2. Autophagy Apoptosis NF-κB PI3K/Akt/mTOR MAPK/ERK Pathway Stem Cell/Wnt
  3. Autophagy Apoptosis NF-κB PI3K Akt MEK ERK
  4. Sophocarpine monohydrate

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.

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Sophocarpine monohydrate Chemical Structure

Sophocarpine monohydrate Chemical Structure

CAS No. : 145572-44-7

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Based on 9 publication(s) in Google Scholar

Other Forms of Sophocarpine monohydrate:

Sophocarpine monohydrate Related Antibodies

Top Publications Citing Use of Products

    Sophocarpine monohydrate purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2023 May 3;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 MedChemExpress. Usage Cited in: Eur J Pharmacol. 2023 May 3;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 MedChemExpress. Usage Cited in: Molecules. 2022, 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.

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    NF-κB NF-κB1/p50 RelA/p65 RelB c-Rel

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    PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

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    Akt Akt1 Akt2 Akt3

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    MEK1 MEK2 MEK5 MEK

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    ERK ERK1 ERK2 ERK5 ERK8

    • Biological Activity

    • Purity & Documentation

    • References

    • Customer Review

    Description

    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

     

    In Vitro

    Sophocarpine monohydrate (0.5-4 mM; 24-48 h) inhibits cell viability, proliferation and migration, induces cell cycle G0/G1 arrest and apoptosis, upregulates PTEN and downregulates PI3K/Akt signaling pathways in glioblastoma cells (U251, C6)[1].
    Sophocarpine monohydrate (0.4 mM; 24-72 h) inhibits cell proliferation and migration, downregulates MEK/ERK phosphorylation and VEGF-A/C/D secretion, and reduces N-cadherin and MMP-9 expression in colorectal cancer cells (HCT116, SW620)[2].
    Sophocarpine monohydrate (50-100 μg/mL; 24 h) inhibits LPS-induced NO, TNF-α, and IL-6 production in RAW 264.7 macrophages, downregulates iNOS and COX-2 protein expression, and inhibits NF-κB activation and p38 and JNK phosphorylation in RAW 264.7 macrophages[3].
    Sophocarpine monohydrate (1-5 μM; 24 h pretreatment + 12 h DOX cotreatment) reduces ROS levels in H9C2 cardiomyocytes, upregulates Nrf2/HO-1 signaling, inhibits DOX (HY-15142A)-induced Bax and cleaved-caspase-3 expression, and upregulates Bcl-2 in H9C2 cardiomyocytes[4].

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

    Sophocarpine monohydrate Related Antibodies

    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].
    In Vivo

    Sophocarpine (35 mg/kg; intraperitoneal injection; once every 2 days; 2 weeks) monohydrate inhibits tumor growth, upregulates PTEN expression, downregulates Akt phosphorylation, and induces tumor cell apoptosis in BALB/c nude mouse subcutaneous and orthotopic glioma transplantation models[1].
    Sophocarpine (10-30 mg/kg; intraperitoneal injection; twice a week; 4 weeks) monohydrate improves cardiac function, reduces CK, CK-MB, and LDH levels, and alleviates oxidative stress and cardiomyocyte apoptosis in a DOX (HY-15142A)-induced cardiac injury model in C57BL/6J mice[4].

    MedChemExpress (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.
    Molecular Weight

    264.36

    Formula

    C15H24N2O2
    CAS No.
    Appearance

    Solid

    Color

    Light yellow to yellow

    SMILES

    O=C1N(C[C@@]2([H])[C@@]3([H])[C@]4([H])CCCN3CCC2)[C@]4([H])CC=C1.O
    Structure Classification
    Initial Source
    Shipping

    Room temperature in continental US; may vary elsewhere.
    Storage
    Powder -20°C 3 years
    4°C 2 years
    In solvent -80°C 6 months
    -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    DMSO : 100 mg/mL (378.27 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

    Preparing
    Stock Solutions
    Concentration Solvent Mass 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
    View the Complete Stock Solution Preparation Table

    * Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
    Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

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    In Vivo:

    Select the appropriate dissolution method based on your experimental animal and administration route.

    For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
    To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day.
    The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

    • Protocol 1

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% Saline

      Solubility: ≥ 2.5 mg/mL (9.46 mM); Clear solution

      This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

      Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

      Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
    • Protocol 2

      Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in Saline)

      Solubility: ≥ 2.5 mg/mL (9.46 mM); Clear solution

      This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

      Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

      Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
    In Vivo Dissolution Calculator
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    Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
    Please enter your animal formula composition:
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    Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
    The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
    Calculation results:
    Working solution concentration: mg/mL
    Method for preparing stock solution: mg drug dissolved in μL  DMSO (Stock solution concentration: mg/mL).
    The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
    Method for preparing in vivo working solution for animal experiments: Take μL DMSO stock solution, add μL . μL , mix evenly, next add μL Tween 80, mix evenly, then add μL Saline.
     If the continuous dosing period exceeds half a month, please choose this protocol carefully.
    Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
    Purity & Documentation

    Purity: 99.91%

    SDS (419 KB)

    COA (251 KB) LCMS (94 KB)

    Handling Instructions (2659 KB)
    References

    Complete Stock Solution Preparation Table

    * Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
    Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

    Optional Solvent Concentration Solvent Mass 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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    Sophocarpine monohydrate Related Classifications

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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:

    Sophocarpine145572-44-7AutophagyApoptosisNF-κBPI3KAktMEKERKNuclear factor-κBNuclear factor-kappaBPhosphoinositide 3-kinasePKBProtein kinase BMitogen-activated protein kinase kinaseMAPKKMAP2KExtracellular signal regulated kinasesInhibitorinhibitorinhibit

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