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  3. Sophocarpine monohydrate

Sophocarpine monohydrate  (Synonyms: 槐果碱水合物)

目录号: HY-N0103A 纯度: 99.91%
COA 产品使用指南 技术支持

Sophocarpine monohydrate 是一种 PTEN 激活剂及 PI3K/AktMEK/ERKNF-κB 信号通路抑制剂。Sophocarpine monohydrate 上调 PTEN 表达抑制 PI3K/Akt 磷酸化,阻滞肿瘤细胞周期并诱导凋亡 (apoptosis)。Sophocarpine monohydrate 抑制 MEK/ERK 磷酸化及 VEGF 分泌,减少肿瘤细胞迁移。Sophocarpine monohydrate 还可抑制 NF-κB 活化及 p38JNK 磷酸化,降低 iNOS、COX-2 等炎症因子表达,同时激活 Nrf2/HO-1 通路减轻氧化应激。Sophocarpine monohydrate 具有抗肿瘤、抗炎、抗氧化及抗凋亡作用,可用于胶质母细胞瘤、结直肠癌等癌症及炎症相关疾病、Doxorubicin (HY-15142A) (DOX) 诱导心脏损伤等领域的研究。

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Sophocarpine monohydrate

Sophocarpine monohydrate Chemical Structure

CAS No. : 145572-44-7

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Customer Review

Other Forms of Sophocarpine monohydrate:

    Sophocarpine monohydrate purchased from MCE. Usage Cited in: Eur J Pharmacol. 2023 Jul 5:950:175745.  [Abstract]

    Sophocarpine (20 mg/kg; i.p.; daily; one week) and LPS together significantly increases the expression of Nrf2 and HO-1 in mice.

    Sophocarpine monohydrate purchased from MCE. Usage Cited in: Eur J Pharmacol. 2023 Jul 5:950:175745.  [Abstract]

    Sophocarpine (20 mg/kg; i.p.; daily; one week) significantly reduces the level of oxidative stress in mice.

    Sophocarpine monohydrate purchased from MCE. Usage Cited in: Molecules. 2022 Nov 15;27(22):7868.

    Sophocarpine (SOP; 20, 40 mg/kg; i.p.; once per day over two weeks) significantly hinders the ISO(Isoproterenol)-induced increase in TLR-4 and phosphorylation of NF-κB in mice.
    • 生物活性

    • 纯度 & 产品资料

    • 参考文献

    生物活性

    Sophocarpine monohydrate is a PTEN activator and an inhibitor of PI3K/Akt, MEK/ERK, and NF-κB signaling pathways. Sophocarpine monohydrate upregulates PTEN expression and inhibits PI3K/Akt phosphorylation, arrests tumor cell cycle and induces apoptosis. Sophocarpine monohydrate inhibits MEK/ERK phosphorylation and VEGF secretion, reducing tumor cell migration. Sophocarpine monohydrate can also inhibit NF-κB activation and p38 and JNK phosphorylation, reduce the expression of inflammatory factors such as iNOS and COX-2, and activate the Nrf2/HO-1 pathway to reduce oxidative stress. Sophocarpine monohydrate has anti-tumor, anti-inflammatory, antioxidant and anti-apoptotic effects, and can be used in the research of cancers such as glioblastoma and colorectal cancer, inflammation-related diseases, and Doxorubicin (HY-15142A)-induced cardiac damage[1][2][3][4].

    IC50 & Target[1]

    PI3K

     

    体外研究
    (In Vitro)

    Sophocarpine monohydrate (0.5-4 mM;24-48 h) 在胶质母细胞瘤细胞 (U251、C6) 中抑制细胞活力、增殖及迁移,诱导细胞周期 G0/G1 期阻滞和凋亡,上调 PTEN 并下调 PI3K/Akt 信号通路[1]
    Sophocarpine monohydrate (0.4 mM;24-72 h) 在结直肠癌细胞 (HCT116、SW620) 中抑制细胞增殖和迁移,下调 MEK/ERK 磷酸化及 VEGF-A/C/D 分泌,减少 N-钙黏蛋白和 MMP-9 表达[2]
    Sophocarpine monohydrate (50-100 μg/mL;24 h) 在 RAW 264.7 巨噬细胞实验中抑制 LPS 诱导的 NO、TNF-α、IL-6 产生,下调 iNOS、COX-2 蛋白表达,抑制 NF-κB 活化及 p38、JNK 磷酸化[3]
    Sophocarpine monohydrate (1-5 μM;24 h 预处理+12 h DOX 共处理) 在 H9C2 心肌细胞实验中降低 ROS 水平,上调 Nrf2/HO-1 信号,抑制 DOX (HY-15142A) 诱导的 Bax、cleaved-caspase-3 表达并上调 Bcl-2[4]

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

    Cell Viability Assay[1]

    Cell Line: U251, C6 glioblastoma cells
    Concentration: 0.5, 1, 2, 4 mM
    Incubation Time: 24-48 h
    Result: Reduced cell viability in a dose- and time-dependent manner, with IC50 around 2 mM at 48 hours, as measured by CCK-8 assay.
    No significant cytotoxicity was observed in primary astrocytes at these concentrations.

