Polyphyllin VI
Based on 6 publication(s) in Google Scholar
Polyphyllin VI, an active saponin, possess anti-cancer activities. Polyphyllin VI induces G2/M cell cycle arrest and triggers apoptosis. Polyphyllin VI induces caspase-1-mediated pyroptosis via the induction of ROS/NF-κB/NLRP3/GSDMD signal axis in non-small cell lung cancer.
For research use only. We do not sell to patients.
- Purity : 99.74%
- CAS No.: 55916-51-3
- Formula: C39H62O13
- Molecular Weight:738.90
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Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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Polyphyllin VI (Standard)Apoptosis Inducer
Publications Citing Use of MedChemExpress (MCE) Polyphyllin VI
More- Cancer Res. 2025 Jun 6. [Abstract]
- ACS Nano. 2024 Nov 12;18(45):31401-31420. [Abstract]
- Dev Cell. 2025 Apr 18:S1534-5807(25)00206-0. [Abstract]
- Int Immunopharmacol. 2025 Jan 10:144:113684. [Abstract]
- Int Immunopharmacol. 2024 Oct 8;143(Pt 1):113334. [Abstract]
- Mediators Inflamm. 2022 Apr 21;2022:8007078. [Abstract]
Customer Validation & Images
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Cell Proliferation/Viability Assay
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Bio/Physico-chemical Assay
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Cell Proliferation/Viability Assay
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Cell Proliferation/Viability Assay
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Flow Cytometry
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| HL-60 | IC50 |
5.2 μg/mL
Compound: 5
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Cytotoxicity against human HL60 cells by MTT assay
Cytotoxicity against human HL60 cells by MTT assay
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[PMID: 11000027] |
In Vitro
Polyphyllin VI (0-16 μM; 48 h) significantly decreases the viability of A549, NCI-H1299 and HepaRG cells in a dose-dependent manner[1][2].
Polyphyllin VI (0.5-2 μM-1 μM; 24 h) significantly increases the percentage of A549, and NCI-H1299 cells in the G2/M stage in a dose-dependent manner[1].
Polyphyllin VI (0-12 μM-1 μM; 24 h) arrests HepaRG cells at S stage [2].
Polyphyllin VI (0-6 μM-1 μM; 24 h) activates the NLRP3 inflammasome[3].
Polyphyllin VI (0-6 μM-1 μM; 24 h) induces pyroptosis via ROS/NF-κB pathway om A549 and NCI-H1299 cells[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:A549, NCI-H1299, and HepaRG cells
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Concentration:0 μM, 2.5 μM, 5.0 μM, 7.5 μM, 10 μM, 12.5 μM (A549, NCI-H1299), 0 μM, 2 μM, 4.0 μM, 6.0 μM, 8.0 μM, 10.0 μM, 12.0 μM, 16.0 μM (HepaRG)
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Incubation Time:48 h (A549, NCI-H1299), 24 h and 48 h (HepaRG)
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Result:Showed the IC50 value in NCI-H1299 cells after 48h treatment was 1.87±0.09 μM, 1.59±0.12 μM in A549[1].
Demonstrated the reduction of HepaRG cell viability ranged from 88.90% to 1.07% after 24 h, and from 79.06% to 0.71% after 48 h[2].
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Cell Line:A549, NCI-H1299 cells
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Concentration:0.5 μM, 1.0 μM, 2.0 μM
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Incubation Time:24 h
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Result:Showed those of A549 cells in G2/M phase were 25.14%±3.31%, 28.40%±4.63%, and 42.66%±1.30%, and NCI-H1299 cells were 27.99%±4.68%, 30.24%±3.61% and 38.51%±5.10% after treatment with 0.5, 1, and 2μM for 24 h, respectively.
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Cell Line:HepaRG cells
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Concentration:0 μM, 2.0 μM, 4.0 μM, 6.0 μM, 8.0 μM, 12.0 μM
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Incubation Time:24 h
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Result:Resulted the ratios of cells in the S and G0/G1 phase changed from 23.62%±0.14% to 34.01%±0.32%, 66.88%±1.15% to 54.00%±0.71%, respectively.
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Cell Line:A549, NCI-H1299 cells
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Concentration:0 μM, 3 μM, 4 μM, 5 μM, 6 μM
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Incubation Time:24 h
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Result:Resulted dose-dependently increasing the protein expression of NLRP3 and ASC, and the cleaved form of caspase-1, IL-1β, IL-18 and GSDMD in A549 and NCI-H1299 cells.
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Cell Line:A549, NCI-H1299 cells
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Concentration:0 μM, 3 μM, 4 μM, 5 μM, 6 μM
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Incubation Time:24 h
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Result:Resulted the expression of caspase-1 was significantly inhibited by N-acetyl-L-cysteine (NAC) in Polyphyllin VI -treated A549 and NCI-H1299 cells.
