2. MAPK/ERK Pathway Metabolic Enzyme/Protease
  3. p38 MAPK Mitochondrial Metabolism
  4. Arvenin I

Arvenin I  (Synonyms: 葫芦素B 2-O-BETA-D-葡萄糖苷)

目录号: HY-N6579
产品使用指南 技术支持

Arvenin I 是一种天然的葫芦素葡萄糖苷，能够在肿瘤竞争性微环境中激活 T 细胞。Arvenin I 通过共价修饰并超活化 MKK3，进而经由 p38MAPK 通路恢复耗竭 T 细胞的线粒体 (mitochondrial) 功能。Arvenin I 对多种癌细胞具有广谱抗增殖作用。Arvenin I 在小鼠模型中单独使用或与免疫检查点抑制剂联用时，均能增强抗肿瘤功效。Arvenin I 可用于结肠癌、乳腺癌、肺癌和卵巢癌等癌症的相关研究[1][2]。

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Arvenin I

Arvenin I Chemical Structure

CAS No. : 65247-27-0

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1 mg ￥3024
1 - 2 周
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Arvenin I 相关抗体

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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

Arvenin I is a natural cucurbitacin glucoside that activates T cells within the cancer-competitive environment. Arvenin I covalently reacts with and hyperactivates MKK3, thereby reviving the mitochondrial fitness of exhausted T cells through the activation of the p38MAPK pathway[1]. Arvenin I exhibits broad-spectrum antiproliferative against cancer cells[2]. Arvenin I enhances antitumor effects both as a monotherapy and in combination with immune checkpoint inhibitors in mice[1]. Arvenin I can be used for cancer research, such as colon cancer, breast cancer, lung cancer, and ovarian cancer[1][2].

体外研究
(In Vitro)

Arvenin I (0.5-4 μM, 48 h) 在无 PHA 和 PMA (HY-18739) 刺激时，未在 Jurkat PD-1 细胞中检测到 IL-2 的诱导，且在 4 μM 浓度下对 Jurkat PD-1 细胞未表现出显著细胞毒性，表明其不能独立激活 T 细胞，而是增强 PHA/PMA 诱导的 T 细胞活化[1]。
Arvenin I (0-30 μM, 24-48 h) 通过其迈克尔受体结构域与 AKT (Cys310) 和 MKK3 (Cys227) 的特定位点半胱氨酸形成共价键，从而激活 MKK3-p38MAPK 信号通路，导致 IL-2 产量增加[1]。
Arvenin I (250 nM, 2 h) 通过 p38MAPK 通路增强原代 CD8+ T 细胞的线粒体生物能量学，表现为提高基础呼吸、最大呼吸及备用呼吸能力[1]。
Arvenin I (1-100 μM, 3 天) 对人类癌细胞系表现出广谱抗增殖活性，在 A-549、HT-29、OVCAR 和 MCF-7细胞中的 IC50 值分别为 17.0、49.4、14.7 和 42.8 μM[2]。

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

Arvenin I 相关抗体:

Western Blot Analysis[1]

Cell Line: HEK293 and Jurkat PD-1 cells
Concentration: 0, 3, 10, and 30 μM for HEK293 cells; 0, 2, and 4 μM for Jurkat PD-1 cells
Incubation Time: 24 h
Result: Caused slightly slower electrophoretic migration of the Western-blotted bands of Flag-AKT wt and Flag-MKK3 wt on SDS-PAGE gels at concentrations as low as 3 μM.
Failed to induce a band shift in mutants where each corresponding cysteine residue was substituted with a serine residue (Flag-AKT C310S and Flag-MKK3 C227S), even at a high concentration of 30 μM.
Markedly increased the phosphorylation of p38MAPK Thr180/Tyr182 in Jurkat hPD-1 cells either in the presence or absence of PHA and PMA.
Had no detectable effects on the phosphorylation of FOXO1 Ser256.
Increased the phosphorylation of MKK3 in Jurkat hPD-1 cells.

Cell Viability Assay[1]

Cell Line: Jurkat PD-1 cells
Concentration: 0.5, 1, 2, and 4 μM
Incubation Time: 48 h
Result: Exhibited no significant cytotoxicity in Jurkat PD-1 cells at 4 μM.

ELISA Assay[1]

Cell Line: Jurkat PD-1, Jurkat MKK3 wild-type and C227S cells
Concentration: 4 μM
Incubation Time: 48 h
Result: Its ability to restore IL-2 production (suppressed by MDA-MB-231 conditioned medium) was dose-dependently canceled by SB203580 (HY-10256).
Potentiated the augmentation of IL-2 production resulting from the overexpression of wild-type MKK3.
体内研究
(In Vivo)

Arvenin I (6 mg/kg, i.p., 腹腔注射，从第 10 天至第 22 天每 3 天一次) 在免疫正常的 MC38 荷瘤小鼠中抑制肿瘤生长，但在 Rag2KO 小鼠中无效，证明其抗肿瘤功效完全依赖于适应性免疫系统[1]。

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

Animal Model: WT C57BL/6N mice (6 weeks old) Subcutaneously injected with MC38 colon cancer cells[1]
Dosage: 6 mg/kg
Administration: i.p., every 3 days from day 10 to day 22
Result: Caused a 40 % inhibition of tumor growth in comparison to the control group, comparable to the efficacy of the PD-L1 antibody (30 μg every 6 day from day 10 to day 22).
Produced approximately 70 % inhibition of tumor growth with a combination with PD-L1 antibody.
Did not lead to significant reductions in body weight or differences in liver toxicity markers, including AST, ALT, and LDH.
Significantly enhanced mitochondrial respiration and upregulated proliferation markers (Ki67) in DLN CD8+ T cells in combination with the PD-L1 antibody.
Increased TNF-α levels but reduced IFN-γ levels in combination with the PD-L1 antibody.
Showed a trend toward decreasing the population of terminally exhausted CD8+ T cells (PD1+ Tim3+) and increasing the proportion of less exhausted CD8+ T cells in the combination group.
Animal Model: Rag2KO C57BL/6N mice (6 weeks old) Subcutaneously injected with MC38 colon cancer cells[1]
Dosage: 6 mg/kg
Administration: i.p., every 3 days from day 10 to day 22
Result: Failed to suppress tumors in immunodeficient mice, thereby demonstrating that its antitumor efficacy is depends on the adaptive immune system.
分子量

720.84

Formula

C38H56O13
CAS 号
中文名称

葫芦素B 2-O-BETA-D-葡萄糖苷
结构分类
初始来源
运输条件

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

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

Arvenin I 相关分类

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Keywords:

Arvenin I65247-27-0葫芦素B 2-O-BETA-D-葡萄糖苷p38 MAPKMitochondrial Metabolismanticancer effectscucurbitacin glucosideT cellscancer-competitiveMKK3mitochondrialp38MAPKMC38Rag2KO miceInhibitorinhibitorinhibit

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