PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32598495-4	2020	Strong CYP3A inhibitor use resulted in an 82% increase in the area under the curve (AUC) and a 72% increase in the maximum concentration (Cmax ) of quizartinib.	quizartinib	148-159	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	7-12	
33415416-10	2021	Because concomitant strong cytochrome P450 3A (CYP3A) inhibitor use significantly increases quizartinib concentration, these results support the clinical recommendation of quizartinib dose reduction in patients concurrently receiving a strong CYP3A inhibitor.	quizartinib	92-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	27-45	
33415416-10	2021	Because concomitant strong cytochrome P450 3A (CYP3A) inhibitor use significantly increases quizartinib concentration, these results support the clinical recommendation of quizartinib dose reduction in patients concurrently receiving a strong CYP3A inhibitor.	quizartinib	92-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	47-52	
33415416-10	2021	Because concomitant strong cytochrome P450 3A (CYP3A) inhibitor use significantly increases quizartinib concentration, these results support the clinical recommendation of quizartinib dose reduction in patients concurrently receiving a strong CYP3A inhibitor.	quizartinib	172-183	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	47-52	
32598495-10	2020	Only concomitant use of strong CYP3A inhibitors had a clinically meaningful effect on quizartinib and AC886 PK exposure.	quizartinib	86-97	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	31-36	
32683457-5	2020	CYP3A4 is the main enzyme responsible for SMIs metabolism, and strong CYP3A4 inhibitors, such azoles, could increase drug exposure and toxicity; therefore dose adjustments (venetoclax, quizartinib, and ivosidenib) or alternative therapies or close monitoring (glasdegib, midostaurin, and gilteritinib) are recommended.	quizartinib	185-196	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6	
32683457-5	2020	CYP3A4 is the main enzyme responsible for SMIs metabolism, and strong CYP3A4 inhibitors, such azoles, could increase drug exposure and toxicity; therefore dose adjustments (venetoclax, quizartinib, and ivosidenib) or alternative therapies or close monitoring (glasdegib, midostaurin, and gilteritinib) are recommended.	quizartinib	185-196	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	70-76	
31173645-0	2019	Effects of CYP3A inhibitors on the pharmacokinetics of quizartinib, a potent and selective FLT3 inhibitor, and its active metabolite.	quizartinib	55-66	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	11-16	
31173645-11	2019	CONCLUSIONS: These results suggest reducing the dose of quizartinib when coadministered with a strong CYP3A inhibitor, but not with a moderate or weak CYP3A inhibitor.	quizartinib	56-67	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	102-107	
30898762-6	2019	We found that CYP3A4 plays a major role in BMSC-mediated inhibition in the activity of 3 different FLT3 TKIs (sorafenib, quizartinib, and gilteritinib) against FLT3/ITD acute myeloid leukemia (AML).	quizartinib	121-132	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	14-20