2. Apoptosis NF-κB Metabolic Enzyme/Protease Immunology/Inflammation Protein Tyrosine Kinase/RTK JAK/STAT Signaling Epigenetics Stem Cell/Wnt PI3K/Akt/mTOR Cell Cycle/DNA Damage Neuronal Signaling
  3. RIP kinase Apoptosis Reactive Oxygen Species (ROS) JAK STAT PI3K Akt Sirtuin Necroptosis Amyloid-β
  4. Ponicidin

Ponicidin (Rubescensine B) is an orally active RIPK1 inhibitor with a Kd value of 135 nM. Ponicidin inhibits the JAK2/STAT3 pathway to induce apoptosis, activates the PI3K/Akt pathway, upregulates SIRT1 expression, alleviates oxidative stress, suppresses inflammatory responses and necroptosis, and blocks cell cycle progression. Ponicidin induces ROS production to exert antiproliferative and antiviral effects, while also improving cognitive function and reducing Aβ plaque deposition. Ponicidin can be used in studies related to hepatocellular carcinoma, Alzheimer's disease, and gastric cancer.

For research use only. We do not sell to patients.

CAS No. : 52617-37-5

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10 mM * 1 mL in DMSO
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Customer Review

Based on 4 publication(s) in Google Scholar

Ponicidin Related Antibodies

Top Publications Citing Use of Products

    Ponicidin purchased from MedChemExpress. Usage Cited in: Phytomedicine. 2023 Jun:114:154785.

    Ponicidin (5, 20 µM; 48 h) suppresses proliferation of NOZ and GBC-SD cells effectively.

    Ponicidin purchased from MedChemExpress. Usage Cited in: Phytomedicine. 2023 Jun:114:154785.

    Ponicidin (5, 20 µM; 24 h) decreases the migration and invasion capabilities of NOZ and GBC-SD cells.

    Ponicidin purchased from MedChemExpress. Usage Cited in: Phytomedicine. 2023 Jun:114:154785.

    Ponicidin (5, 20 µM) significantly reduces the expression of mesenchymal phenotypes biomarkers, vimentin and N-cadherin, while upregulating the expression of E-cadherin (a distinguishing factor of epithelial cells), in NOZ and GBC-SD cells.

    Ponicidin purchased from MedChemExpress. Usage Cited in: Phytomedicine. 2023 Jun:114:154785.

    Ponicidin (10, 20 mg/kg; p.o.; every 2 days for 4 weeks) significantly inhibits subcutaneous tumor growth in mice in a dose-dependent manner.

    View All RIP kinase Isoform Specific Products:

    View All Isoforms
    RIPK1 RIPK2 RIPK3

    View All JAK Isoform Specific Products:

    View All Isoforms
    JAK1 JAK2 JAK3 Tyk2 JAK

    View All STAT Isoform Specific Products:

    View All Isoforms
    STAT3 STAT5 STAT6 STAT1

    View All PI3K Isoform Specific Products:

    View All Isoforms
    PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

    View All Akt Isoform Specific Products:

    View All Isoforms
    Akt Akt1 Akt2 Akt3

    View All Sirtuin Isoform Specific Products:

    View All Isoforms
    Sirtuin SIRT1 SIRT2 SIRT3 SIRT6 SIRT5 SIRT7 SIRT4

    • Biological Activity

    • Purity & Documentation

    • References

    • Customer Review

    Description

    Ponicidin (Rubescensine B) is an orally active RIPK1 inhibitor with a Kd value of 135 nM. Ponicidin inhibits the JAK2/STAT3 pathway to induce apoptosis, activates the PI3K/Akt pathway, upregulates SIRT1 expression, alleviates oxidative stress, suppresses inflammatory responses and necroptosis, and blocks cell cycle progression. Ponicidin induces ROS production to exert antiproliferative and antiviral effects, while also improving cognitive function and reducing Aβ plaque deposition. Ponicidin can be used in studies related to hepatocellular carcinoma, Alzheimer's disease, and gastric cancer[1][2][3][4].

