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Last Updated: 3 years ago

Possible Interaction: Quinidine and Doxorubicin Hydrochloride

Research Papers that Mention the Interaction

Non-toxic concentrations (5-20 microM) of chloroquine, quinine, quinidine , and primaquine potentiated the toxicity of doxorubicin in a concentration-dependent manner.
Biochemical pharmacology  •  2000  |  View Paper
The result demonstrated that verapamil, quinidine , tamoxifen, and oligomycin had an additive effect on the cytotoxicity of adriamycin and vinblastine against RCC8701 and RCC8701/ADR800 tumor cells.
Urology  •  1999  |  View Paper
Verapamil and quinidine lowered the IC50 values of doxorubicin for MDR1-positive cell lines.
Journal of the National Cancer Institute  •  1994  |  View Paper
Results highlight the utility of quinidine as a drug response modulator in a schedule-dependent manner to potentiate the cytotoxicity of ADR and MITO and warrants further studies into a possible role of quinidine to increase the chemotherapeutic efficacy of antineoplastic drugs in the clinics.
Neoplasma  •  1990  |  View Paper
The enhancing effect of quinidine (7.5 micrograms/mL) on sensitivity to ADR was statistically significant only in the group with high MDR1 RNA levels.
Journal of the National Cancer Institute  •  1989  |  View Paper
Chromanol, quinidine , and erythromycin exerted concentration-dependent increases in relaxation time, doxorubicin decreases in contractile force.
Circulation research  •  2010  |  View Paper
In the presence of quinidine , the biliary excretion of doxorubicin was reduced significantly; however, doxorubicinol recovery in bile was not altered.
Quinidine and GF120918 inhibit the transport of P-gp substrates, including doxorubicin.
Quinidine was associated with a decrease in doxorubicin canalicular egress, doxorubicinol formation, and other doxorubicinol pathways.
Cancer research  •  1998  |  View Paper
Substances that are substrates for P-glycoprotein, such as verapamil, vinblastine, vincristine and quinidine , significantly increased doxorubicin concentrations in LLC-PK1 cells.
The Journal of pharmacology and experimental therapeutics  •  1998  |  View Paper
A non-toxic concentration of quinidine (5 microM) enhanced the DNA biosynthesis inhibition induced by ADR (55 to 65%) and MITO (37 to 44%) in P388/ADR cells, indicating reversal of resistance, while in P388/S cells only a minimal increase in DNA biosynthesis inhibition was observed.
Quinidine enhanced the cytotoxicity of both ADR and MITO in P388/S and P388/ADR cells, as assessed by the decrease in color intensity of formazan crystal in the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay.
Quinidine increased the cellular levels of ADR by 53 to 126% in P388/ADR cells in vitro, but failed to indicate such elevated levels of cellular ADR in P388/S cells.
The combination of quinidine at doses of 50 to 100 mg/kg significantly potentiated the antitumor activity of ADR and MITO in P388/ADR bearing mice, whereas the potentiation of ADR and MITO antitumor response was lower in P388/S bearing mice.
Selective cancer therapeutics  •  1990  |  View Paper
The antiarrhythmic drug, quinidine , and the detergent, Tween 80, also potentiated ADR activity in P388R cells to the same extent as VER.
Cancer research  •  1986  |  View Paper
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