    Apoptosis Analysis[1]

    Cell Line: U251 glioblastoma cells
    Concentration: 2 mM
    Incubation Time: 24 h
    Result: Resulted a significant increase in subG1 phase cells (apoptotic cells) and G0/G1 phase arrest.

    Western Blot Analysis[1][2]

    Cell Line: U251 glioblastoma cells[1] HCT116, SW620 colorectal cancer cells[2]
    Concentration: 2 mM for U251 cells; 0.4 mM for HCT116, SW620 cells
    Incubation Time: 24 h, 48 h
    Result: Upregulation of cleaved Caspase-3, P53, and downregulation of Bcl-2, indicating induction of intrinsic apoptosis in U251 cells[1].
    Downregulated phosphorylated MEK (p-MEK), phosphorylated ERK (p-ERK), N-cadherin, and MMP-9 in HCT116, SW620 cells, while VEGF-A/C/D secretion reduced[2].
    体内研究
    (In Vivo)

    Sophocarpine (35 mg/kg;腹腔注射;每 2 天 1 次;2 周) 在 BALB/c 裸鼠皮下及原位胶质瘤移植模型中抑制肿瘤生长,上调 PTEN 表达并下调 Akt 磷酸化,诱导肿瘤细胞凋亡[1]
    Sophocarpine (10-30 mg/kg;腹腔注射;每周 2 次;4 周) 在 C57BL/6J 小鼠的 DOX (HY-15142A) 诱导心脏损伤模型中改善心功能,降低 CK、CK-MB、LDH 水平,减轻氧化应激及心肌细胞凋亡[4]

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

    Animal Model: BALB/c Nude Mouse Glioblastoma Xenograft Model (male, 18-24 g, 6-8 weeks old): subcutaneous and orthotopic U251 glioblastoma xenografts[1]
    Dosage: 35 mg/kg Sophocarpine
    Administration: Intraperitoneal injection, every 2 days for 2 weeks (subcutaneous model); daily for 2 weeks (orthotopic model)
    Result: Significantly reduced subcutaneous tumor volume and weight by 50% compared to control.
    Echocardiography and histology showed no cardiotoxicity.
    Western blot in tumor tissues revealed upregulated PTEN and cleaved Caspase-3, downregulated p-Akt and Bcl-2, indicating activation of the PTEN/PI3K/Akt pathway to induce apoptosis.
    Immunohistochemistry confirmed reduced Ki-67 proliferation marker and increased PTEN expression.
    Animal Model: C57BL/6J Mouse Doxorubicin-Induced Heart Injury Model (male, 25 g, 7 weeks old): Doxorubicin (5 mg/kg weekly×4 weeks) induced cardiotoxicity[4]
    Dosage: 10 mg/kg or 30 mg/kg Sophocarpine
    Administration: Intraperitoneal injection, co-administered with Doxorubicin weekly for the last 2 weeks (after initial 2 weeks of doxorubicin alone), total 4 weeks
    Result: Echocardiography showed improved left ventricular ejection fraction (LVEF) and fractional shortening (LVFS).
    Serum biomarkers CK, CK-MB, and LDH were reduced by 30-40% compared to doxorubicin group.
    DHE staining revealed decreased myocardial superoxide production, while MDA levels were lowered and SOD/GSH increased.
    Western blot showed upregulated Nrf2/HO-1 signaling, reduced NOX-4 and pro-apoptotic proteins (Bax, cleaved-caspase-3, Cyto-C), and increased anti-apoptotic Bcl-2 in heart tissues.
    分子量

    264.36

    Formula

    C15H24N2O2

    CAS 号
    性状

    固体

    颜色

    Light yellow to yellow

    中文名称

    槐果碱水合物

    结构分类
    初始来源
    运输条件

    Room temperature in continental US; may vary elsewhere.

    储存方式
    Powder -20°C 3 years
    4°C 2 years
    In solvent -80°C 6 months
    -20°C 1 month
    溶解性数据
    细胞实验: 

    DMSO 中的溶解度 : 100 mg/mL (378.27 mM; 超声助溶; 吸湿的 DMSO 对产品的溶解度有显著影响,请使用新开封的 DMSO)

    配制储备液
    浓度 溶剂体积 质量 1 mg 5 mg 10 mg
    1 mM 3.7827 mL 18.9136 mL 37.8272 mL
    5 mM 0.7565 mL 3.7827 mL 7.5654 mL
    查看完整储备液配制表

    * 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效
    储备液的保存方式和期限:-80°C, 6 months; -20°C, 1 month。-80°C储存时,请在6个月内使用,-20°C储存时,请在1个月内使用。

