Gene-drug interactions (data source: DGIdb)
Gene Name Entrez ID Drug Name Chembl ID Interaction Types Sources publications
CYP1A1 1543 HYPERICIN CHEMBL286494 NCI 14633740
CYP1A1 1543 2-METHOXYESTRADIOL CHEMBL299613 DrugBank 12810639
CYP1A1 1543 LIOTHYRONINE SODIUM CHEMBL1201119 NCI 1322573
CYP1A1 1543 CHRYSIN CHEMBL117 inhibitor GuideToPharmacologyInteractions
CYP1A1 1543 QUERCETIN CHEMBL50 NCI 10359656
CYP1A1 1543 PHENOBARBITAL CHEMBL40 PharmGKB
CYP1A1 1543 CARBAMAZEPINE CHEMBL108 PharmGKB
CYP1A1 1543 RUTIN CHEMBL226335 NCI 14633740
CYP1A1 1543 BIOCHANIN CHEMBL131921 NCI 15479032
CYP1A1 1543 VALPROIC ACID CHEMBL109 PharmGKB
CYP1A1 1543 RISPERIDONE CHEMBL85 NCI 10048600
CYP1A1 1543 CHEMBL1255648 CHEMBL1255648 NCI 9890552
CYP1A1 1543 PROMETHAZINE CHEMBL643 NCI 4024659
CYP1A1 1543 SPIRONOLACTONE CHEMBL1393 NCI 7079590
CYP1A1 1543 LANSOPRAZOLE CHEMBL480 NCI 8647108
CYP1A1 1543 DAUNORUBICIN CHEMBL178 NCI 15588138
CYP1A1 1543 DOXORUBICIN CHEMBL53463 NCI 15588138

Variant-drug associations (data source: PharmGKB)
Gene Name Variant Alleles Chemical Phenotype Category Significance Notes Sentence Publications Annotation ID
CYP1A1 rs2472297 T caffeine metabolism/PK yes This variant is associated with higher 17X/137X, suggesting they are associated with faster caffeine metabolism. Allele T is associated with increased metabolism of caffeine as compared to allele C. 27702941 1451198580
CYP1A1 rs1048943 AG + GG capecitabine efficacy yes Women with genotypes AG + GG have significantly longer progression-free survival than women with the genotype AA. Genotypes AG + GG are associated with increased response to capecitabine and docetaxel in women with Breast Neoplasms as compared to genotype AA. 22426923 981475614
CYP1A1 rs1048943 C warfarin dosage no No association was found between this variant and warfarin-maintenance dose. Please note that A/G alleles were given (complementary alleles are given here). Allele C is not associated with increased dose of warfarin in people with an international normalized ratio (INR) of 2.0-3.0 as compared to allele T. 22248286 827845820
CYP1A1 rs2606345 AC + CC deferasirox metabolism/PK yes Weight-adjusted trough concentrations (ng/ml/kg). In multivariate analyses, the AA genotype was found to predict drug concentrations below 20,000 ng/ml, which is the trough concentration cutoff value that predicts therapeutic efficacy. The AA genotype was associated with a decreased chance of having drug concentrations above the cutoff for therapeutic efficacy. Genotypes AC + CC is associated with increased concentrations of deferasirox in people with beta-Thalassemia as compared to genotype AA. 25348619 1333193034
CYP1A1 rs3826041 CC warfarin dosage yes All participants were warfarin-naive. Genotype CC is associated with increased dose of warfarin in people with heart valve replacement as compared to genotypes AA + AC. 27740732 1448267332
CYP1A1 rs2606345 AA deferasirox metabolism/PK no The genotype was not associated with area under the concentration curve (AUC) above the effectiveness cutoff of 360 micrograms/mL/h as compared in univariate analysis. Genotype AA is not associated with concentrations of deferasirox in people with beta-Thalassemia as compared to genotypes AC + CC. 27193993 1448101354
CYP1A1 rs4646903 AA + AG deferasirox metabolism/PK no The genotypes were not associated with area under the concentration curve (AUC) above the effectiveness cutoff of 360 micrograms/mL/h as compared in univariate analysis. Genotypes AA + AG are not associated with concentrations of deferasirox in people with beta-Thalassemia as compared to genotype GG. 27193993 1448101346
CYP1A1 rs2606345 AC + CC deferasirox metabolism/PK yes Half life was also longer in CC/CA compared to AA. Authors state "This suggested a homozygous A allele gain of function, thus lower drug concentrations" even though "located in intronic region of CYP1A1 gene". Genotypes AC + CC is associated with increased trough concentration of deferasirox in children with beta-Thalassemia as compared to genotype AA. 28346059 1448612764
CYP1A1 rs2606345 AA + AC exemestane metabolism/PK no No significant difference in exemestane concentrations were seen between the three genotypes. Genotypes AA + AC are not associated with concentrations of exemestane in women with Breast Neoplasms as compared to genotype CC. 27549341 1448495164
CYP1A1 CYP1A1*1, CYP1A1*2A *2A granisetron metabolism/PK yes CYP1a1*2a carriers had a significantly higher granisetron clearance and decreased AUC compared with patients without the allele in pregnant women with nausea and vomiting. CYP1A1 *2A is associated with increased clearance of granisetron as compared to CYP1A1 *1/*1. 27809336 1448426866
CYP1A1 CYP1A1*1, CYP1A1*2A *1/*2A + *2A/*2A exemestane metabolism/PK no No significant difference in exemestane concentrations were seen between the three genotypes. CYP1A1 *1/*2A + *2A/*2A are not associated with concentrations of exemestane in women with Breast Neoplasms as compared to CYP1A1 *1/*1. 27549341 1448495665
CYP1A1 rs2606345 AA antiepileptics efficacy yes Bonferroni-corrected significance level was p<0.017. The AA genotype (as well as the A allele) was overrepresented in female poor responders to antiepileptic drugs. Poor responders were those who had one or more seizures during the 10 months of analysis of patients taking antiepileptics (the study period was a year, but the first 2 months were excluded to allow drugs to reach steady-state levels). Note that no significant results were seen when considering males (n=194, p=0.627) or the total population (n=351, p=0.072). The A allele was found to lower CYP1A1 promoter activity by 70-80%. Genotype AA is associated with decreased response to antiepileptics in women with Epilepsy as compared to genotypes AC + CC. 26951882 1448424049
CYP1A1 rs1048943 C imatinib dosage no No significant association between genotype and chance of requiring an imatinib dose reduction. Please note that alleles have been complemented to the positive strand. Allele C is not associated with dose of imatinib in people with Gastrointestinal Stromal Tumors as compared to allele T. 30713339 1450933440