PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
32665925-3	2020	Females and patients with sepsis, impaired kidney and/or liver function, malnutrition, advanced age, congenital 5-oxoprolinase deficiency and supratherapeutic acetaminophen and flucloxacillin dosage are associated with increased risk.	Floxacillin	177-191	5-oxoprolinase, ATP-hydrolysing	Homo sapiens	112-126
33841856-0	2021	Acute kidney injury following prophylactic flucloxacillin and gentamicin in primary hip and knee arthroplasty.	Floxacillin	43-57	hedgehog interacting protein	Homo sapiens	84-87
33841856-8	2021	Conclusions: Our findings suggest that the use of prophylactic high-dose flucloxacillin and gentamicin should be used with caution in patients undergoing primary hip or knee arthroplasty without a clear advantage in reducing surgical site infections given the association with increased rates of AKI.	Floxacillin	73-87	hedgehog interacting protein	Homo sapiens	162-165
30661239-2	2019	HLA-B*57:01 is an established genetic risk factor for flucloxacillin DILI.	Floxacillin	54-68	major histocompatibility complex, class I, B	Homo sapiens	0-5
32130375-0	2020	Flucloxacillin-Induced Hepatotoxicity - Association with HLA-B*5701.	Floxacillin	0-14	major histocompatibility complex, class I, B	Homo sapiens	57-62
32130375-13	2020	The authors present this case to remind the possibility of moderate/severe drug-induced liver injury to flucloxacillin, an antibiotic commonly used in clinical practice and association with the HLA-B * 5701 allele reported in the literature.	Floxacillin	104-118	major histocompatibility complex, class I, B	Homo sapiens	194-199
30538582-16	2018	Clinical risk factors for flucloxacillin-induced DILI could be used to indicate whom to test for HLA-B*57:01 before treatment.	Floxacillin	26-40	major histocompatibility complex, class I, B	Homo sapiens	97-102
31288895-7	2019	These results revealed that flucloxacillin might have weak pharmacokinetic interactions on midazolam metabolized into 1"-hydroxy midazolam, indicating that there was weak induction to CYP3A by flucloxacillin and that there was at least 30.80 % of metabolic behaviour in change with bioavailability decreased by 38.11 % that took effect to flucloxacillin metabolism for liver injury in CPY3A4 poor metabolic polymorphisms.	Floxacillin	28-42	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	184-189
31288895-7	2019	These results revealed that flucloxacillin might have weak pharmacokinetic interactions on midazolam metabolized into 1"-hydroxy midazolam, indicating that there was weak induction to CYP3A by flucloxacillin and that there was at least 30.80 % of metabolic behaviour in change with bioavailability decreased by 38.11 % that took effect to flucloxacillin metabolism for liver injury in CPY3A4 poor metabolic polymorphisms.	Floxacillin	193-207	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	184-189
31288895-7	2019	These results revealed that flucloxacillin might have weak pharmacokinetic interactions on midazolam metabolized into 1"-hydroxy midazolam, indicating that there was weak induction to CYP3A by flucloxacillin and that there was at least 30.80 % of metabolic behaviour in change with bioavailability decreased by 38.11 % that took effect to flucloxacillin metabolism for liver injury in CPY3A4 poor metabolic polymorphisms.	Floxacillin	193-207	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	184-189
30447161-5	2019	Surprisingly, sulfaphenazole appeared to be a potent inhibitor of 5"-hydroxylation of flucloxacillin by both recombinant CYP3A4 and CYP3A7.	Floxacillin	86-100	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	121-127
30447161-5	2019	Surprisingly, sulfaphenazole appeared to be a potent inhibitor of 5"-hydroxylation of flucloxacillin by both recombinant CYP3A4 and CYP3A7.	Floxacillin	86-100	cytochrome P450 family 3 subfamily A member 7	Homo sapiens	132-138