    • 摩尔计算器

    • 稀释计算器

    Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

    质量
    =
    浓度
    ×
    体积
    ×
    分子量 *

    Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

    This equation is commonly abbreviated as: C1V1 = C2V2

    浓度 (start)

    C1

    ×
    体积 (start)

    V1

    =
    浓度 (final)

    C2

    ×
    体积 (final)

    V2

    动物实验:

    请根据您的 实验动物和给药方式 选择适当的溶解方案。

    以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液,再依次添加助溶剂:
    ——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议您现用现配,当天使用
    以下溶剂前显示的百分比是指该溶剂在您配制终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶

    • 方案 一

      请依序添加每种溶剂: 10% DMSO    40% PEG300    5% Tween-80    45% Saline

      Solubility: ≥ 2.5 mg/mL (9.46 mM); 澄清溶液

      此方案可获得 ≥ 2.5 mg/mL(饱和度未知)的澄清溶液。

      1 mL 工作液为例,取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中,混合均匀;再向上述体系中加入 50 μL Tween-80,混合均匀;然后再继续加入 450 μL 生理盐水 定容至 1 mL

      生理盐水的配制:将 0.9 g 氯化钠,溶解于 ddH₂O 并定容至 100 mL,可以得到澄清透明的生理盐水溶液。
    • 方案 二

      请依序添加每种溶剂: 10% DMSO    90% (20% SBE-β-CD in Saline)

      Solubility: ≥ 2.5 mg/mL (9.46 mM); 澄清溶液

      此方案可获得 ≥ 2.5 mg/mL(饱和度未知)的澄清溶液。

      1 mL 工作液为例,取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液 中,混合均匀。

      2 g SBE-β-CD(磺丁基醚 β-环糊精)粉末定容于 10 mL 的生理盐水中,完全溶解至澄清透明。
    动物溶解方案计算器
    请输入动物实验的基本信息:

    给药剂量

    mg/kg

    动物的平均体重

    g

    每只动物的给药体积

    μL

    动物数量

    由于实验过程有损耗,建议您多配一只动物的量
    请输入您的动物体内配方组成:
    %
    DMSO +
    +
    %
    Tween-80 +
    %
    Saline
    如果您的动物是免疫缺陷鼠或者体弱鼠,建议 DMSO 中的在最后工作液体系中的占比尽量不超过 2%。
    方案所需 助溶剂 包括:DMSO ,均可在 MCE 网站选购。 Tween 80,均可在 MCE 网站选购。
    计算结果
    工作液所需浓度 : mg/mL
    储备液配制方法 : mg 药物溶于 μL  DMSO(母液浓度为 mg/mL)。
    您所需的储备液浓度超过该产品的实测溶解度,以下方案仅供参考,如有需要,请与 MCE 中国技术支持联系。
    动物实验体内工作液的配制方法 : 取 μL DMSO 储备液,加入 μL  μL ,混合均匀至澄清,再加 μL Tween 80,混合均匀至澄清,再加 μL 生理盐水
    连续给药周期超过半月以上,请谨慎选择该方案。
    请确保第一步储备液溶解至澄清状态,从左到右依次添加助溶剂。您可采用超声加热 (超声清洗仪,建议频次 20-40 kHz),涡旋吹打等方式辅助溶解。
    纯度 & 产品资料

    纯度: 99.91%

    参考文献

    完整储备液配制表

    * 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效
    储备液的保存方式和期限:-80°C, 6 months; -20°C, 1 month。-80°C储存时,请在6个月内使用,-20°C储存时,请在1个月内使用。

    可选溶剂 浓度 溶剂体积 质量 1 mg 5 mg 10 mg 25 mg
    DMSO 1 mM 3.7827 mL 18.9136 mL 37.8272 mL 94.5680 mL
    5 mM 0.7565 mL 3.7827 mL 7.5654 mL 18.9136 mL
    10 mM 0.3783 mL 1.8914 mL 3.7827 mL 9.4568 mL
    15 mM 0.2522 mL 1.2609 mL 2.5218 mL 6.3045 mL
    20 mM 0.1891 mL 0.9457 mL 1.8914 mL 4.7284 mL
    25 mM 0.1513 mL 0.7565 mL 1.5131 mL 3.7827 mL
    30 mM 0.1261 mL 0.6305 mL 1.2609 mL 3.1523 mL
    40 mM 0.0946 mL 0.4728 mL 0.9457 mL 2.3642 mL
    50 mM 0.0757 mL 0.3783 mL 0.7565 mL 1.8914 mL
    60 mM 0.0630 mL 0.3152 mL 0.6305 mL 1.5761 mL
    80 mM 0.0473 mL 0.2364 mL 0.4728 mL 1.1821 mL
    100 mM 0.0378 mL 0.1891 mL 0.3783 mL 0.9457 mL
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