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Merck

SML1666

Sigma-Aldrich

4-Hydroxytamoxifen

≥98% (HPLC), solution, Tamoxifen metabolite

别名:

4-OHT,

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About This Item

经验公式(希尔记法):
C26H29NO2
CAS号:
分子量:
387.51
分類程式碼代碼:
12352200
NACRES:
NA.77

product name

4-Hydroxytamoxifen Ready Made Solution, 5 mg/mL in ethanol: isopropanol (95:5)

生物源

synthetic

品質等級

形狀

solution

濃度

5 mg/mL in ethanol: isopropanol (95:5)

運輸包裝

dry ice

儲存溫度

−20°C

InChI

1S/C26H29NO2/c1-4-25(20-8-6-5-7-9-20)26(21-10-14-23(28)15-11-21)22-12-16-24(17-13-22)29-19-18-27(2)3/h5-17,28H,4,18-19H2,1-3H3/b26-25-

InChI 密鑰

TXUZVZSFRXZGTL-QPLCGJKRSA-N

生化/生理作用

4-羟基他莫昔芬是他莫昔芬的活性代谢产物。4-羟基他莫昔芬在人肝脏中由细胞色素 P450 2D6 形成,是一种强效选择性雌激素受体拮抗剂。4-羟基他莫昔芬用于刺激 LC3 脂化,并以超氧化物依赖的方式形成自噬囊泡。在原代培养的人肝细胞中,他莫昔芬和 4-羟基他莫昔芬显著诱导细胞色素 P450 3A4(一种主要的药物代谢酶)。4-羟基他莫昔芬经历反 (E-Z) 异构化—这一过程发生在所有常见的实验室溶剂中。
4-羟基他莫昔芬的反式 异构体具有抗雌激素活性,而 顺式 4-羟基他莫昔芬是雌激素受体的关键激动剂。4-羟基他莫昔芬通过激活 乳腺癌细胞中p38 通路促进凋亡。

準備報告

4-羟基他莫昔芬为 13 mM 溶液。推荐工作浓度为 10-100μM。因此,4-羟基他莫昔芬制备液应在细胞培养基中以 1:130-1:1,300 稀释。

訊號詞

Danger

危險分類

Aquatic Chronic 3 - Carc. 1B - Eye Irrit. 2 - Flam. Liq. 2 - Repr. 1B

儲存類別代碼

3 - Flammable liquids

水污染物質分類(WGK)

WGK 3

閃點(°F)

55.4 °F

閃點(°C)

13 °C


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Characterization of tamoxifen and 4-hydroxytamoxifen glucuronidation by human UGT1A4 variants.
Sun D, et al.
Breast Cancer Research, 8(4), R50-R50 (2006)
Activation of the p38 mitogen-activated protein kinase pathway by estrogen or by 4-hydroxytamoxifen is coupled to estrogen receptor-induced apoptosis.
Zhang C C and Shapiro D J
The Journal of Biological Chemistry, 275(1), 479-486 (2000)
Izumi Kaji et al.
JCI insight, 6(16) (2021-07-02)
Functional loss of myosin Vb (MYO5B) induces a variety of deficits in intestinal epithelial cell function and causes a congenital diarrheal disorder, microvillus inclusion disease (MVID). The impact of MYO5B loss on differentiated cell lineage choice has not been investigated.
Kindlin-2 preserves integrity of the articular cartilage to protect against osteoarthritis.
Wu, et al.
Nature aging, 2, 332-347 (2023)
Jinming Zhao et al.
iScience, 24(12), 103425-103425 (2021-12-09)
We previously showed stabilization of NIK-induced activation of NF-κB non-canonical signaling suppresses MLL-AF9-induced AML. In the current study, we demonstrate that deletion of NF-κB non-canonical RelB prevents the inhibitory effect of NIK stabilization in MLL-AF9 AML. Mechanistically, RelB suppresses its

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