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1 hat contains an antiestrogenic side chain in endoxifen.
2 TPE), and antagonists 4-hydroxytamoxifen and endoxifen.
3 -hydroxytamoxifen, N-desmethyltamoxifen, and endoxifen.
4 e metabolites: 4-hydroxytamoxifen (4OHT) and endoxifen.
5 HT and endoxifen were equivalent to 4OHT and endoxifen.
6 nt with high, but not low, concentrations of endoxifen.
7 r the conversion of N-desmethyl tamoxifen to endoxifen.
8 neration of the potent tamoxifen metabolite, endoxifen.
9 inst the trans isomers of either 4-OH-TAM or endoxifen.
10 for the metabolic activation of tamoxifen to endoxifen.
11 4-OHT], and 4-hydroxy-N-desmethyl-tamoxifen [endoxifen]).
12               Steady-state concentrations of endoxifen (4-hydroxy-N-desmethyltamoxifen), the most pot
13                                              Endoxifen, a cytochrome P450 mediated tamoxifen metaboli
14 tochrome P450 2D6 have reduced production of endoxifen and a higher risk of breast cancer recurrence.
15  transcriptome following treatment with 4HT, endoxifen and ICI, both in the presence and absence of e
16                        All of the effects of endoxifen are concentration dependent and do not occur a
17 esized fixed ring (FR) analogues of 4OHT and endoxifen as well as FR E and Z isomers with methoxy and
18 ications with high therapeutic potential for endoxifen, as monotherapy or in combination, by applying
19                   Additionally, we show that endoxifen blocks ERalpha transcriptional activity and in
20                                              Endoxifen clearance was unaffected by CYP2D6 genotype.
21 om 20 mg to 40 mg in IM and PM patients, the endoxifen concentration rose significantly; in IM there
22             As expected, the median baseline endoxifen concentration was higher in EM (34.3 ng/mL) co
23 M and IM patients (P = .84); however, the PM endoxifen concentration was still significantly lower.
24 ased at 160 mg per day given lack of MTD and endoxifen concentrations > 1,900 ng/mL.
25                               Alterations in endoxifen concentrations also dramatically altered the g
26 n with impaired CYP2D6 metabolism have lower endoxifen concentrations and a greater risk of breast ca
27                                              Endoxifen concentrations and CYP2D6 genotypes were assoc
28 al Register: NTR1509) study was to associate endoxifen concentrations and CYP2D6 genotypes with clini
29 rfere with CYP2D6 function, thereby reducing endoxifen concentrations and potentially increasing the
30             No association was found between endoxifen concentrations and RFSt (adjusted hazard ratio
31 re was no longer a significant difference in endoxifen concentrations between EM and IM patients (P =
32 hat doubling the tamoxifen dose can increase endoxifen concentrations in IM and PM patients.
33  revealed substantial differences related to endoxifen concentrations including significant induction
34                   Also, neither categorizing endoxifen concentrations into quartiles nor using 5.9 ng
35  clinical study shows no association between endoxifen concentrations or CYP2D6 genotypes and clinica
36                                              Endoxifen concentrations were analyzed as a continuous v
37 whether the key active tamoxifen metabolite, endoxifen, could be increased by genotype-guided tamoxif
38 ble in glia with minimal tissue damage after endoxifen delivery via microfluidic polymer implants.
39                                          (Z)-endoxifen (endoxifen) is the active metabolite of tamoxi
40 ifen was not confirmed, potentially owing to endoxifen exposure differences.
41 nd demonstrates the potential of repurposing endoxifen for GBM treatment.
42                             The amide-linked endoxifen-gefitinib drug conjugates 17b and 17c demonstr
43                 The E-isomers of FR 4OHT and endoxifen had no estrogenic activity at therapeutic seru
44                                 In addition, endoxifen has known estrogen-independent effects, such a
45  Early-phase clinical trials have shown that endoxifen has promising effects in patients with hormone
46 nduction following stereotaxic injections of endoxifen in CX3CR1creERT2 mice, we carried out chronic
47 tic insight into the potential importance of endoxifen in the suppression of breast cancer growth and
48  and, unlike 4-hydroxytamoxifen (4OHTAM) and Endoxifen, induced cell growth to a level comparable to
49                                              Endoxifen is a potent antiestrogen that binds and blocks
50         Here, we provide novel evidence that endoxifen is a potent antiestrogen that functions in par
51                                      Purpose Endoxifen is a tamoxifen metabolite with potent antiestr
52                                              Endoxifen is known to be a potent anti-estrogen and its
53        These results support the theory that endoxifen is the primary metabolite responsible for the
54                               (Z)-endoxifen (endoxifen) is the active metabolite of tamoxifen.
55 ajor active metabolites of TAM, 4-OH-TAM and endoxifen, is by glucuronidation via the UDP-glucuronosy
56                                   The median endoxifen level per mg oral tamoxifen among poor, interm
57 les were retrieved for CYP2D6 genotyping and endoxifen measurements by Amplichip (Roche Diagnostics,
58                    Here, we demonstrate that endoxifen-mediated recruitment of ERalpha to known targe
59                            Patients received endoxifen once daily at seven dose levels (20 to 160 mg)
60  containing the antiestrogenic side chain of endoxifen or a free hydroxyl.
61 crine-refractory metastatic breast cancer, Z-endoxifen provides substantial drug exposure unaffected
62 ty against the trans isomers of 4-OH-TAM and endoxifen, respectively, compared with wild-type UGT2B7(
63 occupied by the antiestrogenic side chain of endoxifen results in early apoptosis similar to planar E
64  Taken together, these data demonstrate that endoxifen's mechanism of action is different from that o
65 tiforme (GBM) emerged as a top candidate for endoxifen's therapeutic potential.
66 t has been postulated that concentrations of endoxifen, the active metabolite of tamoxifen, are a bet
67        Although in a retrospective study, an endoxifen threshold of 5.9 ng/mL for efficacy was descri
68 sifying patients into quartiles and using an endoxifen threshold of 5.9 ng/mL.
69 thods We performed a phase I study of oral Z-endoxifen to determine its toxicities, maximum tolerated
70 pite these observations, the contribution of endoxifen to the overall drug effectiveness of tamoxifen
71 s in the CRT435 GBM cell line confirmed that endoxifen treatment reduced cell proliferation and induc
72 nchymal delivery of the tamoxifen metabolite endoxifen using inducible cre reporter mice.
73  advantages over tamoxifen in breast cancer, endoxifen warrants investigation in other cancer types.
74 uronidation against trans-4-OH-TAM and trans-endoxifen was 28% (P < 0.001) and 27% (P = 0.002) lower,
75 .0-7.9] vs 3.8 [IQR, 1.3-7.9] ng/g), whereas endoxifen was abundant in the oral tamoxifen group and m
76                 The FR Z-isomers of 4OHT and endoxifen were equivalent to 4OHT and endoxifen.
77  series of compounds connecting tamoxifen or endoxifen with the EGFR-inhibitor gefitinib via a covale