30447161-6	2019	CONCLUSIONS AND IMPLICATIONS: The combined results show that the 5"-hydroxylation of flucloxacillin is primarily catalysed by CYP3A4, CYP3A7 and CYP2C9.	Floxacillin	85-99	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	126-132
30447161-6	2019	CONCLUSIONS AND IMPLICATIONS: The combined results show that the 5"-hydroxylation of flucloxacillin is primarily catalysed by CYP3A4, CYP3A7 and CYP2C9.	Floxacillin	85-99	cytochrome P450 family 3 subfamily A member 7	Homo sapiens	134-140
30447161-6	2019	CONCLUSIONS AND IMPLICATIONS: The combined results show that the 5"-hydroxylation of flucloxacillin is primarily catalysed by CYP3A4, CYP3A7 and CYP2C9.	Floxacillin	85-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
28346841-1	2017	HLA-B*57:01 is strongly associated with severe adverse drug reaction induced by the anti-HIV drug abacavir (ABC) and antibiotic flucloxacillin.	Floxacillin	128-142	major histocompatibility complex, class I, B	Homo sapiens	0-5
29436218-4	2018	Weak flucloxacillin-specific T cell responses were detected in donors expressing HLA-B*57:01 and HLA-B*58:01.	Floxacillin	5-19	major histocompatibility complex, class I, B	Homo sapiens	81-86
29436218-4	2018	Weak flucloxacillin-specific T cell responses were detected in donors expressing HLA-B*57:01 and HLA-B*58:01.	Floxacillin	5-19	major histocompatibility complex, class I, B	Homo sapiens	97-102
28346841-10	2017	The newly established real-time PCR assay provides a rapid and reliable tool for HLA-B*57:01 allele screening before the prescription of ABC and flucloxacillin in clinical practice.	Floxacillin	145-159	major histocompatibility complex, class I, B	Homo sapiens	81-86
28444390-6	2017	High-mobility group box 1 protein (HMGB1) and lactate dehydrogenase release as well as adenosine triphosphate depletion occurred in a drug-, time-, and concentration-dependent manner with SMX-NO and flucloxacillin, whereas isoniazid and amoxicillin were nontoxic.	Floxacillin	199-213	high mobility group box 1	Homo sapiens	0-25
28444390-6	2017	High-mobility group box 1 protein (HMGB1) and lactate dehydrogenase release as well as adenosine triphosphate depletion occurred in a drug-, time-, and concentration-dependent manner with SMX-NO and flucloxacillin, whereas isoniazid and amoxicillin were nontoxic.	Floxacillin	199-213	high mobility group box 1	Homo sapiens	35-40
28444390-10	2017	SMX-NO/flucloxacillin stimulated secretion of TNF-alpha, IL-6, IL-1alpha, and IL-1-beta.	Floxacillin	7-21	interleukin 1 beta	Homo sapiens	78-87
28444390-10	2017	SMX-NO/flucloxacillin stimulated secretion of TNF-alpha, IL-6, IL-1alpha, and IL-1-beta.	Floxacillin	7-21	tumor necrosis factor	Homo sapiens	46-55
28444390-10	2017	SMX-NO/flucloxacillin stimulated secretion of TNF-alpha, IL-6, IL-1alpha, and IL-1-beta.	Floxacillin	7-21	interleukin 6	Homo sapiens	57-61
28444390-10	2017	SMX-NO/flucloxacillin stimulated secretion of TNF-alpha, IL-6, IL-1alpha, and IL-1-beta.	Floxacillin	7-21	interleukin 1 alpha	Homo sapiens	63-72
28253087-5	2017	We found that the genetic risk variants that were identified genome-wide, and replication confirmed, are mainly related to polymorphisms in the human leukocyte antigen (HLA) region that include HLA-DQB1*06:02 for amoxicillin-clavulanate, HLA-B*57:01 for flucloxacillin, HLA-DRB1*15:01 for lumiracoxib, and HLA-DRB1*07:01 for lapatinib and ximelagatran-induced hepatotoxicity.	Floxacillin	254-268	major histocompatibility complex, class II, DR beta 1	Homo sapiens	169-172
28253087-5	2017	We found that the genetic risk variants that were identified genome-wide, and replication confirmed, are mainly related to polymorphisms in the human leukocyte antigen (HLA) region that include HLA-DQB1*06:02 for amoxicillin-clavulanate, HLA-B*57:01 for flucloxacillin, HLA-DRB1*15:01 for lumiracoxib, and HLA-DRB1*07:01 for lapatinib and ximelagatran-induced hepatotoxicity.	Floxacillin	254-268	major histocompatibility complex, class II, DQ beta 1	Homo sapiens	194-202
