2. Autophagy Apoptosis Immunology/Inflammation Metabolic Enzyme/Protease NF-κB
  3. Mitophagy Autophagy Ferroptosis Interleukin Related IFNAR Reactive Oxygen Species (ROS)
  4. Platycodin D2

Platycodin D2 is an orally active triterpenoid saponin found in Platycodon grandiflorum. Platycodin D2 induces mitophagy in cancer cells through NIX, thereby activating the P21/CyclinA2 pathway and promoting cell senescence. Platycodin D2 induces mitochondrial dysfunction, enhances autophagy, inhibits hepatocellular carcinoma cell proliferation, and exhibits anti-tumor activity against multiple cancer cell types. Platycodin D2 promotes mRNA expression of T-bet, GATA-3, Th1 cytokines IL-2 and IFN-γ, and Th2 cytokines IL-4 and IL-10, enhances splenocyte proliferation, and acts as a vaccine adjuvant with low rabbit red blood cell hemolytic activity. Platycodin D2 induces mitochondrial ROS production, incomplete autophagy, and ferroptosis to inhibit breast cancer cell proliferation. Platycodin D2 can be used for the research of cancer, inflammation and immunology.

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Platycodin D2

Platycodin D2 Chemical Structure

CAS No. : 66663-90-9

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Based on 3 publication(s) in Google Scholar

Platycodin D2 Related Antibodies

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Description

Platycodin D2 is an orally active triterpenoid saponin found in Platycodon grandiflorum. Platycodin D2 induces mitophagy in cancer cells through NIX, thereby activating the P21/CyclinA2 pathway and promoting cell senescence. Platycodin D2 induces mitochondrial dysfunction, enhances autophagy, inhibits hepatocellular carcinoma cell proliferation, and exhibits anti-tumor activity against multiple cancer cell types. Platycodin D2 promotes mRNA expression of T-bet, GATA-3, Th1 cytokines IL-2 and IFN-γ, and Th2 cytokines IL-4 and IL-10, enhances splenocyte proliferation, and acts as a vaccine adjuvant with low rabbit red blood cell hemolytic activity. Platycodin D2 induces mitochondrial ROS production, incomplete autophagy, and ferroptosis to inhibit breast cancer cell proliferation. Platycodin D2 can be used for the research of cancer, inflammation and immunology[1][2][3].

IC50 & Target[2]

IL-2

 

IL-4

 

IL-10

 

Cellular Effect
Cell Line Type Value Description References
HCT-15 IC50
5.7 μM
Compound: 8, deapio-platycodin D
Antiproliferative activity against human HCT15/CL02 cells after 48 hrs by sulforhodamine B assay
Antiproliferative activity against human HCT15/CL02 cells after 48 hrs by sulforhodamine B assay
[PMID: 20939516]
HCT-15 IC50
9.6 μM
Compound: 8, deapio-platycodin D
Antiproliferative activity against human HCT15 cells after 48 hrs by sulforhodamine B assay
Antiproliferative activity against human HCT15 cells after 48 hrs by sulforhodamine B assay
[PMID: 20939516]
MES-SA IC50
3.5 μM
Compound: 8, deapio-platycodin D
Antiproliferative activity against human MESSA cells after 48 hrs by sulforhodamine B assay
Antiproliferative activity against human MESSA cells after 48 hrs by sulforhodamine B assay
[PMID: 20939516]
MES-SA/Dx5 IC50
5.2 μM
Compound: 8, deapio-platycodin D
Antiproliferative activity against human MESSA/DX5 cells after 48 hrs by sulforhodamine B assay
Antiproliferative activity against human MESSA/DX5 cells after 48 hrs by sulforhodamine B assay
[PMID: 20939516]
In Vitro

