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CAS No. 72496-41-4
Pirarubicin is an anthracycline antibiotic, and also a DNA/RNA synthesis inhibitor by intercalating into DNA and interacts with topoisomerase II, used as an antineoplastic agent.
Selleck's Pirarubicin has been cited by 9 publications
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|Description||Pirarubicin is an anthracycline antibiotic, and also a DNA/RNA synthesis inhibitor by intercalating into DNA and interacts with topoisomerase II, used as an antineoplastic agent.|
Pirarubicin is rapidly taken up by M5076 cells and the intracellular concentration of pirarubicin reaches more than 2.5-fold that of doxorubicin. Pirarubicin is more effective than doxorubicin in terms of the 50% cell growth-inhibitory concentration in vitro.  Pirarubicin causes G0/G1 cell cycle arrest in MG-63 cells. Pirarubicin suppresses the expression of PCNA, cyclin D1, cyclin E and Bcl-2, and increases Bax expression in MG-63 cells.  Pirarubicin markedly relaxes contractions induced by noradrenaline (0.1 μM) in the aorta with endothelium, but not in that without endothelium. Pirarubicin-induced relaxation is inhibited by methylene blue (5 μM), hydroquinone (100 μM), phenidone (50 μM), haemoglobin (1 μM) and p-bromophenacyl bromide (50 μM), but not by indomethacin (25 μM).  Pirarubicin is approximately 2-5 times more potent than Adriamycin in SKUT1B, HEC1A, and BG1 cell lines. Pirarubicin also displays a reverse dose-response pattern of G2 block so that at high dose, cell cycle kinetics would mirror those of untreated controls. 
|In vivo||Pirarubicin reduces the tumor weight to 60% of the control level in M5076 solid tumor-bearing mice, although doxorubicin has no effect.  Pirarubicin and Epirubicin are effective against V x 2 tumor when injected via the hepatic intra-arterial (h.i.a.) route, the activity of Pirarubicin is stronger than that of Epirubicin. |
-  Sugiyama T, et al. Jpn J Cancer Res, 1999, 90(7), 775-780.
-  Liu SY, et al. Chemotherapy, 2010, 56(2), 101-107.
-  Hirano S, et al. J Pharm Pharmacol, 1991, 43(12), 848-854.
|In vitro||DMSO||7 mg/mL (11.15 mM)|
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