PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34099830-1	2021	Recent studies suggested that ibrutinib, a Bruton tyrosine kinase (BTK) inhibitor, developed for the treatment of chronic lymphocytic leukemia, may prevent NLRP3 inflammasome activation in macrophages, IL-1beta secretion and subsequent development of inflammation and organ fibrosis.	ibrutinib	30-39	NLR family pyrin domain containing 3	Homo sapiens	156-161	
29383704-4	2018	We have recently identified platelet TLR4, NLRP3, and Bruton tyrosine kinase (BTK) as critical regulators of platelet aggregation and thrombus formation, suggesting that the BTK inhibitor ibrutinib is a potential therapeutic target.	ibrutinib	188-197	NLR family pyrin domain containing 3	Homo sapiens	43-48	
28216434-6	2017	RESULTS: Here we show that BTK is a critical regulator of NLRP3 inflammasome activation: pharmacologic (using the US Food and Drug Administration-approved inhibitor ibrutinib) and genetic (in patients with XLA and Btk knockout mice) BTK ablation in primary immune cells led to reduced IL-1beta processing and secretion in response to nigericin and the Staphylococcus aureus toxin leukocidin AB (LukAB).	ibrutinib	165-174	NLR family pyrin domain containing 3	Homo sapiens	58-63