PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
20356791-3	2010	A well known hypolipidemic drug, bezafibrate, has been tested to stimulate expression of mutated gene for CPT 2, but it may represent a challenge for a series of other fatty acid mitochondrial disorders to restore the capacity for normal long-chain fatty oxidation in muscle.	Bezafibrate	33-44	carnitine palmitoyltransferase 2	Homo sapiens	106-111	
21816645-5	2011	L-carnitine, a substrate of CPT II, boosted the effects of bezafibrate on cellular ATP levels in WT and IAE fibroblasts, even in severe IAE fibroblasts with thermolabile compound variations of F352C+V368I at 37 C and 41 C. The results suggest the potential usefulness of bezafibrate for the treatment of IAE.	Bezafibrate	59-70	carnitine palmitoyltransferase 2	Homo sapiens	28-34	
21816645-5	2011	L-carnitine, a substrate of CPT II, boosted the effects of bezafibrate on cellular ATP levels in WT and IAE fibroblasts, even in severe IAE fibroblasts with thermolabile compound variations of F352C+V368I at 37 C and 41 C. The results suggest the potential usefulness of bezafibrate for the treatment of IAE.	Bezafibrate	271-282	carnitine palmitoyltransferase 2	Homo sapiens	28-34	
18033029-5	2007	The demonstration that fibrates can induce correction of carnitine palmitoyl-transferase II deficiency in patients cells, lead to the development of an open-labelled therapeutic trial with bezafibrate in patients with CPTII deficiency, which is actually ongoing.	Bezafibrate	189-200	carnitine palmitoyltransferase 2	Homo sapiens	218-223	
12840153-5	2003	Data obtained show that bezafibrate treatment of mild-type CPTII-deficient cells resulted in a time- and dose- dependent increase in CPTII mRNA (from +47% to +66%) and residual enzyme activity (from +54% to 135%), and led to normalization of 3H-palmitate and 3H-myristate cellular oxidation rates.	Bezafibrate	24-35	carnitine palmitoyltransferase 2	Homo sapiens	59-64	
12840153-5	2003	Data obtained show that bezafibrate treatment of mild-type CPTII-deficient cells resulted in a time- and dose- dependent increase in CPTII mRNA (from +47% to +66%) and residual enzyme activity (from +54% to 135%), and led to normalization of 3H-palmitate and 3H-myristate cellular oxidation rates.	Bezafibrate	24-35	carnitine palmitoyltransferase 2	Homo sapiens	133-138