PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34169526-6	2021	Ruxolitinib PK was adequately described with a 2-compartment model with first-order absorption and elimination with distribution volumes normalized to mean body weight (91.5 kg) and a separate typical CL for participants administered efavirenz (a known CYP3A4 inducer).	ruxolitinib	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	253-259	
34505930-12	2021	CONCLUSION: Ruxolitinib exposure is increased in GvHD patients in comparison to myelofibrosis patients due to reduced clearance and comedication with CYP3A4 or CYP2C9 inhibitors.	ruxolitinib	12-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	150-156	
30069628-10	2018	The metabolization of ruxolitinib through CYP3A4 needs to be considered particularly if co-administered with potent CYP3A4 inhibitors.	ruxolitinib	22-33	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-48	
30069628-10	2018	The metabolization of ruxolitinib through CYP3A4 needs to be considered particularly if co-administered with potent CYP3A4 inhibitors.	ruxolitinib	22-33	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	116-122	
30645821-14	2016	Ruxolitinib is mainly metabolised by cytochrome P450 isoenzymes CYP3A4 and CYP2C9, creating a risk of multiple drug interactions.	ruxolitinib	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	64-70	
25670523-2	2015	A ruxolitinib physiologically based pharmacokinetic model was constructed using all baseline PK data in healthy subjects, and verified by retrospective predictions of observed drug-drug interactions with rifampin (a potent CYP3A4 inducer), ketoconazole (a potent CYP3A4 reversible inhibitor) and erythromycin (a moderate time-dependent inhibitor of CYP3A4).	ruxolitinib	2-13	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	223-229	
25670523-2	2015	A ruxolitinib physiologically based pharmacokinetic model was constructed using all baseline PK data in healthy subjects, and verified by retrospective predictions of observed drug-drug interactions with rifampin (a potent CYP3A4 inducer), ketoconazole (a potent CYP3A4 reversible inhibitor) and erythromycin (a moderate time-dependent inhibitor of CYP3A4).	ruxolitinib	2-13	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	263-269	
25670523-2	2015	A ruxolitinib physiologically based pharmacokinetic model was constructed using all baseline PK data in healthy subjects, and verified by retrospective predictions of observed drug-drug interactions with rifampin (a potent CYP3A4 inducer), ketoconazole (a potent CYP3A4 reversible inhibitor) and erythromycin (a moderate time-dependent inhibitor of CYP3A4).	ruxolitinib	2-13	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	263-269	
25670523-3	2015	The model prospectively predicts that 100-200 mg daily dose of fluconazole, a dual inhibitor of CYP3A4 and 2C9, would increase ruxolitinib plasma concentration area under the curve by ~two-fold, and that as a perpetrator, ruxolitinib is highly unlikely to have any discernible effect on digoxin, a sensitive P-glycoprotein substrate.	ruxolitinib	127-138	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	96-110	
24756798-6	2014	The metabolization of ruxolitinib through CYP3A4 needs to be considered particularly if co-administered with potent CYP3A4 inhibitors.	ruxolitinib	22-33	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-48	
24756798-6	2014	The metabolization of ruxolitinib through CYP3A4 needs to be considered particularly if co-administered with potent CYP3A4 inhibitors.	ruxolitinib	22-33	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	116-122	
21602517-1	2012	Ruxolitinib, a selective Janus kinase (JAK) 1&2 inhibitor in development for the treatment of myeloproliferative neoplasms, is primarily metabolized by CYP3A4.	ruxolitinib	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	156-162	
21602517-2	2012	The effects of inhibition or induction of CYP3A4 on single oral dose ruxolitinib pharmacokinetics (PK) and pharmacodynamics (PD) were evaluated in healthy volunteers.	ruxolitinib	69-80	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-48	
21602517-3	2012	Coadministration of ketoconazole (a potent CYP3A4 inhibitor) and erythromycin (a moderate CYP3A4 inhibitor) increased total ruxolitinib plasma exposure (AUC(0- )) by 91% and 27%, respectively, and ruxolitinib PD, as measured by the inhibition of interleukin (IL)-6-stimulated STAT3 phosphorylation in whole blood, was generally consistent with the PK observed.	ruxolitinib	124-135	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	43-49	