28253087-5	2017	We found that the genetic risk variants that were identified genome-wide, and replication confirmed, are mainly related to polymorphisms in the human leukocyte antigen (HLA) region that include HLA-DQB1*06:02 for amoxicillin-clavulanate, HLA-B*57:01 for flucloxacillin, HLA-DRB1*15:01 for lumiracoxib, and HLA-DRB1*07:01 for lapatinib and ximelagatran-induced hepatotoxicity.	Floxacillin	254-268	major histocompatibility complex, class I, B	Homo sapiens	238-243
28253087-5	2017	We found that the genetic risk variants that were identified genome-wide, and replication confirmed, are mainly related to polymorphisms in the human leukocyte antigen (HLA) region that include HLA-DQB1*06:02 for amoxicillin-clavulanate, HLA-B*57:01 for flucloxacillin, HLA-DRB1*15:01 for lumiracoxib, and HLA-DRB1*07:01 for lapatinib and ximelagatran-induced hepatotoxicity.	Floxacillin	254-268	major histocompatibility complex, class II, DR beta 1	Homo sapiens	270-278
28253087-5	2017	We found that the genetic risk variants that were identified genome-wide, and replication confirmed, are mainly related to polymorphisms in the human leukocyte antigen (HLA) region that include HLA-DQB1*06:02 for amoxicillin-clavulanate, HLA-B*57:01 for flucloxacillin, HLA-DRB1*15:01 for lumiracoxib, and HLA-DRB1*07:01 for lapatinib and ximelagatran-induced hepatotoxicity.	Floxacillin	254-268	major histocompatibility complex, class II, DR beta 1	Homo sapiens	306-314
28253087-6	2017	Additionally, polymorphisms in ST6 beta-galactosamide alpha-2, 6-sialyltranferase-1 (ST6GAL1), which plays a role in systemic inflammatory response, and variants in intron of family with sequence similarity-65 member-B (FAM65B) that play roles in liver inflammation displayed association with flucloxacillin and antituberculosis drug-induced hepatotoxicity, respectively.	Floxacillin	293-307	ST6 beta-galactoside alpha-2,6-sialyltransferase 1	Homo sapiens	31-83
27637899-8	2016	Furthermore, responses were detected to carbamazepine (in HLA-B*15:02 donors), flucloxacillin (in 1 HLA-B*57:01 donor) and oxypurinol (in HLA-B*58:01 donors), which are associated with HLA-class I-restricted forms of hypersensitivity.	Floxacillin	79-93	major histocompatibility complex, class I, B	Homo sapiens	100-105
28017537-2	2017	For example, it is well-established that HLA-B*15:02 and HLA-B*57:01 are associated with carbamazepine-induced Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) and abacavir-induced hypersensitivity/flucloxacillin-induced liver injury, respectively.	Floxacillin	213-227	major histocompatibility complex, class I, B	Homo sapiens	41-46
28017537-2	2017	For example, it is well-established that HLA-B*15:02 and HLA-B*57:01 are associated with carbamazepine-induced Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) and abacavir-induced hypersensitivity/flucloxacillin-induced liver injury, respectively.	Floxacillin	213-227	major histocompatibility complex, class I, B	Homo sapiens	57-62
28017537-6	2017	Finally, HLA-B*57:01-restricted activation of T-cells from patients with flucloxacillin-induced liver injury is dependent on processing of drug protein adducts.	Floxacillin	73-87	major histocompatibility complex, class I, B	Homo sapiens	9-14
28856081-4	2017	The presence of the HLA-B*57:01 allele has been associated with an 81-fold increased risk of flucloxacillin DILI.	Floxacillin	93-107	major histocompatibility complex, class I, B	Homo sapiens	20-25
