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H1792

Sigma-Aldrich

贯叶金丝桃素 二环己基铵盐

别名:

Hyp-DCHA, 贯叶金丝桃素-DCHA

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About This Item

经验公式（希尔记法）:
C35H52O4·C12H23N
CAS号:
238074-03-8
分子量:
718.10
MDL號碼:
MFCD04000098
分類程式碼代碼:
12352200
PubChem物質ID:
329815179
NACRES:
NA.25

化驗

≥98% (HPLC)

品質等級

100

形狀

powder

儲存條件

protect from light

顏色

white to off-white

溶解度

DMSO: ≥10 mg/mL

儲存溫度

−20°C

SMILES 字串

C1CCC(CC1)NC2CCCCC2.CC(C)C(=O)[C@@]34C(O)=C(C\C=C(\C)C)C(=O)[C@@](C\C=C(\C)C)(C[C@H](C\C=C(/C)C)[C@@]3(C)CC\C=C(\C)C)C4=O

InChI

1S/C35H52O4.C12H23N/c1-22(2)13-12-19-33(11)27(16-14-23(3)4)21-34(20-18-25(7)8)30(37)28(17-15-24(5)6)31(38)35(33,32(34)39)29(36)26(9)10;1-3-7-11(8-4-1)13-12-9-5-2-6-10-12/h13-15,18,26-27,38H,12,16-17,19-21H2,1-11H3;11-13H,1-10H2/t27-,33+,34+,35-;/m0./s1

InChI 密鑰

ZUYCAROZOLUHJY-DNSWOBEMSA-N

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生化／生理作用

贯叶金丝桃素的稳定盐。贯叶金丝桃素被认为是负责圣约翰草′提取物的抗抑郁和抗焦虑特性的主要活性成分。它通过激活瞬时受体电位离子通道TRPC6充当单胺（包括5-羟色胺，去甲肾上腺素，多巴胺以及GABA和谷氨酸）的再摄取抑制剂。激活TRPC6可诱导钠和钙进入细胞，从而抑制单胺再摄取。它也是孕烷X受体（PXR）的激活剂，它是CYP3A4转录的关键调节剂，CYP3A4是细胞色素（CYP）P450酶系统的成员。最近的研究发现了其他神经系统作用，对炎症的作用以及抗菌、抗肿瘤和抗血管生成作用。
贯叶金丝桃素被认为是负责圣约翰草′提取物的抗抑郁和抗焦虑特性的主要活性成分。它通过激活瞬时受体电位离子通道TRPC6充当单胺（包括5-羟色胺，去甲肾上腺素，多巴胺以及GABA和谷氨酸）的再摄取抑制剂。它也是孕烷X受体（PXR）的激活剂，它是CYP3A4转录的关键调节剂，CYP3A4是细胞色素（CYP）P450酶系统的成员。最近的研究发现它对阿尔茨海默氏′病（AD）神经病理学具有神经保护作用，包括在体外分解淀粉样蛋白β聚集体和改善体内空间记忆的能力。

訊號詞

Danger

危險聲明

H302 - H314 - H400

危險分類

Acute Tox. 4 Oral - Aquatic Acute 1 - Eye Dam. 1 - Skin Corr. 1B

儲存類別代碼

8A - Combustible, corrosive hazardous materials

水污染物質分類（WGK）

WGK 3

閃點（°F）

Not applicable

閃點（°C）

Not applicable

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Cyclooxygenase-2-derived prostaglandin E(2) (PGE(2)) stimulates tumor cell growth and progression. However, the mechanisms by which PGE(2) increases tumor growth remain incompletely understood. In studies performed in non-small cell lung carcinoma (NSCLC) cells, we found that PGE(2) stimulates the expression of
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Signal transducer and activator of transcription-3 (STAT3) is downstream of growth factor and cytokine receptors, and regulates key oncogenic pathways in non-small cell lung cancer (NSCLC). Activation of STAT3 by cellular Src (c-Src) promotes tumor progression. We hypothesized that c-Src
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