21602517-4	2012	Pretreatment with rifampin, a potent CYP3A4 inducer, decreased ruxolitinib AUC(0- ) by 71% while resulting in only a 10% decrease in the overall PD activity.	ruxolitinib	63-74	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	37-43	
21602517-6	2012	The collective PK/PD data suggest that starting doses of ruxolitinib should be reduced by 50% if coadministered with a potent CYP3A4 inhibitor, whereas adjustments in ruxolitinib starting doses may not be needed when coadministered with inducers or mild/moderate inhibitors of CYP3A4.	ruxolitinib	57-68	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	126-132	
32234672-6	2020	IL-22 was next found to activate the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) 3 pathway, whose inhibition by the JAK inhibitor ruxolitinib fully prevented the IL-22-mediated CYP3A4, CYP2B6 and NTCP repression in HepaRG cells.	ruxolitinib	161-172	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	208-214	
31941838-9	2020	Furthermore, miR-543 upregulation promotes the expression of genes related to drug metabolism, including CYP3A4, which is involved in ruxolitinib metabolism.	ruxolitinib	134-145	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	105-111	
31145690-0	2019	Drug-drug interaction (DDI) assessments of ruxolitinib, a dual substrate of CYP3A4 and CYP2C9, using a verified physiologically based pharmacokinetic (PBPK) model to support regulatory submissions.	ruxolitinib	43-54	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	76-82	
31145690-1	2019	Ruxolitinib is mainly metabolized by cytochrome P450 (CYP) enzymes CYP3A4 and CYP2C9 followed by minor contributions of other hepatic CYP enzymes in vitro.	ruxolitinib	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	67-73	
31145690-2	2019	A physiologically based pharmacokinetic (PBPK) model was established to evaluate the changes in the ruxolitinib systemic exposures with co-administration of CYP3A4 and CYP2C9 perpetrators.	ruxolitinib	100-111	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	157-163	
31145690-3	2019	The fractions metabolized in the liver via oxidation by CYP enzymes (fm,CYP3A4 = 0.75, fm,CYP2C9 = 0.19, and fm,CYPothers = 0.06) for an initial ruxolitinib model based on in vitro data were optimized (0.43, 0.56, and 0.01, respectively) using the observed exposure changes of ruxolitinib (10 mg) with co-administered ketoconazole (200 mg).	ruxolitinib	145-156	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	72-78	
31145690-7	2019	The estimated AUC ratios of ruxolitinib by co-administration of the moderate CYP3A4 inhibitor erythromycin (500 mg) and the strong CYP3A4 inducer rifampicin (600 mg) were within a 20% error compared with the clinically observed values.	ruxolitinib	28-39	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	77-83	
31145690-7	2019	The estimated AUC ratios of ruxolitinib by co-administration of the moderate CYP3A4 inhibitor erythromycin (500 mg) and the strong CYP3A4 inducer rifampicin (600 mg) were within a 20% error compared with the clinically observed values.	ruxolitinib	28-39	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	131-137	
31145690-9	2019	Furthermore, an AUC increase of ruxolitinib in the absence or presence of the dual CYP3A4 and CYP2C9 inhibitor fluconazole (100-400 mg) was prospectively estimated to be 1.94- to 4.31-fold.	ruxolitinib	32-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	83-89	
31145690-11	2019	A ruxolitinib PBPK model with optimized fm,CYP3A4 and fm,CYP2C9 was established to evaluate victim DDI risks.	ruxolitinib	2-13	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	43-49	
24589536-5	2014	Ruxolitinib is primarily metabolized by the cytochrome P-450 (CYP) 3A4 isoenzyme system; therefore, if concomitant use with a strong CYP3A4 inhibitor is unavoidable, an initial dosage reduction is warranted.	ruxolitinib	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	44-70	
24589536-5	2014	Ruxolitinib is primarily metabolized by the cytochrome P-450 (CYP) 3A4 isoenzyme system; therefore, if concomitant use with a strong CYP3A4 inhibitor is unavoidable, an initial dosage reduction is warranted.	ruxolitinib	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	133-139