Daunomycin (Daunorubicin) and Adriamycin

A, Dimarco

doi:10.1007/978-3-642-65806-8_31

Cited by 11 publications

(11 citation statements)

References 47 publications

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“…Control starting I11 (nonheated) consisted of 97% pharmacologically active drug and 3% aglycones. The aglycones are pharmacologically inactive (16). Compounds released from microspheres prepared a t 135-145" for 10 min consisted of 74% pharmacologically active I11 (identical Rf as starting 111) with the remaining 2696, consisting of aglycones.…”

Section: Results a N D Discussionmentioning

confidence: 99%

Magnetic Microspheres: Synthesis of a Novel Parenteral Drug Carrier

Widder

Flouret

Senyei

1979

Journal of Pharmaceutical Sciences

186

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Section: Results a N D Discussionmentioning

confidence: 99%

Magnetic Microspheres: Synthesis of a Novel Parenteral Drug Carrier

Widder

Flouret

Senyei

1979

Journal of Pharmaceutical Sciences

186

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“…Dox can interfere with the growth of cells by intercalating into the DNA strands, inhibiting further DNA and RNA biosynthesis, and eventually causing cell death. [4][5][6] This interference does not shorten cell cycle, but reduces cell amounts in cell cycle and accumulates block cells in a certain phase to cease cell cycle. 21 In this study, FCM of H22 cells was performed to test the possible changes in the cell cycle distribution and the percentage of apoptosis (hypodiploids) in response to the treatment, and the results were as shown in Table II.…”

Section: Fcm Analysismentioning

confidence: 99%

“…[1][2][3] It can interfere with the growth of cancer cells by intercalating into the DNA strands, inhibiting further DNA and RNA biosynthesis, and eventually causing cell death. [4][5][6] However, like many other drugs used to treat cancers, doxorubicin hydrochloride (Dox) by systematic administration has short circular retention time to reduce bioavailability and causes acute toxicity (e.g., hairloss, nausea, and vomiting) as well as irreversible cardiac toxicity, which restricts the repeated clinic administration.…”

Section: Introductionmentioning

confidence: 99%

Doxorubicin‐loaded ultrafine PEG‐PLA fiber mats against hepatocarcinoma

Jing

Song

et al. 2011

J of Applied Polymer Sci

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The purpose of this study was to evaluate both cytotoxicity in vitro and in vivo anticancer activities of implantable doxorubicin hydrocloride (Dox)-loaded diblock copolymer poly(ethylene glycol)-b-poly(L-lactic acid) (PEG-PLA) fiber mats (hereafter medicated mats). For in vitro evaluation, SMMC7721 cells were directly exposed to the medicated fiber mats, followed with MTT assay. For in vivo evaluation, the medicated mats were locally implanted into H22 tumor-bearing mice, followed with detection of Fas protein and flow cytometry analysis. The results showed that in vitro cytotoxicity of medicated fibers were sustained throughout the whole experiment process with the degradation of fiber matrix, while that of pure Dox was reduced in six days; medicated fibers had superior in vivo anticancer activities to pure Dox (P < 0.01). In conclusion, Doxorubicin-loaded PEG-PLA electrospun fiber mats had the properties of loading doxorubicin hydrochloride (Dox) and sustained release of Dox from medicated fiber matrix and apparently retained both in vitro cytotoxicity and in vivo anticancer activities in a long term. Medicated fiber mats are therefore suitable for a local therapy device.

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“…Both ADR and MITO intercalate into double stranded DNA and induce formation of DNA strand breaks (6,7). Further in vivo and in vitro cross resistance pattern of MITO has been shown in human and murine tumors displaying the pleiotropic or multidrug resistant (MDR) phenomenon (8)(9)(10), which is characterized by a simultaneous expression of resistance to a variety of functionally and structurally unrelated compounds (11,12).…”

mentioning

confidence: 99%

Evaluation of Quinidine Effect on the Antitumor Activity of Adriamycin and Mitoxantrone in Adriamycin-Sensitive and -Resistant P388 Leukemia Cells

Parekh¹,

Chitnis²

1990

Selective Cancer Therapeutics

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Utilizing the P388 murine leukemia cells sensitive (P388/S) and resistant (P388/ADR) to Adriamycin (ADR), we evaluated the effect of quinidine, an anti-arrhythmic agent, on the cytotoxic activity of ADR and Mitoxantrone (MITO), both in vitro as well as in vivo. 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. A dose dependent inhibition of 3H-thymidine and 3H-uridine incorporation was observed when the P388/S and P388/ADR cells were exposed to quinidine alone. 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. 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. 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. This enhanced intracellular accumulation of ADR in P388/ADR cells, explains the therapeutic efficacy of ADR and MITO in P388/ADR, both in vitro as well as in vivo. Results suggest the efficacy of quinidine to ameliorate the antitumor effects of ADR and MITO in drug resistant tumor cells.

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Daunomycin (Daunorubicin) and Adriamycin

Cited by 11 publications

References 47 publications

Magnetic Microspheres: Synthesis of a Novel Parenteral Drug Carrier

Magnetic Microspheres: Synthesis of a Novel Parenteral Drug Carrier

Doxorubicin‐loaded ultrafine PEG‐PLA fiber mats against hepatocarcinoma

Evaluation of Quinidine Effect on the Antitumor Activity of Adriamycin and Mitoxantrone in Adriamycin-Sensitive and -Resistant P388 Leukemia Cells

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