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