Pirarubicin (Theprubicin) is an anthracycline antibiotic. It is also a DNA/RNA synthesis inhibitor that intercalates into DNA and interacts with topoisomerase II, utilized 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. [1] 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. [2] 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). [3] 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. [4]

Pirarubicin reduces the tumor weight to 60% of the control level in M5076 solid tumor-bearing mice, although doxorubicin has no effect. [1] 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. [5]