Can someone explain to me what is the relationship between Finasteride and CYP3A? I ask this because something does not come back. The substance I’ve been taking (Oxerutin) reports a common strangeness with CYP3A’s Finasteride. “In vitro data on a possible modulation of CYP3A activity by the components of the oxerutin (quercetin and rutin present in traces) are discordant.”(Italian Drug Agency) WTF?
Axalotl There is a connection between the two things Finasteride-Oxerutin. This enzyme.
It seems that: “Finasteride is extensively metabolized in the liver, primarily via the CYP3A subfamily, involving CYP3A4-mediated hydroxylation and oxidation” Cindy H. Chau, Douglas K. Price, Cathee Till, Phyllis J. Goodman, Xiaohong Chen, Robin J. Leach, Teresa L. Johnson-Pais, Ann W. Hsing, Ashraful Hoque, Catherine M. Finasteride Concentrations and Prostate Cancer Risk: Results from the Prostate Cancer Prevention Trial. PLoS One. 2015; 10(5): e0126672. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4425512/
Oxerutin activate CYP 3A4.
“Quercetin and rutin are popular flavonoids in plant foods, herbs, and dietary supplements. Cyclosporine (CSP), an immunosuppressant with a narrow therapeutic window, is a substrate of P-glycoprotein (P-gp) and cytochrome P-450 3A4 (CYP3A4). This study investigated the effects of quercetin and rutin on CSP pharmacokinetics from Neoral and relevant mechanisms. Rats were orally administered Neoral with and without quercetin or rutin. The blood CSP concentration was assayed by a specific monoclonal fluorescence polarization immunoassay. The results showed that quercetin and rutin significantly decreased the C(max) of CSP by 67.8 and 63.2% and reduced the AUC(0-540) by 43.3 and 57.2%, respectively. The in vitro studies indicated that the quercetin and rutin induced the functions of P-gp and CYP3A4. In conclusion, quercetin and rutin decreased the bioavailability of CSP through activating P-gp and CYP3A.” ( Yu CP, Wu PP, Hou YC, Lin SP, Tsai SY, Chen CT, Chao PD. Quercetin and rutin reduced the bioavailability of cyclosporine from Neoral, an immunosuppressant, through activating P-glycoprotein and CYP 3A4. Yu CP, et al. J Agric Food Chem. 2011. https://www.ncbi.nlm.nih.gov/m/pubmed/21466223/
Cyp3a deficiency enhances androgen receptor
“Testosterone regulates cellular functions in the prostate through activation of the androgen receptor (AR), which may enhance expression levels of cholesterogenic enzymes through activation of sterol regulatory element-binding protein2 (SREBP2). Because testosterone is inactivated to 6β-hydroxytestosterone by cytochrome P450 3A (CYP3A), we examined the effects of Cyp3a deficiency on circulating testosterone levels and its effects on activation of the AR and expression levels of cholesterogenic enzymes in the prostate using Cyp3a-knockout (Cyp3a(-/-)) mice. The results showed that Cyp3a(-/-) mice had remarkably increased free testosterone levels in plasma along with suppressed testosterone 6β-hydroxylation activities in liver microsomes, suggesting that Cyp3a is a major determinant of systemic levels of testosterone in mice. The results also showed that mRNA expression levels of the AR target genes were increased significantly, and that AR bindings to the promoter region of the AR target genes were more abundant in the prostates of Cyp3a(-/-) mice. These findings suggest that AR activation was stimulated in the prostate of Cyp3a(-/-) mice. In addition, the protein expression levels of SREBP cleavage-activating protein (SCAP), mRNA expression levels of SREBP2 target genes and total cholesterol contents were increased in the prostates of Cyp3a(-/-) mice. The findings suggest that Cyp3a deficiency stimulated the expression of Scap via activation of the AR, which elevated cholesterogenic gene expression levels through activation of SREBP2 and increased total cholesterol contents in the prostate” (Hashimoto M, Kobayashi K, Yamazaki M, Kazuki Y, Takehara S, Oshimura M, Chiba K. Cyp3a deficiency enhances androgen receptor activity and cholesterol synthesis in the mouse prostate. Hashimoto M, et al. J Steroid Biochem Mol Biol. 2016. https://www.ncbi.nlm.nih.gov/m/pubmed/27137100/
Has Oxerutin raised the level of CYP3A in the liver blocking AR?
What the fuck? Oxerutin has been raised this enzyme in the liver?
you’re bugging for no reason. finasteride is metabolized by an enzyme located in the liver known as CYP3A4. this is irrelevant
Read by courtesy. What I hypothesized raises that enzyme that does not work Testosterone. It could be different from Finasteride. I assumed Oxerutin.