PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33750129-2	2021	However, recent experimental evidence suggested that the inhibition and/or depletion of topoisomerase IIbeta (TOP2B) by dexrazoxane could be cardioprotective.	Dexrazoxane	120-131	DNA topoisomerase II beta	Homo sapiens	110-115	
33750129-3	2021	Hence, we evaluated a series of dexrazoxane analogues and found that their cardioprotective activity strongly correlated with their interaction with TOP2B in cardiomyocytes, but was independent of their iron chelation ability.	Dexrazoxane	32-43	DNA topoisomerase II beta	Homo sapiens	149-154	
34551586-0	2021	Clinically Translatable Prevention of Anthracycline Cardiotoxicity by Dexrazoxane Is Mediated by Topoisomerase II Beta and Not Metal Chelation.	Dexrazoxane	70-81	DNA topoisomerase II beta	Homo sapiens	97-118	
34551586-9	2021	DEX, but not ADR-925, inhibited and depleted TOP2B and prevented daunorubicin-induced genotoxic damage.	Dexrazoxane	0-3	DNA topoisomerase II beta	Homo sapiens	45-50	
34551586-10	2021	TOP2B dependency of the cardioprotective effects was probed and supported by experiments with diastereomers of a new DEX derivative.	Dexrazoxane	117-120	DNA topoisomerase II beta	Homo sapiens	0-5	
30792806-1	2018	Following systematic scrutiny of the evidence in support of the hypothesis that the cardioprotective mechanism of action of dexrazoxane is mediated by a "depletion" or "downregulation" of Top2beta protein levels in heart tissue, the author concludes that this hypothesis is untenable.	Dexrazoxane	124-135	DNA topoisomerase II beta	Homo sapiens	188-196