27637899-8	2016	Furthermore, responses were detected to carbamazepine (in HLA-B*15:02 donors), flucloxacillin (in 1 HLA-B*57:01 donor) and oxypurinol (in HLA-B*58:01 donors), which are associated with HLA-class I-restricted forms of hypersensitivity.	Floxacillin	79-93	major histocompatibility complex, class I, B	Homo sapiens	100-105
23635947-8	2013	Several HLA alleles also demonstrate drug-specific associations with DILI, such as HLA-A*33:03 for ticlopidine, HLA-B*57:01 for flucloxacillin and HLA-DQA1*02:01 for lapatinib.	Floxacillin	128-142	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	8-11
25877613-4	2015	CD8+ T-cells from lymph nodes of flucloxacillin-sensitized mice were stimulated to proliferate, secrete interferon (IFN-gamma) and granzyme B, and induce hepatocyte apoptosis in a concentration-dependent manner following ex vivo stimulation.	Floxacillin	33-47	interferon gamma	Mus musculus	96-125
25877613-4	2015	CD8+ T-cells from lymph nodes of flucloxacillin-sensitized mice were stimulated to proliferate, secrete interferon (IFN-gamma) and granzyme B, and induce hepatocyte apoptosis in a concentration-dependent manner following ex vivo stimulation.	Floxacillin	33-47	granzyme B	Mus musculus	131-141
25080918-2	2014	Several HLA-B alleles proved to be associated with SADRs for drugs such as carbamazepine, allopurinol, lamotrigine, and flucloxacillin.	Floxacillin	120-134	major histocompatibility complex, class I, B	Homo sapiens	8-13
23807564-14	2013	Furthermore, flucloxacillin was able to induce 3A4/2C8 expression mediated by PXR in a genotype dependent manner.	Floxacillin	13-27	nuclear receptor subfamily 1 group I member 2	Homo sapiens	78-81
24777842-7	2015	Interestingly, HLA-B*57:01 is associated with both abacavir DISI and flucloxacillin DILI but the reasons for the different phenotype of ADR remains unknown.	Floxacillin	69-83	major histocompatibility complex, class I, B	Homo sapiens	15-20
24652713-9	2015	TLR4-associated-signal transduction may be involved in FLX-induced liver injury, and IL-17 is an exacerbating factor.	Floxacillin	55-58	toll-like receptor 4	Mus musculus	0-4
24731753-0	2014	T cells infiltrate the liver and kill hepatocytes in HLA-B(*)57:01-associated floxacillin-induced liver injury.	Floxacillin	78-89	major histocompatibility complex, class I, B	Homo sapiens	53-58
24731753-3	2014	Recent studies have identified the HLA-B(*)57:01 allele as a risk factor for floxacillin (FLUX)-induced liver injury and have suggested a role for cytotoxic CD8(+) T cells in the pathomechanism of liver injury caused by FLUX.	Floxacillin	77-88	major histocompatibility complex, class I, B	Homo sapiens	35-40
21136982-5	2009	Affinity, cation exchange and reversed phase chromatography prior to MS revealed in vivo modification of HSA with flucloxacillin in tolerant patients, with up to nine modified lysine residues being detected in each patient, and with modification of Lys190 and Lys212 being detected in 8/8 patients.	Floxacillin	114-128	albumin	Homo sapiens	105-108
23596311-2	2013	A particularly interesting example is flucloxacillin (FLUX)-DILI, which is associated with the HLA-B*57:01 allele.	Floxacillin	38-52	major histocompatibility complex, class I, B	Homo sapiens	95-100
21501118-2	2011	HLA-B*5701 is strongly associated with hypersensitivity to the HIV drug abacavir, liver toxicity from the antibiotic flucloxacillin and is a marker for slow progression of HIV AIDS.	Floxacillin	117-131	major histocompatibility complex, class I, B	Homo sapiens	0-5
19483685-0	2009	HLA-B*5701 genotype is a major determinant of drug-induced liver injury due to flucloxacillin.	Floxacillin	79-93	major histocompatibility complex, class I, B	Homo sapiens	0-5
19483685-5	2009	Further MHC genotyping, which included 64 flucloxacillin-tolerant controls, confirmed the association with HLA-B*5701 (OR = 80.6, P = 9.0 x 10(-19)).	Floxacillin	42-56	major histocompatibility complex, class I, B	Homo sapiens	107-112