    IC50 & Target

    Apoptosis[1]
    In Vitro

    Ponicidin (5-40 μM; 24-72 h) inhibits the viability of QGY-7701 and HepG-2 human hepatocellular carcinoma cells in a dose- and time-dependent manner, with treatment at 40 μM for 72 h reducing cell viability to 9.3% (QGY-7701) and 12.7% (HepG-2), respectively[1].
    Ponicidin (40 μM; 48-72 h) downregulates the mRNA and protein expression of Survivin and Bcl-2, while upregulating the mRNA and protein expression of Bax, in QGY-7701 and HepG-2 human hepatocellular carcinoma cells[1].
    Ponicidin (1-50 μM; 24 h) shows no significant cytotoxicity against HT-22 mouse hippocampal neuronal cells, while Ponicidin (10 μM; 2 h pre-incubation) significantly restores the cell viability reduced by Aβ1-42 exposure[2].
    Ponicidin (10 μM; pre-incubated for 2 h) significantly alleviates Aβ1-42-induced neuroinflammation in HT-22 mouse hippocampal neuron cells by downregulating pro-inflammatory cytokines (TNF-α, IL-1β) and upregulating the anti-inflammatory factor IL-10[2].
    Ponicidin (10 μM; preincubated for 2 h) significantly reduces Aβ1-42-induced intracellular ROS production and oxidative stress in HT-22 mouse hippocampal neuronal cells by decreasing lipid peroxidation levels and restoring antioxidant enzyme activity[2].
    Ponicidin (10 μM; 2 h pre-incubation) significantly upregulates the expression of SIRT1 in Aβ1-42-treated HT-22 mouse hippocampal neurons and modulates the activation of the PI3K/Akt pathway, while SIRT1 inhibitors reverse these effects[2].
    Ponicidin (10 μM; 2 h pre-incubation) significantly enhances the expression of BDNF and NGF in Aβ1-42-treated HT-22 mouse hippocampal neuron cells via a SIRT1-mediated mechanism[2].
    Ponicidin (10-50 μM; 48 h) induces dose-dependent apoptosis in human gastric cancer MKN28 cells, with the proportion of early apoptotic cells reaching 59.03% at the concentration of 50 μM[3].
    Ponicidin (10-50 μM; 48 h) induces dose-dependent G0-G1 cell cycle arrest in human gastric cancer MKN28 cells, increasing the proportion of G0-G1 phase cells to 60.68% at a concentration of 50 μM. It also reduces the proportions of cells in S phase and G2-M phase[3].
    Ponicidin (10-50 μM; 1-48 h) induces time- and dose-dependent activation of caspase-3 in human gastric cancer MKN28 cells, with its activity reaching 28.76% at 50 μM for 48 h[3].
    Ponicidin (1.56-100 μM; 8 h) exhibits a CC50 of 59.360 μM in BV2 microglial cells, and shows low cytotoxicity at a concentration of 5 μM[4].
    Ponicidin (5 μM; 8.5 h) inhibits Z-VAD (LZ) (HY-164388)-induced secretion of TNF-α (IC50 = 3.56 μM) and IL-6 (IC50 = 2.635 μM) in BV2 microglia, with significant inhibitory effects observed at a concentration of 5 μM[4].
    Ponicidin (5 μM; 8.5 h) inhibits TZ-induced LDH release and protects HT22 neuronal cells from necroptosis-associated membrane damage[4].
    Ponicidin (5 μM; 8.5 h) inhibits neuronal necroptosis by blocking the RIPK1-RIPK3-MLKL signaling cascade, and reduces the phosphorylation levels of RIPK1, RIPK3 and MLKL in TZ-stimulated HT22 neuronal cells[4].

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

    Ponicidin Related Antibodies

    Apoptosis Analysis[1]

    Cell Line: QGY-7701, HepG-2 human hepatocellular carcinoma cell lines
    Concentration: 5, 10, 20, 30 and 40 μM
    Incubation Time: 24, 48, 72 h
    Result: Increased the percentage of sub-G1 apoptotic cells in both cell lines in a dose- and time-dependent manner.
    Induced an apoptotic rate of 51.5% in HepG-2 cells after 40 μM treatment for 72 h.
    Induced an apoptotic rate of 63.3% in QGY-7701 cells after 40 μM treatment for 72 h.

    Western Blot Analysis[3]

    Cell Line: human gastric carcinoma MKN28 cells
    Concentration: 10, 25 and 50 μM
    Incubation Time: 6 h (JAK2/STAT3 phosphorylation assay); 48 h (apoptosis/signaling protein assay)
    Result: Dose-dependently decreased phosphorylation of JAK2 and STAT3 without altering total JAK2 or STAT3 protein levels after 6 h treatment.
    Dose-dependently decreased protein levels of VEGF, VEGFR2, and Bcl-2, while increasing protein levels of Bax and the active form of caspase-3 after 48 h treatment.

    Western Blot Analysis[4]

    Cell Line: LZ-stimulated BV2 mouse microglial cells
    Concentration: 5 μM
    Incubation Time: 30 min (pre-incubation); 4 h (LZ stimulation)
    Result: Effectively reduced LZ-induced phosphorylation of RIPK1, JAK1, and STAT1, and simultaneously downregulated protein levels of TNF-α and IL-6, with no significant effect on total RIPK1, JAK1, or STAT1 protein levels.

    Western Blot Analysis[4]

    Cell Line: TZ-stimulated HT22 mouse hippocampal neuronal cells
    Concentration: 5 μM
    Incubation Time: 30 min (pre-incubation); 4 h (TZ stimulation)
    Result: Effectively reduced TZ-induced phosphorylation of RIPK1, RIPK3, and MLKL, with no significant effect on total RIPK1, RIPK3, or MLKL protein levels.

