PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33878513-5	2021	RESULTS: We found that CUDC-101 and gemcitabine interacted synergistically to reduce NHL cell viability and to induce the apoptotic death of these cells via the EGFR/ PI3K/Akt and Erk pathways, which were regulated by HDAC signaling pathways.	7-(4-(3-ethynylphenylamino)-7-methoxyquinazolin-6-yloxy)-N-hydroxyheptanamide	23-31	AKT serine/threonine kinase 1	Homo sapiens	172-175	
30662800-5	2018	In addition, CUDC-101 enhanced gemcitabine-induced apoptosis via inhibited PI3K/Akt/mTOR and Erk pathway activation, as indicated by the phosphorylation status of Akt, 4EBP1, S6 and Erk.	7-(4-(3-ethynylphenylamino)-7-methoxyquinazolin-6-yloxy)-N-hydroxyheptanamide	13-21	AKT serine/threonine kinase 1	Homo sapiens	163-166	
20388807-4	2010	Because of its integrated histone deacetylase inhibition, CUDC-101 synergistically blocked key regulators of EGFR/HER2 signaling pathways, also attenuating multiple compensatory pathways, such as AKT, HER3, and MET, which enable cancer cells to escape the effects of conventional EGFR/HER2 inhibitors.	7-(4-(3-ethynylphenylamino)-7-methoxyquinazolin-6-yloxy)-N-hydroxyheptanamide	58-66	AKT serine/threonine kinase 1	Homo sapiens	196-199	
30662800-5	2018	In addition, CUDC-101 enhanced gemcitabine-induced apoptosis via inhibited PI3K/Akt/mTOR and Erk pathway activation, as indicated by the phosphorylation status of Akt, 4EBP1, S6 and Erk.	7-(4-(3-ethynylphenylamino)-7-methoxyquinazolin-6-yloxy)-N-hydroxyheptanamide	13-21	AKT serine/threonine kinase 1	Homo sapiens	80-83