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1 bit but not rodent members of the cytochrome P450 3A.
2 pha, albumin, cytokeratin 18, and cytochrome P450 3A.
3 ifampin and phenobarbital, which also induce p450 3A activity, have been reported to significantly de
4 stration, only mild inhibition of cytochrome P450 3A, and no evidence of cardiac- or phototoxicity in
5 inhibitors of the hepatic enzyme, cytochrome P450 3A, and the drug transporter, P-glycoprotein, which
6                 Hepatic cytochromes P450 3A (P450s 3A) are endoplasmic reticulum (ER)-proteins, respo
7 However, MG132 has been reported to suppress P450s 3A as a result of impaired nuclear factor-kappaB a
8 nd TIPS on intestinal and hepatic cytochrome P450 3A (CYP3A) activity.
9 icardipine-treated rats will form cytochrome P450 3A (CYP3A) aggregates when incubated at 37 degrees
10 -carbonitrile (PCN), which induce cytochrome P450 3A (CYP3A) expression and protect the body from har
11                                   Cytochrome P450 3A (CYP3A) is an enzyme of paramount importance to
12                                   Cytochrome P450 3A (CYP3A) is the most abundant CYP450 enzyme in th
13                             Human cytochrome P450 3A (CYP3A) members are major drug-metabolizing enzy
14 ction is due to increased hepatic cytochrome P450 3a (Cyp3a) protein expression and activity.
15                 Many genes of the cytochrome P450 3A (CYP3A) subfamily, including several human and r
16 matic increase in the activity of cytochrome P450 3A (CYP3A), which catalyzes side-chain hydroxylatio
17 ites catalyzed by enzymes such as cytochrome P450 3A (CYP3A).
18                  The human liver cytochromes P450 3A (CYP3As), orthologous to the rat glucocorticoid
19 with drug efflux transporters and cytochrome P450 3A drug-metabolizing enzymes.
20 ole, but not sulfaphenazole, suggesting that P450 3A enzymes are responsible for this activity in the
21  quinidine (QIN), substrates specific to cyt P450 3A enzymes, were used to demonstrate applicability
22 gnane X receptor (hPXR) activates cytochrome P450-3A expression in response to a wide variety of xeno
23 tions between ritonavir, a potent cytochrome P450 3A inhibitor, and other cytochrome P450 3A substrat
24                                   Cytochrome P450 3A is the most important CYP subfamily in humans, a
25 itically ill patients rely on the cytochrome P450 3A isoform for their elimination.
26 gree of sequence homology between cytochrome P450 3A isoforms (i.e., CYP3A4 and CYP3A5), they have th
27 itazone is not metabolized by the cytochrome p450 3A isozyme family, it is a potential inducer of thi
28 monophosphate (NMP), anticipating cytochrome P450 3A-mediated oxidative cleavage to the NMP in hepato
29  medications whose clearance is dependent on P450 3A metabolism is warranted.
30 al induction of the gene encoding cytochrome P450 3A oxygenase (CYP3A) causes a prominent class of da
31                          Hepatic cytochromes P450 3A (P450s 3A) are endoplasmic reticulum (ER)-protei
32 rial cytochromes P450 can be used to predict P450 3A residues that contribute to regiospecific steroi
33 vir is an inhibitor of the enzyme cytochrome P450 3A, responsible for the metabolism of both cyclospo
34                    Members of the cytochrome P450 3A subfamily catalyze the metabolism of endogenous
35 idazolam, two clinically relevant cytochrome P450 3A substrates, after cardiac arrest and to investig
36 rome P450 3A inhibitor, and other cytochrome P450 3A substrates, such as tacrolimus.