In Vivo
Polyphyllin VI (2.5-10 mg/kg; i.p.; 10 consecutive days) activates NLRP3 inflammasome in A549-bearing athymic nude mice[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:A549 tumor xenografts subcutaneously inoculated into the right flank of the nude mice[1]
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Dosage:2 mg/kg, 3 mg/kg, 4 mg/kg
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Administration:Intraperitoneal Injection (i.p.)
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Result:Resulted the reduction of tumor volume to 25.63%, 41.71%, and 40.41%, respectively, after 2 mg/kg, 3 mg/kg and 4 mg/kg treatment.
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Animal Model:A549 tumor xenografts subcutaneously inoculated into the right flank of the nude mice[3]
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Dosage:2.5 mg/kg, 5 mg/kg, 10 mg/kg
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Administration:Intraperitoneal Injection (i.p.)
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Result:Showed the expression of NLRP3, caspase-1, IL-1β and GSDMD was increasing in a dose manner.
Chemical Information
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CAS No. 55916-51-3
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Appearance Solid
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Molecular Weight 738.90
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Formula C39H62O13
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Color White to off-white
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SMILES
O[C@]1([C@@]2([H])O[C@]3(CC[C@@H](C)CO3)[C@H]1C)[C@]([C@@]4([H])C2)(CC[C@@]5([H])[C@@]4([H])CC=C6[C@@]5(CC[C@H](O[C@@](O[C@H](CO)[C@@H](O)[C@@H]7O)([H])[C@@H]7O[C@@](O[C@@H](C)[C@H](O)[C@H]8O)([H])[C@@H]8O)C6)C)C
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Publications (6)
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Journal Impact Factor
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Most Recent
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Cancer Res
Genome-Wide CRISPR Screening Reveals that mTOR Inhibition Initiates Ferritinophagy and Ferroptosis in Head and Neck Cancer. [Abstract]2025 Jun 6. PMID: 40479615
Polyphyllin VI purchased from MedChemExpress. Usage Cited in: Cancer Res. 2025 Jun 6. [Abstract]
Cell viability of Cal27 treated with INK128 (50 nM) for 72 hours was measured. From left to right, Z-VAD, Necrostatin-1 and Ac-FEID-CMK were used in combination with INK128. Positive controls were Etoposide (1.5 μM) and Polyphyllin VI (PPVI, 5 μM; 72 h). Cell viability was compared between monotherapy and combination therapy (mean ± SD, n = 6).
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ACS Nano
Targeted Positron Emission Tomography-Tracked Biomimetic Codelivery Synergistically Amplifies Ferroptosis and Pyroptosis for Inducing Lung Cancer Regression and Anti-PD-L1 Immunotherapy Efficacy. [Abstract]2024 Nov 12;18(45):31401-31420. PMID: 39475541
Polyphyllin VI purchased from MedChemExpress. Usage Cited in: ACS Nano. 2024 Nov 12;18(45):31401-31420. [Abstract]
Polyphyllin VI (PPVI, 24 h) exhibited IC50 values of 6.41 μM and 16.26 μM in A549 and H1299 cells, respectively.
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Dev Cell
2025 Apr 18:S1534-5807(25)00206-0. PMID: 40280135
Polyphyllin VI purchased from MedChemExpress. Usage Cited in: Dev Cell. 2025 Apr 18:S1534-5807(25)00206-0. [Abstract]
Measurement of caspase 1 (CASP1) activity in control A549 cells and A549 cells withCCN1 overexpression following treatment with RSL3 (0.5 μM, 24 h) or erastin (10 μM, 24h). Treatment with Polyphyllin VI (2 μM, 24 h) was set as the positive control to induce CASP1 activity.
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Int Immunopharmacol
2025 Jan 10:144:113684. PMID: 39602960 -
Int Immunopharmacol
Stachyose ameliorates myocardial ischemia-reperfusion injury by inhibiting cardiomyocyte ferroptosis and macrophage pyroptosis. [Abstract]2024 Oct 8;143(Pt 1):113334. PMID: 39383784 -
Mediators Inflamm
Downregulated XBP-1 Rescues Cerebral Ischemia/Reperfusion Injury-Induced Pyroptosis via the NLRP3/Caspase-1/GSDMD Axis. [Abstract]2022 Apr 21;2022:8007078. PMID: 35497095
Polyphyllin VI purchased from MedChemExpress. Usage Cited in: Mediators Inflamm. 2022 Apr 21;2022:8007078. [Abstract]
The HT22 cells were, respectively, pretreated with Z-YVAD-FMK (20 μM) and Polyphyllin VI (4 μM) 30 min before exposing to OGD/R for 24 h. Cell viability was detected in HT22 cells using a CCK-8 assay.
Polyphyllin VI purchased from MedChemExpress. Usage Cited in: Mediators Inflamm. 2022 Apr 21;2022:8007078. [Abstract]
The HT22 cells were, respectively, pretreated with XBP-1 siRNA, 24 h before exposing to OGD/R for 24 h and Z-YVAD-FMK (20 μM) and Polyphyllin VI (4 μM) 30 min before exposing to OGD/R for 24 h. The quantity of necrotic cells and pyroptotic cells were analyzed by Annexin V and PI staining in each group.
