2. Protein Tyrosine Kinase/RTK PI3K/Akt/mTOR Neuronal Signaling Apoptosis GPCR/G Protein MAPK/ERK Pathway
  3. Akt mTOR VEGFR Ferroptosis PI3K Cannabinoid Receptor p38 MAPK
  4. Auriculasin

Auriculasin 是一种抗癌剂，可靶向 VEGFR2、PI3K/AKT/mTOR、MAPK 等信号通路。Auriculasin 可抑制细胞增殖、诱导细胞凋亡 (apoptosis)、抑制血管生成；并能够促进线粒体氧化应激和铁死亡 (ferroptosis)。Auriculasin 还对大麻素受体 CB1 具有活性，IC50 为 8.92 μM。Auriculasin 可用于癌症研究，尤其是前列腺癌、非小细胞肺癌等相关疾病，以及抗血管生成药物开发的研究。

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Auriculasin

Auriculasin Chemical Structure

CAS No. : 60297-37-2

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1 mg ￥4200
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Auriculasin 相关抗体

Top Publications Citing Use of Products

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Akt Akt1 Akt2 Akt3

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mTOR mTORC1 mTORC2

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VEGFR1/Flt-1 VEGFR2/KDR/Flk-1 VEGFR3/Flt-4

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PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

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CB1 CB2

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p38 MAPK p38α p38β MAPK13 p38δ p38γ

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Auriculasin is an anticancer agent that inhibits VEGFR2, PI3K/AKT/mTOR, MAPK. Auriculasin can inhibit cell proliferation, induce cell apoptosis, and inhibit angiogenesis, and promotes mitochondrial oxidative stress and ferroptosis. Auriculasin is also active at the cannabinoid receptor CB1 with an IC50 of 8.92 μM. Auriculasin can be used in cancer research, especially related diseases such as prostate cancer and non-small cell lung cancer, as well as research on the development of anti-angiogenic drugs[1][2][3][4][5].

IC50 & Target

CB1

8.92 μM (IC50)

VEGFR2

 

体外研究
(In Vitro)

Auriculasin (2.5-10 μM；6-24 h) 以剂量和时间依赖性方式抑制人脐静脉内皮细胞 (HUVECs) 的增殖[1]。
Auriculasin (5-10 μM；12 h) 抑制 VEGF 诱导的 HUVECs 迁移和侵袭[1]。
Auriculasin (5-10 μM；6 h) 抑制 HUVECs 的毛细血管样结构形成[1]。
Auriculasin (5-10 μM；6 天) 抑制大鼠主动脉环的微血管出芽[1]。
Auriculasin (5-10 μM；24 h 或 30 min-1 h) 下调 HUVECs 中 Bcl-2、Bcl-XL、VEGF 的表达，并抑制 VEGFR2 及其下游 Akt、mTOR 等的磷酸化[1]。
Auriculasin (2.5-10 μM；24 h) 抑制 RC-58T/h/SA#4 原发性前列腺癌细胞活力，与 TRAIL 联用效果更显著，且对 RWPE-1 前列腺上皮细胞毒性低[2]。
Auriculasin (5 μM) 联合 TRAIL (100 ng/mL；24 h) 诱导 RC-58T/h/SA#4 细胞凋亡[2]。
Auriculasin (1-10 μM；24 h) 降低 LNCa P前列腺癌细胞活力，对 RWPE-1 细胞无影响[3]。
Auriculasin (1-5 μM；24 h) 诱导 LNCaP 细胞凋亡，表现为 sub-G1 群体增加、DNA 片段化等[3]。
Auriculasin (2.5-5 μM；12-24 h) 增加 LNCaP 细胞内 ROS 生成[3]。
Auriculasin 降低 NSCLC A549 细胞活力，促进线粒体氧化应激和铁死亡[4]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Auriculasin 相关抗体:

Cell Migration Assay [1]

Cell Line: HUVECs
Concentration: 5 μM, 7.5 μM, 10 μM
Incubation Time: 12 h
Result: Inhibited VEGF-induced migration in wound-healing assay and invasion in trans-well assay.
体内研究
(In Vivo)

Auriculasin (5、10 μg/mL；皮下注射；单剂量) 在 C57BL/6 小鼠模型中，减少血红蛋白含量、内皮细胞积累和 VEGF 表达，抑制血管生成[1]。
Auriculasin (5、10 mg/kg；口服灌胃；每 2 天一次；21 天) 在裸鼠 LNCaP 前列腺癌异种移植模型中，降低肿瘤大小、重量和体积，且无明显毒性[3]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: 5-week-old male C57BL/6 mice, Matrigel plug model[1]
Dosage: 5 μg/mL, 10 μg/mL (in Matrigel with 20 units of heparin and 150 ng/mL VEGF)
Administration: Subcutaneous injection, single dose, 7 days
Result: Co-treated with Matrigel plugs and VEGF, showed marked reduction of red blood cells, lighter color, significantly reduced hemoglobin concentrations, dramatically blocked VEGF-induced vasculature formation, and reduced area of VEGF-staining cells compared to the VEGF alone group.
分子量

420.45

Formula

C25H24O6
CAS 号
性状

固体

颜色

White to off-white

运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

-20°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

纯度 & 产品资料
参考文献

Auriculasin 相关分类

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Auriculasin60297-37-2AktmTORVEGFRFerroptosisPI3KCannabinoid Receptorp38 MAPKPKBProtein kinase BMammalian target of RapamycinVascular endothelial growth factor receptorPhosphoinositide 3-kinaseCannabinoid receptorLimonium leptophyllumInhibitorinhibitorinhibit

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