22987284-0	2013	Human leukocyte antigen (HLA)-B*57:01-restricted activation of drug-specific T cells provides the immunological basis for flucloxacillin-induced liver injury.	Floxacillin	122-136	major histocompatibility complex, class I, B	Homo sapiens	0-31
22987284-2	2013	For flucloxacillin, a delay in the reaction onset and identification of human leukocyte antigen (HLA)-B*57:01 as a susceptibility factor are indicative of an immune pathogenesis.	Floxacillin	4-18	major histocompatibility complex, class I, B	Homo sapiens	78-103
22987284-3	2013	Thus, we characterize flucloxacillin-responsive CD4+ and CD8+ T cells from patients with liver injury and show that naive CD45RA+CD8+ T cells from volunteers expressing HLA-B*57:01 are activated with flucloxacillin when dendritic cells present the drug antigen.	Floxacillin	22-36	CD4 molecule	Homo sapiens	48-51
22987284-3	2013	Thus, we characterize flucloxacillin-responsive CD4+ and CD8+ T cells from patients with liver injury and show that naive CD45RA+CD8+ T cells from volunteers expressing HLA-B*57:01 are activated with flucloxacillin when dendritic cells present the drug antigen.	Floxacillin	22-36	CD8a molecule	Homo sapiens	57-60
22987284-3	2013	Thus, we characterize flucloxacillin-responsive CD4+ and CD8+ T cells from patients with liver injury and show that naive CD45RA+CD8+ T cells from volunteers expressing HLA-B*57:01 are activated with flucloxacillin when dendritic cells present the drug antigen.	Floxacillin	22-36	CD8a molecule	Homo sapiens	129-132
22987284-3	2013	Thus, we characterize flucloxacillin-responsive CD4+ and CD8+ T cells from patients with liver injury and show that naive CD45RA+CD8+ T cells from volunteers expressing HLA-B*57:01 are activated with flucloxacillin when dendritic cells present the drug antigen.	Floxacillin	22-36	major histocompatibility complex, class I, B	Homo sapiens	169-174
22987284-3	2013	Thus, we characterize flucloxacillin-responsive CD4+ and CD8+ T cells from patients with liver injury and show that naive CD45RA+CD8+ T cells from volunteers expressing HLA-B*57:01 are activated with flucloxacillin when dendritic cells present the drug antigen.	Floxacillin	200-214	CD8a molecule	Homo sapiens	129-132
22987284-3	2013	Thus, we characterize flucloxacillin-responsive CD4+ and CD8+ T cells from patients with liver injury and show that naive CD45RA+CD8+ T cells from volunteers expressing HLA-B*57:01 are activated with flucloxacillin when dendritic cells present the drug antigen.	Floxacillin	200-214	major histocompatibility complex, class I, B	Homo sapiens	169-174
22987284-6	2013	Activation of CD8+ clones with flucloxacillin was processing-dependent and restricted by HLA-B*57:01 and the closely related HLA-B*58:01.	Floxacillin	31-45	CD8a molecule	Homo sapiens	14-17
22987284-6	2013	Activation of CD8+ clones with flucloxacillin was processing-dependent and restricted by HLA-B*57:01 and the closely related HLA-B*58:01.	Floxacillin	31-45	major histocompatibility complex, class I, B	Homo sapiens	89-94
22987284-6	2013	Activation of CD8+ clones with flucloxacillin was processing-dependent and restricted by HLA-B*57:01 and the closely related HLA-B*58:01.	Floxacillin	31-45	major histocompatibility complex, class I, B	Homo sapiens	125-130
23032409-0	2013	The safety of flucloxacillin in HIV-infected patients with positive HLA-B*5701 genotype.	Floxacillin	14-28	major histocompatibility complex, class I, B	Homo sapiens	68-73
23032409-1	2013	Positive HLA-B*5701 genotype has recently been identified as the main genetic risk factor for flucloxacillin drug-induced liver injury (DILI).	Floxacillin	94-108	major histocompatibility complex, class I, B	Homo sapiens	9-14