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (135.34 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 1 mg/mL (1.35 mM); Clear solution
This protocol yields a clear solution of ≥ 1 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (10.0 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.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 1 mg/mL (1.35 mM); Clear solution
This protocol yields a clear solution of ≥ 1 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (10.0 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
Please enter the basic information of animal experiments:
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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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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
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).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
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.
Protocols
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Flow cytometric DNA-content cell-cycle staining
Flow cytometric DNA-content cell-cycle staining measures the fluorescence intensity of DNA-bound fluorochromes in single cells or nuclei to estimate DNA content distributions, allowing assignment of populations to G0/G1, S, and G2/M phases by DNA histogram deconvolution. Propidium iodide (PI) intercalates into DNA, and PI fluorescence is proportional to cellular DNA content when staining is performed under conditions that make DNA accessible and minimize non-DNA signal. Cells with G2/M DNA content are expected to show approximately twice the fluorescence intensity of G0/G1 cells, while S-phase cells occupy intermediate fluorescence values. PI-based DNA-content analysis can also detect cells with fractional DNA content, often reported as sub-G1, when DNA fragmentation and extraction during staining reduce retained DNA signal in apoptotic cells. DAPI is an alternative DNA fluorochrome for univariate DNA-content analysis, while bivariate approaches combining DNA content with proliferation
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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BrdU Incorporation Assay
Bromodeoxyuridine (BrdU) incorporation assay is based on the principle that BrdU, a thymidine analog, is incorporated into newly synthesized DNA during the S phase of the cell cycle, thereby serving as a marker of DNA replication and cellular proliferation. Incorporated BrdU can be detected using anti-BrdU antibodies following DNA denaturation, enabling visualization or quantification of proliferating cells through immunochemical detection methods such as immunofluorescence or immunohistochemistry.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Protocol for Cell Cycle
Cell-cycle analysis by flow cytometry measures DNA content in single cells to estimate the fraction of cells in G0/G1, S, and G2/M phases. Propidium iodide intercalates into DNA, and after RNA removal with RNase, fluorescence intensity reflects cellular DNA content: 2N cells are assigned to G0/G1, cells between 2N and 4N to S phase, and 4N cells to G2/M. DNA-content analysis alone cannot reliably separate G0 from G1 or G2 from M. Ki-67 can distinguish quiescent G0 cells from cycling cells, EdU or BrdU incorporation marks active DNA synthesis in S phase, and phospho-histone H3 staining identifies mitotic cells within the 4N population.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
Purity & Documentation
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Data Sheet (286 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Lin Z, et al. Anti-lung Cancer Effects of Polyphyllin VI and VII Potentially Correlate with Apoptosis In Vitro and In Vivo. Phytother Res. 2015 Oct;29(10):1568-76. [Content Brief]
[2]. Liu Y, et al. Molecular Mechanisms of Apoptosis in HepaRG Cell Line Induced by Polyphyllin VI via the Fas Death Pathway and Mitochondrial-Dependent Pathway. Toxins (Basel). 2018 May 15;10(5). pii: E201. [Content Brief]
[3]. Jin-Feng Teng, et al. Polyphyllin VI Induces Caspase-1-Mediated Pyroptosis via the Induction of ROS/NF-κB/NLRP3/GSDMD Signal Axis in Non-Small Cell Lung Cancer. Cancers (Basel). 2020 Jan 13;12(1):193. [Content Brief]
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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 1.3534 mL | 6.7668 mL | 13.5336 mL | 33.8341 mL |
| 5 mM | 0.2707 mL | 1.3534 mL | 2.7067 mL | 6.7668 mL | |
| 10 mM | 0.1353 mL | 0.6767 mL | 1.3534 mL | 3.3834 mL | |
| 15 mM | 0.0902 mL | 0.4511 mL | 0.9022 mL | 2.2556 mL | |
| 20 mM | 0.0677 mL | 0.3383 mL | 0.6767 mL | 1.6917 mL | |
| 25 mM | 0.0541 mL | 0.2707 mL | 0.5413 mL | 1.3534 mL | |
| 30 mM | 0.0451 mL | 0.2256 mL | 0.4511 mL | 1.1278 mL | |
| 40 mM | 0.0338 mL | 0.1692 mL | 0.3383 mL | 0.8459 mL | |
| 50 mM | 0.0271 mL | 0.1353 mL | 0.2707 mL | 0.6767 mL | |
| 60 mM | 0.0226 mL | 0.1128 mL | 0.2256 mL | 0.5639 mL | |
| 80 mM | 0.0169 mL | 0.0846 mL | 0.1692 mL | 0.4229 mL | |
| 100 mM | 0.0135 mL | 0.0677 mL | 0.1353 mL | 0.3383 mL |
Polyphyllin VI Related Classifications
HY-N0816 Related Classifications
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