Platycodin D2 (1-100 μM; 48 h) specifically inhibits proliferation of Huh-7, MHCC97H, HCCLM3, HepG-2, SK-Hep1, and Huh-6 HCC cells with an IC50 of 10.2-12.7 μM, while having no significant cytotoxic effect on THLE-2 and L02 normal liver cells (IC50 >200 μM)[1].
Platycodin D2 (10 μM; 48 h) does not significantly induce apoptosis in Huh-7 or HCCLM3 HCC cells[1].
Platycodin D2 (10 μM; 24-48 h) induces robust autophagy in Huh-7 and HCCLM3 HCC cells, as evidenced by increased LC3 puncta formation, elevated autophagic flux, autophagolysosome formation, and altered expression of autophagy-related proteins, without affecting apoptosis-related proteins[1].
Platycodin D2 (5, 10 μM; 48 h) induces mitochondrial dysfunction in Huh-7 and HCCLM3 HCC cells, evidenced by increased ROS production, reduced mitochondrial membrane potential, and selective mitophagy via LC3 co-localization with damaged mitochondria[1].
Platycodin D2 (10 μM; 48 h) induces mitophagy in HCCLM3 HCC cells via NIX, as silencing NIX abrogates PD2's effects on autophagy, cell viability, mitochondrial function, and downstream P21/CyclinA2 expression[1].
Platycodin D2 (10 μM; 48 h) induces G2/M phase arrest and senescence in Huh-7 and HCCLM3 HCC cells, evidenced by altered cell cycle distribution, upregulated SASP gene expression, shifted expression of senescence-related proteins, increased β-galactosidase activity, reduced Lamin B1 levels, and nuclear γ-H2A.X aggregation[1].
Platycodin D2 (3.906-125 μg/mL; 30 min) exhibits haemolytic activity against 0.5% rabbit red blood cell suspensions with an HD50 of 18.57 μg/mL[2].
Platycodin D2 (0.0016-1.0 μg/mL; 16 h) significantly enhances mRNA expression of Th1 (IL-2, IFN-γ, T-bet) and Th2 (IL-4, IL-10, GATA-3) cytokines and transcription factors in Con A-stimulated naive ICR mouse splenocytes[2].
Platycodin D2 (5-50 μM; 48 h) potently inhibits the proliferation of MCF7, SKBR3, and Hs578T breast cancer cells with IC50 values of 14.62 μM, 29.60 μM, and 5.24 μM, respectively, after 48 h of incubation[3].
Platycodin D2 (5-50 μM; 48 h) blocks autophagy flux in MCF7, SKBR3, and Hs578T breast cancer cells by increasing LC3II/I and p62 expression while decreasing Syntaxin 17, SNAP29, VAMP8, and Lamp2b expression after 48 h of incubation[3].
Platycodin D2 (5-50 μM; 48 h) induces ferroptosis in MCF7, SKBR3, and Hs578T breast cancer cells by decreasing SLC7A11, GSH and GPX4 expression after 48 h of incubation[3].
Platycodin D2 (5-50 μM; 48 h) increases intracellular ferrous ion levels in MCF7, SKBR3, and Hs578T breast cancer cells after 48 h of incubation, a hallmark of ferroptosis[3].
Platycodin D2 (5-50 μM; 48 h) upregulates mitochondrial outer membrane protein TOM20 expression in MCF7, SKBR3, and Hs578T breast cancer cells after 48 h of incubation, indicating mitochondrial damage[3].
Platycodin D2 (5-50 μM; 48 h) increases intracellular MDA levels in MCF7, SKBR3, and Hs578T breast cancer cells after 48 h of incubation, indicating enhanced lipid peroxidation associated with ferroptosis[3].
Platycodin D2 (5-50 μM; 48 h) decreases intracellular SOD levels in MCF7, SKBR3, and Hs578T breast cancer cells after 48 h of incubation, reducing antioxidant capacity and promoting ferroptosis[3].
Platycodin D2 (5-50 μM; 48 h) increases mitochondrial ROS production and reduces mitochondrial membrane potential in MCF7, SKBR3, and Hs578T breast cancer cells after 48 h of incubation, contributing to mitochondrial damage[3].

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

Platycodin D2 Related Antibodies

Cell Viability Assay[1]

Cell Line: Huh-7, MHCC97H, HCCLM3, HepG-2, SK-Hep1, Huh-6 hepatocellular carcinoma (HCC) cells, THLE-2, L02 normal liver cells
Concentration: 1, 5, 10, 20, 50, 100 μM
Incubation Time: 48 h
Result: Significantly reduced viability of all tested HCC cell lines, with IC50 values of 10.2 μM (Huh-7), 11.5 μM (MHCC97H), 10.4 μM (HCCLM3), 11.2 μM (HepG-2), 12.7 μM (SK-Hep1), and 11.8 μM (Huh-6).
Had no obvious inhibitory effect on normal THLE-2 and L02 liver cells, with IC50 values >200 μM for both.

