1 ur studies demonstrated that doxorubicin and aclarubicin also significantly augmented rAAV transducti

2 r topoII catalytic inhibitors (merbarone and aclarubicin), as well as collaterally sensitive to the D

3                                 We show that aclarubicin effectively induces incorporation of exon 7

4 ect effect of widely used anticancer agents (aclarubicin, ICRF-193, VM26, doxorubicin, camptothecin,

5            Here, we report that the compound aclarubicin increases the retention of exon 7 into the S

6                             Aclacinomycin A (aclarubicin) is an anthracycline anticancer agent with d

7 that pretreatment of cells with merbarone or aclarubicin, known catalytic inhibitors of topo II, woul

8 icin, but not to other catalytic inhibitors, aclarubicin or SN-22995.

9     In addition, another anthracycline drug, aclarubicin, shows similar effects on enhancing nucleoso

10                           In the presence of aclarubicin, the differential sensitivity of BRCA-profic

11 he anthracycline derivatives doxorubicin and aclarubicin were chosen for analysis because they have b

12 dent sensitivity was confirmed by the use of aclarubicin, which is a catalytic inhibitor of topoisome

13 ger with duplex DNA, which is different from aclarubicin, which only inhibits Tdp1 with the double-st