ライフサイエンスコーパス: endoxifen

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1 e metabolites: 4-hydroxytamoxifen (4OHT) and endoxifen.

2 HT and endoxifen were equivalent to 4OHT and endoxifen.

3 nt with high, but not low, concentrations of endoxifen.

4 r the conversion of N-desmethyl tamoxifen to endoxifen.

5 neration of the potent tamoxifen metabolite, endoxifen.

6 inst the trans isomers of either 4-OH-TAM or endoxifen.

7 for the metabolic activation of tamoxifen to endoxifen.

8 -hydroxytamoxifen, N-desmethyltamoxifen, and endoxifen.

9 4-OHT], and 4-hydroxy-N-desmethyl-tamoxifen [endoxifen]).

10 Steady-state concentrations of endoxifen (4-hydroxy-N-desmethyltamoxifen), the most pot

11 Endoxifen, a cytochrome P450 mediated tamoxifen metaboli

12 tochrome P450 2D6 have reduced production of endoxifen and a higher risk of breast cancer recurrence.

13 transcriptome following treatment with 4HT, endoxifen and ICI, both in the presence and absence of e

14 All of the effects of endoxifen are concentration dependent and do not occur a

15 esized fixed ring (FR) analogues of 4OHT and endoxifen as well as FR E and Z isomers with methoxy and

16 Additionally, we show that endoxifen blocks ERalpha transcriptional activity and in

17 Endoxifen clearance was unaffected by CYP2D6 genotype.

18 om 20 mg to 40 mg in IM and PM patients, the endoxifen concentration rose significantly; in IM there

19 As expected, the median baseline endoxifen concentration was higher in EM (34.3 ng/mL) co

20 M and IM patients (P = .84); however, the PM endoxifen concentration was still significantly lower.

21 ased at 160 mg per day given lack of MTD and endoxifen concentrations > 1,900 ng/mL.

22 Alterations in endoxifen concentrations also dramatically altered the g

23 n with impaired CYP2D6 metabolism have lower endoxifen concentrations and a greater risk of breast ca

24 rfere with CYP2D6 function, thereby reducing endoxifen concentrations and potentially increasing the

25 re was no longer a significant difference in endoxifen concentrations between EM and IM patients (P =

26 hat doubling the tamoxifen dose can increase endoxifen concentrations in IM and PM patients.

27 revealed substantial differences related to endoxifen concentrations including significant induction

28 whether the key active tamoxifen metabolite, endoxifen, could be increased by genotype-guided tamoxif

29 The E-isomers of FR 4OHT and endoxifen had no estrogenic activity at therapeutic seru

30 tic insight into the potential importance of endoxifen in the suppression of breast cancer growth and

31 and, unlike 4-hydroxytamoxifen (4OHTAM) and Endoxifen, induced cell growth to a level comparable to

32 Here, we provide novel evidence that endoxifen is a potent antiestrogen that functions in par

33 Purpose Endoxifen is a tamoxifen metabolite with potent antiestr

34 Endoxifen is known to be a potent anti-estrogen and its

35 These results support the theory that endoxifen is the primary metabolite responsible for the

36 ajor active metabolites of TAM, 4-OH-TAM and endoxifen, is by glucuronidation via the UDP-glucuronosy

37 Here, we demonstrate that endoxifen-mediated recruitment of ERalpha to known targe

38 Patients received endoxifen once daily at seven dose levels (20 to 160 mg)

39 crine-refractory metastatic breast cancer, Z-endoxifen provides substantial drug exposure unaffected

40 ty against the trans isomers of 4-OH-TAM and endoxifen, respectively, compared with wild-type UGT2B7(

41 Taken together, these data demonstrate that endoxifen's mechanism of action is different from that o

42 thods We performed a phase I study of oral Z-endoxifen to determine its toxicities, maximum tolerated

43 pite these observations, the contribution of endoxifen to the overall drug effectiveness of tamoxifen

44 uronidation against trans-4-OH-TAM and trans-endoxifen was 28% (P < 0.001) and 27% (P = 0.002) lower,

45 The FR Z-isomers of 4OHT and endoxifen were equivalent to 4OHT and endoxifen.

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