Cell Autophagy Assay[1]

Cell Line: Huh-7, HCCLM3 HCC cells
Concentration: 10 μM
Incubation Time: 24 h; 48 h
Result: Significantly increased the number of EGFP-LC3 puncta per cell (20 puncta for HCCLM3, 60 puncta for Huh-7, compared to near-zero in controls).
Showed significantly more red fluorescence than green fluorescence via mRFP-GFP-LC3 staining, indicating increased autophagic flux.
Revealed abundant autophagolysosomes in PD2-treated cells via transmission electron microscopy.
Increased LC3-II and Beclin 1 expression, and decreased P62 expression via Western blotting, while apoptosis-related proteins (Cleaved-caspase3, PARP, Cleaved-PARP) showed no significant changes.

Cell Cycle Analysis[1]

Cell Line: Huh-7, HCCLM3 HCC cells
Concentration: 10 μM
Incubation Time: 48 h
Result: Induced G2/M phase arrest in HCC cells, with G2/M phase percentage increasing.
Showed significant upregulation of SASP genes (IL-6, IL-8, MMP3, TGF-β, IGFBP3, CXCL-1) in both cell lines via Real Time qPCR.
Revealed upregulated P21 and γ-H2A.X, and downregulated CDK1, CyclinA2, E2F, and p-RB via Western blotting.
Showed a significant increase in β-galactosidase positive cells, reduced Lamin B1 fluorescence and nuclear aggregation of γ-H2A.X in PD2-treated cells via β-galactosidase staining and immunofluorescence.

Western Blot Analysis[3]

Cell Line: MCF7, SKBR3, Hs578T
Concentration: 5, 10, 20 μM (MCF7, Hs578T); 25, 50 μM (SKBR3)
Incubation Time: 48 h
Result: Upregulated the expression of LC3II/I and p62 proteins in all three breast cancer cell lines.
Downregulated the expression of Syntaxin 17, SNAP29, VAMP8, and Lamp2b proteins in all three breast cancer cell lines.\nDownregulated the expression of ferroptosis-related proteins SLC7A11 and GPX4 in all three breast cancer cell lines.\nSignificantly upregulated the expression of TOM20 in all three breast cancer cell lines.
In Vivo

Platycodin D2 (5-10 mg/kg; intratumoral injection; once every 3 days; 4 doses) significantly inhibits HCC tumor growth in female BALB/c nude mice in vivo in a dose-dependent manner, with 10 mg/kg achieving near-complete tumor volume reduction, and induces mitophagy and cell senescence via upregulation of LC3-II, NIX, and P21 and downregulation of Cyclin A2[1].
Platycodin D2 (25-100 μg; s.c.; on Day 1 and Day 15) elicits balanced Th1 and Th2 immune responses in OVA (HY-W250978)-immunized ICR mice, significantly enhancing splenocyte proliferation, OVA-specific antibody titers at tested doses[2].
Platycodin D2 (2.5-5 mg/kg; i.g.; once every 2 days; 5 total doses) significantly inhibits breast cancer tumor growth in nude mice, with the 5 mg/kg dose reducing tumor volume by 80.5%, and mediates this effect via autophagy flux blockage and ferroptosis[3].

