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'''Zosuquidar''' is a [[Chemical compound|compound]] of [[antineoplastic]] [[drug]] candidates currently under development. It is now in "[[Phase 3]]" of clinical tests in the United States. Its action mechanism consists of the [[Enzyme inhibition|inhibition]] of [[P-glycoprotein]]s; other drugs with this mechanism include [[tariquidar]] and [[laniquidar]]. P-glycoproteins are [[protein]]s which |
'''Zosuquidar''' is a [[Chemical compound|compound]] of [[antineoplastic]] [[drug]] candidates currently under development. It is now in "[[Phase 3]]" of clinical tests in the United States. Its action mechanism consists of the [[Enzyme inhibition|inhibition]] of [[P-glycoprotein]]s; other drugs with this mechanism include [[tariquidar]] and [[laniquidar]]. P-glycoproteins are [[protein]]s which |
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convert the [[energy]] derived from the [[hydrolysis]] of [[Adenosine triphosphate|ATP]] to structural changes in protein molecules, in order to perform [[coupling]], thus discharging [[medicine]] from cells. If P-glycoprotein coded with the MDR1 [[gene]] manifests itself in [[cancer cell]]s, it discharges much of the antineoplastic drugs from the cells, making [[cancer cell]]s [[medicine tolerance|medicine tolerant]], and rendering antineoplastic drugs ineffective. This protein also manifests itself in normal organs not affected by the cancer (such as the liver, small intestine, and skin cells in blood vessels of the brain), and participates in the transportation of medicine. The compound Zosuquidar inhibits this P-glycoprotein, causing the cancer cells to lose their medicine tolerance, and making antineoplastic drugs effective. |
convert the [[energy]] derived from the [[hydrolysis]] of [[Adenosine triphosphate|ATP]] to structural changes in protein molecules, in order to perform [[coupling]], thus discharging [[medicine]] from cells. If P-glycoprotein coded with the MDR1 [[gene]] manifests itself in [[cancer cell]]s, it discharges much of the antineoplastic drugs from the cells, making [[cancer cell]]s [[medicine tolerance|medicine tolerant]], and rendering antineoplastic drugs ineffective. This protein also manifests itself in normal organs not affected by the cancer (such as the liver, small intestine, and skin cells in blood vessels of the brain), and participates in the transportation of medicine. The compound Zosuquidar inhibits this P-glycoprotein, causing the cancer cells to lose their medicine tolerance, and making antineoplastic drugs effective. |
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==Chemistry== |
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Reaction of [[dibenzosuberone]] with the difluorocarbene from [[chlorodifluoroacetate]] |
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affords the cyclopropyl adduct. Reduction of the ketone with borohydride proceeds to afford the derivative wherein the fused cyclpropyl and alcohol are on the same side of the seven-membered ring. The carbinol is then converted to the halide with thionyl chloride apparently with retention of configuration. Displacement with piperazine monoformamide leads to the alkylated product in which the groups are now anti. Hydrolysis of the formamide grouping then affords secondary |
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amine. In a convergent sequence, [[5-hydroxyquinoline]] is allowed to react with the tosyl derivative of chiral [[glycidol]]. |
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[[File:Zosuquidar.png|500px]] |
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{{Cite journal|doi=10.1016/0960-894X(95)00426-T|title=Methanodibenzosuberylpiperazines as potent multidrug resistance reversal agents|year=1995|last1=Pfister|first1=J|journal=Bioorganic & Medicinal Chemistry Letters|volume=5|pages=2473}} |
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==References== |
==References== |
Revision as of 18:15, 23 May 2010
Clinical data | |
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ATC code |
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CAS Number | |
PubChem CID | |
CompTox Dashboard (EPA) | |
ECHA InfoCard | 100.236.552 |
Chemical and physical data | |
Formula | C32H31F2N3O2 |
Molar mass | 527.61 g/mol g·mol−1 |
3D model (JSmol) | |
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Zosuquidar is a compound of antineoplastic drug candidates currently under development. It is now in "Phase 3" of clinical tests in the United States. Its action mechanism consists of the inhibition of P-glycoproteins; other drugs with this mechanism include tariquidar and laniquidar. P-glycoproteins are proteins which convert the energy derived from the hydrolysis of ATP to structural changes in protein molecules, in order to perform coupling, thus discharging medicine from cells. If P-glycoprotein coded with the MDR1 gene manifests itself in cancer cells, it discharges much of the antineoplastic drugs from the cells, making cancer cells medicine tolerant, and rendering antineoplastic drugs ineffective. This protein also manifests itself in normal organs not affected by the cancer (such as the liver, small intestine, and skin cells in blood vessels of the brain), and participates in the transportation of medicine. The compound Zosuquidar inhibits this P-glycoprotein, causing the cancer cells to lose their medicine tolerance, and making antineoplastic drugs effective.