23032409-3	2013	Considering the high prevalence of soft-tissue infections in HIV patients, we conducted a retrospective study to investigate whether flucloxacillin use was associated with adverse events in HIV patients known to be HLA-B*5701 positive.	Floxacillin	133-147	major histocompatibility complex, class I, B	Homo sapiens	215-220
20222094-0	2010	A role for the pregnane X receptor in flucloxacillin-induced liver injury.	Floxacillin	38-52	nuclear receptor subfamily 1 group I member 2	Homo sapiens	15-34
20222094-2	2010	There is some evidence that flucloxacillin is a human pregnane X receptor (PXR) agonist.	Floxacillin	28-42	nuclear receptor subfamily 1 group I member 2	Homo sapiens	54-73
20222094-2	2010	There is some evidence that flucloxacillin is a human pregnane X receptor (PXR) agonist.	Floxacillin	28-42	nuclear receptor subfamily 1 group I member 2	Homo sapiens	75-78
20222094-3	2010	This study was designed to investigate the relevance of PXR to flucloxacillin toxicity and to identify genes changing in expression in response to flucloxacillin.	Floxacillin	63-77	nuclear receptor subfamily 1 group I member 2	Homo sapiens	56-59
20222094-5	2010	The ability of flucloxacillin to act as a PXR agonist was investigated with reporter gene experiments.	Floxacillin	15-29	nuclear receptor subfamily 1 group I member 2	Homo sapiens	42-45
20222094-10	2010	Using a luciferase-everted repeat separated by 6 base pairs element construct, we confirmed that flucloxacillin was a PXR agonist.	Floxacillin	97-111	nuclear receptor subfamily 1 group I member 2	Homo sapiens	118-121
20222094-11	2010	We found a difference in the distribution of a PXR polymorphism (rs3814055; C-25385T) between flucloxacillin DILI cases and controls with the CC genotype associated with an increased risk of disease (odds ratio = 3.37, 95% confidence interval = 1.55-7.30, P = 0.0023).	Floxacillin	94-108	nuclear receptor subfamily 1 group I member 2	Homo sapiens	47-50
20222094-13	2010	CONCLUSION: Flucloxacillin is a PXR agonist at pharmacologically relevant concentrations, and a functionally significant upstream PXR polymorphism is a risk factor for flucloxacillin-induced DILI.	Floxacillin	12-26	nuclear receptor subfamily 1 group I member 2	Homo sapiens	32-35
20222094-13	2010	CONCLUSION: Flucloxacillin is a PXR agonist at pharmacologically relevant concentrations, and a functionally significant upstream PXR polymorphism is a risk factor for flucloxacillin-induced DILI.	Floxacillin	168-182	nuclear receptor subfamily 1 group I member 2	Homo sapiens	130-133
18998265-5	2008	The first line of therapy for cellulitis remains a small spectrum, beta-lactamase resistant penicillin, such as flucloxacillin for 10 days.	Floxacillin	112-126	beta-lactamase	Staphylococcus aureus	67-81
16943303-5	2006	Moreover, flucloxacillin-specific T cell clones could be generated from peripheral blood, they expressed CD4 and the alphabeta-T cell receptor, and showed a heterogeneous cytokine secretion pattern with no clear commitment to either a Th1- or Th2-type response.	Floxacillin	10-24	CD4 molecule	Homo sapiens	105-108
1234495-10	1975	The elimination rate of flucloxacillin in haemodialysis patients (T1/2 : 2h 53 min) corresponds with the extra-renal elimination rate in healthy subjects.	Floxacillin	24-38	interleukin 1 receptor like 1	Homo sapiens	66-78
16472102-0	2006	Induction of cytochrome P450 3A4 and P-glycoprotein by the isoxazolyl-penicillin antibiotic flucloxacillin.	Floxacillin	92-106	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	13-32
16472102-0	2006	Induction of cytochrome P450 3A4 and P-glycoprotein by the isoxazolyl-penicillin antibiotic flucloxacillin.	Floxacillin	92-106	ATP binding cassette subfamily B member 1	Homo sapiens	37-51
16472102-4	2006	However, incubation of human LS 180 colorectal adenocarcinoma cells with flucloxacillin led to a dose-dependent induction of MDR1 as well as of CYP3A4 mRNA, which was also confirmed in primary human hepatocytes.	Floxacillin	73-87	ATP binding cassette subfamily B member 1	Homo sapiens	125-129
