Browse our anti-CYP3A5 (CYP3A5) Antibodies

Human Cytochrome P450, Family 3, Subfamily A, Polypeptide 5 (CYP3A5) interaction partners

1. Kidney donor non-expressor genotype is a risk factor for calcineurin inhibitor nephrotoxicity after transplantation

2. Clinical characteristics and CYP3A5/CYP3A4/POR genotypes were collected.

3. There was no significant association between Tac-related nephrotoxicity and donor CYP3A5 and ABCB1 genotype.

4. No significant association was identified between CYP3A5*3 and the 1-year outcome of patients with ischemic stroke.

5. CP3A5 genetic variants were not associated with treatment resistance when compared to responders to clopidogrel therapy.

6. The authors results show that CYP3A5 polymorphism had a significant impact on tacrolimus pharmacokinetics in this population.

7. CYP3A5 polymorphism is associated with kidney graft rejection.

8. in skin, gene expression of CYP3A5 was significantly greater than that of CYP3A4

9. Concerning CEP72, our results are in line with the findings from the St Jude cohort of children treated for ALL with higher vincristine doses during chronic treatment. Larger high-throughput genetic analyses may be warranted to evaluate variants in other candidate genes such as CYP3A5 and reveal new nonpreviously reported alleles that may be peculiar to this region of the world

10. CYP3A5 genotype and its impact on vincristine pharmacokinetics and development of neuropathy in Kenyan children with cancer.

11. ABCB1 C1236T, ABCB1 G2677 T/A genotype and BMI are probably the factors influencing the clinical efficacy of tacrolimus in treating patients with nephrotic syndrome.

12. Polymorphism in CYP3A5 gene is associated with reduced sorafenib metabolism and increased toxicity in Chinese hepatocellular carcinoma patients.

13. Therapeutic drug monitoring and detection of CYP3A5 gene polymorphism was essential for dosage optimization in patients with myasthenia gravis

14. CYP3A5 genotype is the single most important determinant of tacrolimus metabolite.

15. non-relapse and relapse according to relapse and non-relapse, then the relation between the SNP of CYP3A5 gene and MRD1 gene loci and the risk of cytogenetic relapse in chronic myeloid leukemia patients

16. Use of CYP3A5 genotyping to guide the initial dosing of Tac when converting the immunosuppression therapy from CsA to Tac.

17. Contrasting results have been reported on the role of rs628031 and rs683369 polymorphisms of SLC22A1 and rs776746 of CYP3A5 on imatinib treatment response in patients with chronic myeloid leukemia. The present meta-analysis supports the association of SLC22A1 and CYP3A5 genotypes with clinical imatinib response rates of chronic myeloid leukemia patients. [review]

18. The combined genotype of CYP3A5*1/*3 and CYP2C19*1/*1 was associated with a low level of VASP phosphorylation, while either genotype was not. A multivariate analysis showed that high residual platelet reactivity during the cilostazol treatment, which was defined by a low response of platelet VASP phosphorylation to cilostazol, was an independent risk factor for the recurrence of thrombotic events.

19. Donor SUMO4 rs237025 genetic variant was associated with higher tacrolimus C/D ratios in the early period after liver transplantation, which might be related to the down-regulation of CYP3A5 enzyme through the NF-kB signalling pathway.

20. We analyzed tacrolimus trough concentrations in 1345 adult EA recipients with two CYP3A5 LoF alleles in a genome-wide association study. Only CYP3A4*22 was identified and no additional variants were genome-wide significant