PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
21470995-7	2011	RESULTS: XL184 and vandetanib most effectively inhibited cell proliferation, RET autophosphorylation in combination with a reduction of RET expression, and ERK phosphorylation in MTC-TT and MZ-CRC-1, respectively.	vandetanib	19-29	EPH receptor B2	Homo sapiens	156-159	
34190716-6	2021	There was no statistically significant difference in ERK activation compared with placebo (P=0.45); however, ERK activation was reduced 74% compared with pretreatment biopsy with vandetinib treatment (P=0.005) without a significant reduction in the placebo group (-29%, P=0.55).	vandetanib	179-189	EPH receptor B2	Homo sapiens	109-112	
34190716-11	2021	In accordance with the investigational hypothesis, there was a nonsignificant trend with vandetanib treatment of reduction in p-ERK and increased effects in Ret expressing tumors.	vandetanib	89-99	EPH receptor B2	Homo sapiens	128-131	
28842826-10	2018	Vandetanib produces a significant decrease in vascular and neuronal densities and reduction in the expression of molecules involved in survival and proliferation processes such as phospho-Akt/Akt and phospho-Erk/Erk.	vandetanib	0-10	EPH receptor B2	Homo sapiens	208-211	
28842826-10	2018	Vandetanib produces a significant decrease in vascular and neuronal densities and reduction in the expression of molecules involved in survival and proliferation processes such as phospho-Akt/Akt and phospho-Erk/Erk.	vandetanib	0-10	EPH receptor B2	Homo sapiens	212-215	
20139705-0	2010	ZD6474, a dual tyrosine kinase inhibitor of EGFR and VEGFR-2, inhibits MAPK/ERK and AKT/PI3-K and induces apoptosis in breast cancer cells.	vandetanib	0-6	EPH receptor B2	Homo sapiens	76-79	
19318229-5	2009	ZD6474 and ZD1839 inhibited EGF-induced phosphorylation of EGFR, AKT and ERK, whereas VEGF-induced phosphorylation of VEGFR2 was completely inhibited with 0.1 microM SU11248.	vandetanib	0-6	EPH receptor B2	Homo sapiens	73-76