16472102-4	2006	However, incubation of human LS 180 colorectal adenocarcinoma cells with flucloxacillin led to a dose-dependent induction of MDR1 as well as of CYP3A4 mRNA, which was also confirmed in primary human hepatocytes.	Floxacillin	73-87	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	144-150
16472102-5	2006	At high concentrations, flucloxacillin activated the human Pregnane-X-Receptor, PXR, a ligand-dependent transcription factor that is the target of many drugs that induce CYP3A4, with consequences for the metabolism of other drugs.	Floxacillin	24-38	nuclear receptor subfamily 1 group I member 2	Homo sapiens	59-78
16472102-5	2006	At high concentrations, flucloxacillin activated the human Pregnane-X-Receptor, PXR, a ligand-dependent transcription factor that is the target of many drugs that induce CYP3A4, with consequences for the metabolism of other drugs.	Floxacillin	24-38	nuclear receptor subfamily 1 group I member 2	Homo sapiens	80-83
16472102-5	2006	At high concentrations, flucloxacillin activated the human Pregnane-X-Receptor, PXR, a ligand-dependent transcription factor that is the target of many drugs that induce CYP3A4, with consequences for the metabolism of other drugs.	Floxacillin	24-38	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	170-176
16472102-9	2006	These findings indicate that flucloxacillin has the potential to induce expression of both CYP3A4 as well as P-glycoprotein, most likely through activation of the nuclear hormone receptor PXR.	Floxacillin	29-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	91-97
16472102-9	2006	These findings indicate that flucloxacillin has the potential to induce expression of both CYP3A4 as well as P-glycoprotein, most likely through activation of the nuclear hormone receptor PXR.	Floxacillin	29-43	ATP binding cassette subfamily B member 1	Homo sapiens	109-123
16472102-9	2006	These findings indicate that flucloxacillin has the potential to induce expression of both CYP3A4 as well as P-glycoprotein, most likely through activation of the nuclear hormone receptor PXR.	Floxacillin	29-43	nuclear receptor subfamily 1 group I member 2	Homo sapiens	188-191
35346142-10	2022	Presumably the underlying mechanism is activation of the pregnane X receptor by flucloxacillin, which can induce cytochrome P450, uridine glucuronosyl transferase (UGT1A4) and P-glycoprotein.	Floxacillin	80-94	nuclear receptor subfamily 1 group I member 2	Homo sapiens	57-76
35346142-10	2022	Presumably the underlying mechanism is activation of the pregnane X receptor by flucloxacillin, which can induce cytochrome P450, uridine glucuronosyl transferase (UGT1A4) and P-glycoprotein.	Floxacillin	80-94	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	164-170
3312020-4	1987	Patients receiving flucloxacillin showed increased numbers of Klebsiella spp.	Floxacillin	19-33	histocompatibility minor 13	Homo sapiens	73-76
3987776-3	1985	After the first infusion of flucloxacillin (5 min), the distribution phase was rapid (t 1/2 alpha = 0.13 h).	Floxacillin	28-42	interleukin 1 receptor like 1	Homo sapiens	86-97
11409940-7	2001	Cytotoxicity in BEC preparations (9/13) was also induced by the supernatants of human liver microsomes and of recombinant human cytochrome P450 (CYP)3A4 preincubated with flucloxacillin (500 mg/L).	Floxacillin	171-185	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	128-152
11409940-12	2001	In conclusion, hepatocytes mainly via CYP3A4 activity, generate flucloxacillin metabolite(s) including 5"-hydroxymethylflucloxacillin that may induce cytotoxicity in susceptible BEC.	Floxacillin	64-78	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	38-44
