10-Deacetyl-7-xylosyl paclitaxel is a Paclitaxel (a microtubule stabilizing agent; enhances tubulin polymerization) derivative with improved pharmacological features. IC50 value: Target: Microtubule inhibitor 10-Deacetyl-7-xylosyl paclitaxel induced mitotic cell cycle arrest and apoptosis as measured by flow cytometry, DNA laddering, and transmission electron microscopy. Pro-apoptotic Bax and Bad protein expression was up-regulated and anti-apoptotic Bcl-2 and Bcl-XL expression down-regulated, which lead to a disturbance of the mitochondrial membrane permeability and to the activation of caspase-9. In turn, caspase-9 activated downstream caspases-3 and -6, but not caspase-8. Bid was also activated by caspase-3. Reversely, treatment with a caspase-10-specific inhibitor could not protect PC-3 cells from 7-xylosyl-10-deacetyl-paclitaxel-triggered apoptosis. Moreover, 7-xylosyl-10-deacetylpaclitaxel had no effect on the expression of CD95 and NF-kappaB proteins, indicating that apoptosis was induced through the mitochondrial-dependent pathway in PC-3 cells. 10-Deacetyl-7-xylosyl paclitaxel is a Paclitaxel (a microtubule stabilizing agent; enhances tubulin polymerization) derivative with improved pharmacological features. IC50 value: Target: Microtubule inhibitor 10-Deacetyl-7-xylosyl paclitaxel induced mitotic cell cycle arrest and apoptosis as measured by flow cytometry, DNA laddering, and transmission electron microscopy. Pro-apoptotic Bax and Bad protein expression was up-regulated and anti-apoptotic Bcl-2 and Bcl-XL expression down-regulated, which lead to a disturbance of the mitochondrial membrane permeability and to the activation of caspase-9. In turn, caspase-9 activated downstream caspases-3 and -6, but not caspase-8. Bid was also activated by caspase-3. Reversely, treatment with a caspase-10-specific inhibitor could not protect PC-3 cells from 7-xylosyl-10-deacetyl-paclitaxel-triggered apoptosis. Moreover, 7-xylosyl-10-deacetylpaclitaxel had no effect on the expression of CD95 and NF-kappaB proteins, indicating that apoptosis was induced through the mitochondrial-dependent pathway in PC-3 cells.
10-Deacetyl-7-xylosylpaclitaxel
10-Deacetyl-7-xylosyl paclitaxel is a Paclitaxel (a microtubule stabilizing agent; enhances tubulin polymerization) derivative with improved pharmacological features. IC50 value: Target: Microtubule inhibitor 10-Deacetyl-7-xylosyl paclitaxel induced mitotic cell cycle arrest and apoptosis as measured by flow cytometry, DNA laddering, and transmission electron microscopy. Pro-apoptotic Bax and Bad protein expression was up-regulated and anti-apoptotic Bcl-2 and Bcl-XL expression down-regulated, which lead to a disturbance of the mitochondrial membrane permeability and to the activation of caspase-9. In turn, caspase-9 activated downstream caspases-3 and -6, but not caspase-8. Bid was also activated by caspase-3. Reversely, treatment with a caspase-10-specific inhibitor could not protect PC-3 cells from 7-xylosyl-10-deacetyl-paclitaxel-triggered apoptosis. Moreover, 7-xylosyl-10-deacetylpaclitaxel had no effect on the expression of CD95 and NF-kappaB proteins, indicating that apoptosis was induced through the mitochondrial-dependent pathway in PC-3 cells. 10-Deacetyl-7-xylosyl paclitaxel is a Paclitaxel (a microtubule stabilizing agent; enhances tubulin polymerization) derivative with improved pharmacological features. IC50 value: Target: Microtubule inhibitor 10-Deacetyl-7-xylosyl paclitaxel induced mitotic cell cycle arrest and apoptosis as measured by flow cytometry, DNA laddering, and transmission electron microscopy. Pro-apoptotic Bax and Bad protein expression was up-regulated and anti-apoptotic Bcl-2 and Bcl-XL expression down-regulated, which lead to a disturbance of the mitochondrial membrane permeability and to the activation of caspase-9. In turn, caspase-9 activated downstream caspases-3 and -6, but not caspase-8. Bid was also activated by caspase-3. Reversely, treatment with a caspase-10-specific inhibitor could not protect PC-3 cells from 7-xylosyl-10-deacetyl-paclitaxel-triggered apoptosis. Moreover, 7-xylosyl-10-deacetylpaclitaxel had no effect on the expression of CD95 and NF-kappaB proteins, indicating that apoptosis was induced through the mitochondrial-dependent pathway in PC-3 cells.
10-DEACETYL-7-XYLOTAXOL
10-Deacetyl-7-xylosyl paclitaxel is a Paclitaxel (a microtubule stabilizing agent; enhances tubulin polymerization) derivative with improved pharmacological features. IC50 value: Target: Microtubule inhibitor 10-Deacetyl-7-xylosyl paclitaxel induced mitotic cell cycle arrest and apoptosis as measured by flow cytometry, DNA laddering, and transmission electron microscopy. Pro-apoptotic Bax and Bad protein expression was up-regulated and anti-apoptotic Bcl-2 and Bcl-XL expression down-regulated, which lead to a disturbance of the mitochondrial membrane permeability and to the activation of caspase-9. In turn, caspase-9 activated downstream caspases-3 and -6, but not caspase-8. Bid was also activated by caspase-3. Reversely, treatment with a caspase-10-specific inhibitor could not protect PC-3 cells from 7-xylosyl-10-deacetyl-paclitaxel-triggered apoptosis. Moreover, 7-xylosyl-10-deacetylpaclitaxel had no effect on the expression of CD95 and NF-kappaB proteins, indicating that apoptosis was induced through the mitochondrial-dependent pathway in PC-3 cells. 10-Deacetyl-7-xylosyl paclitaxel is a Paclitaxel (a microtubule stabilizing agent; enhances tubulin polymerization) derivative with improved pharmacological features. IC50 value: Target: Microtubule inhibitor 10-Deacetyl-7-xylosyl paclitaxel induced mitotic cell cycle arrest and apoptosis as measured by flow cytometry, DNA laddering, and transmission electron microscopy. Pro-apoptotic Bax and Bad protein expression was up-regulated and anti-apoptotic Bcl-2 and Bcl-XL expression down-regulated, which lead to a disturbance of the mitochondrial membrane permeability and to the activation of caspase-9. In turn, caspase-9 activated downstream caspases-3 and -6, but not caspase-8. Bid was also activated by caspase-3. Reversely, treatment with a caspase-10-specific inhibitor could not protect PC-3 cells from 7-xylosyl-10-deacetyl-paclitaxel-triggered apoptosis. Moreover, 7-xylosyl-10-deacetylpaclitaxel had no effect on the expression of CD95 and NF-kappaB proteins, indicating that apoptosis was induced through the mitochondrial-dependent pathway in PC-3 cells.
6-sulfanylhexyl alpha-D-mannopyranosyl-(1->2)-alpha-D-mannopyranosyl-(1->2)-alpha-D-mannopyranosyl-(1->6)-alpha-D-mannopyranosyl-(1->4)-2-amino-2-deoxy-beta-D-glucopyranoside
7-(beta-xylosyl)-10-deacetyltaxol
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