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

Animal Model: BALB/c nude mice (female, 5-6 weeks old, injected with 5×106 HCCLM3 cells in the right limb)[1]
Dosage: 5 mg/kg; 10 mg/kg
Administration: intratumoral injection; once every 3 days; 4 doses
Result: Significantly inhibited tumor growth compared to the control group.
Reduced mean tumor volume to ~100 mm3 by week 4 at 5 mg/kg dose.
Reduced mean tumor volume to near 0 mm3 by week 4 at 10 mg/kg dose.
Maintained higher body weights than the control and 5-FU groups throughout the study.
Dose-dependently increased mean density of LC3-II, NIX, and P21 in tumor tissues.
Dose-dependently decreased mean density of Ki67 and Cyclin A2 in tumor tissues.
Animal Model: OVA-immunized ICR mice (female, 6 weeks old, 18-22 g)[2]
Dosage: 25 μg; 50 μg; 75 μg; 100 μg
Administration: s.c.; on Day 1 and Day 15
Result: Significantly increased Con A- and LPS-stimulated splenocyte proliferation at 25 μg and 50 μg compared to the OVA control group (P<0.01 or P<0.001).
Significantly enhanced OVA-induced splenocyte proliferation at all four tested doses compared to the OVA control group (P<0.05 or P<0.01).
Significantly enhanced serum OVA-specific IgG, IgG1, IgG2a, and IgG2b antibody titers at all four tested doses compared to the OVA control group (P<0.01 or P<0.001).
Resulted in significantly higher IgG and IgG1 titers at 75 μg and 100 μg than the Alum-treated group (P<0.05).
Animal Model: BALB/c nude mice (female, 4-5 weeks old, subcutaneous MCF7 cell implantation tumor-bearing model)[3]
Dosage: 2.5 mg/kg; 5 mg/kg
Administration: p.o.; once every 2 days; 5 total doses
Result: Reduced tumor volume by 80.5% at 5 mg/kg compared to control.
Reduced tumor volume by 65.8% at 2.5 mg/kg compared to control.
Did not affect mouse body weight.
Downregulated ferroptosis-related proteins SLC7A11 and GPX4 in tumor tissues.
Upregulated autophagy-related proteins LC3II and p62 in tumor tissues.
Increased ROS levels in tumor tissues.
Increased lipid peroxidation in tumor tissues.
Molecular Weight

1387.46

Formula

C63H102O33
CAS No.
Appearance

Solid

Color

Off-white to light yellow

SMILES

O[C@H]([C@@H]([C@@H](O[C@@]1([H])[C@@H]([C@H]([C@H](O)CO1)O[C@@]2([H])[C@@H]([C@](CO)(O)CO2)O)O)[C@H](C)O3)O)[C@]3([H])O[C@H]([C@H]([C@@H](O)CO4)O)[C@@H]4OC([C@]56[C@](CC(C)(C)CC6)([H])C7=CC[C@@]([C@@]8([C@@](C(CO)([C@@H](O[C@@]9([H])[C@@H]([C@H]([C@H](O)[C@@H](CO)O9)O[C@]%10([H])O[C@@H]([C@@H](O)[C@H](O)[C@H]%10O)CO)O)[C@@H](O)C8)CO)([H])CC%11)C)([H])[C@]%11(C)[C@]7(C)C[C@H]5O)=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 (72.07 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 0.7207 mL 3.6037 mL 7.2074 mL
5 mM 0.1441 mL 0.7207 mL 1.4415 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 (1.80 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 (1.80 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: 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).
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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: 99.84%

SDS (251 KB)

COA (252 KB) RP-HPLC (211 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 0.7207 mL 3.6037 mL 7.2074 mL 18.0185 mL
5 mM 0.1441 mL 0.7207 mL 1.4415 mL 3.6037 mL
10 mM 0.0721 mL 0.3604 mL 0.7207 mL 1.8019 mL
15 mM 0.0480 mL 0.2402 mL 0.4805 mL 1.2012 mL
20 mM 0.0360 mL 0.1802 mL 0.3604 mL 0.9009 mL
25 mM 0.0288 mL 0.1441 mL 0.2883 mL 0.7207 mL
30 mM 0.0240 mL 0.1201 mL 0.2402 mL 0.6006 mL
40 mM 0.0180 mL 0.0901 mL 0.1802 mL 0.4505 mL
50 mM 0.0144 mL 0.0721 mL 0.1441 mL 0.3604 mL
60 mM 0.0120 mL 0.0601 mL 0.1201 mL 0.3003 mL
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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:

Platycodin D266663-90-9Platycodin D 2Platycodin D-2MitophagyAutophagyFerroptosisInterleukin RelatedIFNARReactive Oxygen Species (ROS)Mitochondrial AutophagyILInterferon-α/β receptorInterferon-alpha/beta receptorMCF7HCCLM3hepatocellular carcinomaP21Platycodon grandiflorumbreast cancerHuh-7MHCC97HCyclinA2NIXInhibitorinhibitorinhibit

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