9259029-5	1997	In most Western countries with a relatively low incidence of MRSA, penicillin-derivatives, such as flucloxacillin (or cloxacillin, methicillin and nafcillin) will be the drug of choice, because of their good in-vitro activity, low toxicity, good clinical efficacy and relatively low cost.	Floxacillin	99-113	solute carrier family 9 member A6	Homo sapiens	61-65
35464148-0	2022	Severe acidosis due to 5-oxoprolinase inhibition by flucloxacillin in a patient with shoulder prosthesis joint infection.	Floxacillin	52-66	5-oxoprolinase, ATP-hydrolysing	Homo sapiens	23-37
35464148-2	2022	Inhibition of 5-oxoprolinase by flucloxacillin was found to be the cause of the metabolic derailment.	Floxacillin	32-46	5-oxoprolinase, ATP-hydrolysing	Homo sapiens	14-28
33963595-7	2021	Free flucloxacillin clearance depended on probenecid, allometrically-scaled fat free mass (FFM), and eGFR.	Floxacillin	5-19	epidermal growth factor receptor	Homo sapiens	101-105
33963595-9	2021	CONCLUSION: The simulation results reported can be used to identify dose regimens which optimise flucloxacillin exposure according to eGFR and FFM.	Floxacillin	97-111	epidermal growth factor receptor	Homo sapiens	134-138
32712713-4	2020	Several case reports have reported that flucloxacillin appeared to decrease levels of drugs metabolized by CYP3A4 and P-gp.	Floxacillin	40-54	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	107-113
32712713-4	2020	Several case reports have reported that flucloxacillin appeared to decrease levels of drugs metabolized by CYP3A4 and P-gp.	Floxacillin	40-54	ATP binding cassette subfamily B member 1	Homo sapiens	118-122
32712713-11	2020	CONCLUSIONS: Flucloxacillin decreases tacrolimus trough levels, possibly through a CYP3A4 and/or P-gp-inducing effect.	Floxacillin	13-27	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	83-89
32712713-11	2020	CONCLUSIONS: Flucloxacillin decreases tacrolimus trough levels, possibly through a CYP3A4 and/or P-gp-inducing effect.	Floxacillin	13-27	ATP binding cassette subfamily B member 1	Homo sapiens	97-101
32799554-7	2020	Thus, the in silico drug repurposing technique is a highly effective approach for identifying an existing drug molecule having an antiobesity therapeutic activity against the human FABP4, and Floxacillin was selected as safe and effective drug for candidates for developing an antiobesity therapy.	Floxacillin	192-203	fatty acid binding protein 4	Homo sapiens	181-186
32726429-0	2020	Identification of flucloxacillin-haptenated HLA-B*57:01 ligands: evidence of antigen processing and presentation.	Floxacillin	18-32	major histocompatibility complex, class I, B	Homo sapiens	44-49
32726429-4	2020	In this study, the binding of flucloxacillin to immune cells was characterized and the nature of the peptides presented by human leukocyte antigen HLA-B*57:01 was analyzed using mass spectrometric based immunopeptidomics methods.	Floxacillin	30-44	major histocompatibility complex, class I, B	Homo sapiens	147-152
32726429-6	2020	Of the peptides eluted from flucloxacillin-treated C1R-B*57:01 cells, 6 putative peptides were annotated as flucloxacillin-modified HLA-B*57:01 peptide ligands (Data are available via ProteomeXchange with identifier PXD020137).	Floxacillin	28-42	major histocompatibility complex, class I, B	Homo sapiens	132-137
32726429-6	2020	Of the peptides eluted from flucloxacillin-treated C1R-B*57:01 cells, 6 putative peptides were annotated as flucloxacillin-modified HLA-B*57:01 peptide ligands (Data are available via ProteomeXchange with identifier PXD020137).	Floxacillin	108-122	major histocompatibility complex, class I, B	Homo sapiens	132-137
32521723-3	2020	As FLU is binding to both Sudlow"s site I and site II of human serum albumin (HSA), competitive and allosteric interactions with other drugs, highly bound to the same sites, seem conceivable.	Floxacillin	3-6	albumin	Homo sapiens	63-76