    Cell Cytotoxicity Assay[4]

    Cell Line: HT22 mouse hippocampal neuronal cells treated with LZ-stimulated BV2 microglial cell-conditioned medium
    Concentration: 5 μM
    Incubation Time: 8 h (treated concurrently with BV2-LZ-su)
    Result: Significantly reduced LDH release induced by BV2-LZ-su, decreasing relative LDH release from ~100% to ~70% and preserving cell membrane integrity.
    In Vivo

    Ponicidin (5-10 mg/kg/day; oral; daily; 30 days) significantly improves cognitive function, reduces Aβ plaque deposition, and inhibits neuroinflammation and necroptosis in 5×FAD transgenic mice[4].

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

    Animal Model: 5×FAD transgenic mice (male, 12 weeks old)[4]
    Dosage: 5 mg/kg/day; 10 mg/kg/day
    Administration: oral; daily; 30 days
    Result: Increased novel arm entries and reduced novel arm latency (5 mg/kg, T-maze).
    Increased novel arm travel distance, increased novel arm entries, and reduced novel arm latency (10 mg/kg, T-maze).
    Increased novel arm travel distance and increased novel arm entries (5 mg/kg, Y-maze).
    Increased novel arm travel distance, increased novel arm entries, and reduced novel arm latency (10 mg/kg, Y-maze).
    Reduced target zone latency, reduced target zone errors, and reduced target zone deviation (10 mg/kg, Barnes maze).
    Increased P-point duration in the probe trial (10 mg/kg, Morris water maze).
    Reduced brain APP expression, reduced phosphorylation of RIPK1, RIPK3, MLKL, JAK1, and STAT1, and reduced brain TNF-α and IL-6 protein levels (5 mg/kg and 10 mg/kg, Western blot).
    Reduced amyloid-beta (Aβ) plaque deposition in the cortex and hippocampus (10 mg/kg, immunohistochemistry).
    Molecular Weight

    362.42

    Formula

    C20H26O6
    CAS No.
    Appearance

    Solid

    Color

    White to off-white

    SMILES

    O[C@]12[C@]3(C4=O)[C@]5([H])C6([C@](O[C@@]3([H])[C@](CC5)([H])C4=C)([H])O2)[C@](C(C)(CC[C@@H]6O)C)([H])[C@@H]1O
    Structure Classification
    Initial Source
    Shipping

    Room temperature in continental US; may vary elsewhere.
    Storage

    4°C, protect from light

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

    Solvent & Solubility
    In Vitro: 

    DMSO : 125 mg/mL (344.90 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 2.7592 mL 13.7961 mL 27.5923 mL
    5 mM 0.5518 mL 2.7592 mL 5.5185 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 (protect from light). 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: ≥ 2.08 mg/mL (5.74 mM); Clear solution

      This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).

      Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 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: ≥ 2.08 mg/mL (5.74 mM); Clear solution

      This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).

      Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 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).

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

    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: 99.93%

    SDS (392 KB)

    COA (267 KB) HNMR (263 KB) LCMS (96 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 (protect from light). 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 2.7592 mL 13.7961 mL 27.5923 mL 68.9807 mL
    5 mM 0.5518 mL 2.7592 mL 5.5185 mL 13.7961 mL
    10 mM 0.2759 mL 1.3796 mL 2.7592 mL 6.8981 mL
    15 mM 0.1839 mL 0.9197 mL 1.8395 mL 4.5987 mL
    20 mM 0.1380 mL 0.6898 mL 1.3796 mL 3.4490 mL
    25 mM 0.1104 mL 0.5518 mL 1.1037 mL 2.7592 mL
    30 mM 0.0920 mL 0.4599 mL 0.9197 mL 2.2994 mL
    40 mM 0.0690 mL 0.3449 mL 0.6898 mL 1.7245 mL
    50 mM 0.0552 mL 0.2759 mL 0.5518 mL 1.3796 mL
    60 mM 0.0460 mL 0.2299 mL 0.4599 mL 1.1497 mL
    80 mM 0.0345 mL 0.1725 mL 0.3449 mL 0.8623 mL
    100 mM 0.0276 mL 0.1380 mL 0.2759 mL 0.6898 mL
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    Ponicidin Related Classifications

    Help & FAQs
    • 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:

    Ponicidin52617-37-5Rubescensine BRIP kinaseApoptosisReactive Oxygen Species (ROS)JAKSTATPI3KAktSirtuinNecroptosisAmyloid-βReceptor-interacting protein kinasesRIPKJanus kinasePhosphoinositide 3-kinasePKBProtein kinase Bβ-amyloid peptideAβAbetaPI3K/Akt pathwaymouse RIPK1JAK2/STAT3 pathwayAlzheimer's diseaseSIRT1HepG-2HT-22 mouse hippocampal neuronal cellsQGY-7701gastric carcinomahepatocellular carcinomaInhibitorinhibitorinhibit

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