Hydroxylation at C-3′ of doxorubicin alters the selected phenotype of cellular drug resistance

Leonard Lothstein; Trevor W. Sweatman; Waldemar Priebe

doi:10.1016/0960-894X(95)00300-I

Hydroxylation at C-3′ of doxorubicin alters the selected phenotype of cellular drug resistance

Leonard Lothstein, Trevor W. Sweatman, Waldemar Priebe

Experimental Therapeutics

Research output: Contribution to journal › Article › peer-review

13 Scopus citations

Abstract

Hydroxylation at C-3′ of doxorubicin (DOX) yields the uncharged congener hydroxyrubicin, which circumvents P-glycoprotein-mediated drug resistance without loss of topoisomerase II inhibitory activity. Hydroxyrubicin-resistant cells exhibit a phenotype that is uniquely different from DOX resistance by expressing non-functional P-glycoprotein and hypersensitivity to anti-mitotic drugs.

Original language	English (US)
Pages (from-to)	1807-1812
Number of pages	6
Journal	Bioorganic and Medicinal Chemistry Letters
Volume	5
Issue number	16
DOIs	https://doi.org/10.1016/0960-894X(95)00300-I
State	Published - Aug 17 1995

ASJC Scopus subject areas

Biochemistry
Molecular Medicine
Molecular Biology
Pharmaceutical Science
Drug Discovery
Clinical Biochemistry
Organic Chemistry

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10.1016/0960-894X(95)00300-I

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title = "Hydroxylation at C-3′ of doxorubicin alters the selected phenotype of cellular drug resistance",

abstract = "Hydroxylation at C-3′ of doxorubicin (DOX) yields the uncharged congener hydroxyrubicin, which circumvents P-glycoprotein-mediated drug resistance without loss of topoisomerase II inhibitory activity. Hydroxyrubicin-resistant cells exhibit a phenotype that is uniquely different from DOX resistance by expressing non-functional P-glycoprotein and hypersensitivity to anti-mitotic drugs.",

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AU - Sweatman, Trevor W.

AU - Priebe, Waldemar

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AB - Hydroxylation at C-3′ of doxorubicin (DOX) yields the uncharged congener hydroxyrubicin, which circumvents P-glycoprotein-mediated drug resistance without loss of topoisomerase II inhibitory activity. Hydroxyrubicin-resistant cells exhibit a phenotype that is uniquely different from DOX resistance by expressing non-functional P-glycoprotein and hypersensitivity to anti-mitotic drugs.

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Hydroxylation at C-3′ of doxorubicin alters the selected phenotype of cellular drug resistance

Abstract

ASJC Scopus subject areas

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