Cat. No.: HY-N5008

Macranthoside B

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Macranthoside B is an apoptosis inducer with in vitro and in vivo anticancer activity. Macranthoside B induces autophagy and ferroptosis in cancer cells. Macranthoside B induces intracellular ROS accumulation, activates AMPK, inhibits mTOR and P70S6 kinase phosphorylation, and modulates Bcl-2/Bax expression. Macranthoside B activates caspase-3, caspase-9, and the intrinsic caspase cascade, induces PARP cleavage/degradation, and inhibits NRF2 signaling. Macranthoside B disrupts iron homeostasis via NCOA4-dependent ferritinophagy, up-regulates Lip-ROS, reduces mitochondrial membrane potential, and activates the JNK pathway. Macranthoside B can be used for the research of ovarian cancer, hepatoma, gastric carcinoma, breast carcinoma, colon carcinoma, glioma, melanoma, adenocarcinoma of the esophagogastric junction, and cervical cancer.

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Pureté: 99.95%
CAS No.: 146100-02-9
Formule: C₅₃H₈₆O₂₂
Masse moléculaire:1075.24

Stockage:

4°C, sealed storage, away from moisture and light

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

Macranthoside B Chemical Structure

CAS No.: 146100-02-9

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Activité biologique
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- In Vivo
Chemical Information
Solvant et solubilité
- In Vitro
Pureté et documentation
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Activité biologique

Description

IC₅₀ & Target^[1]^[2]

mTOR

AMPK

Caspase-9

Caspase 3

Bcl-2

Bax

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In Vitro

Macranthoside B (1.25-20 μM; 24-72 h) inhibits proliferation of human ovarian carcinoma A2780 cells in a time- and concentration-dependent manner, with IC₅₀ values ranging from 7.52 μM to 14.66 μM, and exhibits lower cytotoxicity toward normal human embryonic lung fibroblast HFL1 cells^[1].
Macranthoside B (5-20 μM; 6 h treatment, followed by 15 days of growth) dose-dependently inhibits clonogenicity of human ovarian carcinoma A2780 cells, with an IC₅₀ of 8.46 μM^[1].
Macranthoside B (5-20 μM; 48 h) dose-dependently activates AMPK and inhibits the mTOR/P70S6K pathway in human ovarian carcinoma A2780 cells^[1].
Macranthoside B (2.55-80 μM; 48 h) potently inhibits the proliferation of human HepG2, MGC-803, MCF-7, SW1116, U251, rat C6, and mouse B16F1, B16F10 cancer cells in vitro, with IC₅₀ values ranging from 10 μM to 18 μM^[2].
Macranthoside B (0-40 μM; 24, 48 h) inhibits the viability of SKGT-4, OE-19, and OE-33 AEG cells in a concentration-dependent manner, with 48 h IC₅₀ values ranging from 4.74 to 8.59 μM, and is less potent against normal NGEC cells^[3].
Macranthoside B (8-10 μM; 24 h) inhibits the colony-forming ability of SKGT-4 and OE-19 AEG cells in a concentration-dependent manner, with significant suppression at 8 μM and 10 μM^[3].
Macranthoside B (10-15 μM; 48 h) inhibits the proliferation of SKGT-4 and OE-19 AEG cells in a concentration-dependent manner, with significant reduction in EDU-positive cells at 10 μM and 15 μM^[3].
Macranthoside B (8-10 μM; 36 h) inhibits the migration and invasion of SKGT-4 and OE-19 AEG cells in a concentration-dependent manner, with significant suppression at 8 μM and 10 μM^[3].
Macranthoside B (5-20 μM; 24-48 h) dose-dependently induces apoptosis in human ovarian carcinoma A2780 cells, and this apoptosis is reduced by pretreatment with the autophagy inhibitor 3-Methyladenine (HY-19312) or the pan-caspase inhibitor Z-VAD-FMK (HY-16658B)^[1].
Macranthoside B (5-20 μM; 48 h) dose-dependently upregulates pro-apoptotic markers (cleaved caspase-3, cleaved caspase-9, cleaved PARP) and the autophagy marker LC3-II in human ovarian carcinoma A2780 cells; inhibition of autophagy reduces apoptosis, while inhibition of apoptosis enhances autophagy, and inhibition of ROS or AMPK reduces both apoptosis and autophagy^[1].
Macranthoside B (20 μM; 48 h) induces apoptotic nuclear morphological changes in human ovarian carcinoma A2780 cells after 48 h of incubation^[1].
Macranthoside B (10-20 μM) dose-dependently induces autophagic puncta formation in GFP-LC3-expressing human ovarian carcinoma A2780 cells^[1].
Macranthoside B (15 μM; 48 h) activates autophagy in SKGT-4 and OE-19 AEG cells, increasing LC3B puncta, autophagic vacuoles, and LC3B II/P62 protein levels, while impairing autophagic flux^[3].
Macranthoside B (10 μM; 24-48 h) increases intracellular ROS levels in human ovarian carcinoma A2780 cells^[1].
Macranthoside B (30-40 μM; 4 h) induces morphological changes characteristic of early apoptosis, including cell rounding, chromatin condensation, and karyopyknosis, in human hepatoma HepG2 cells^[2].
Macranthoside B (40 μM; 4 h) induces apoptosis in human hepatoma HepG2 cells, with 39.02% of cells entering early apoptosis and 13.45% entering late apoptosis/necrosis^[2].
Macranthoside B (30-40 μM; 4 h) induces apoptosis in human hepatoma HepG2 cells via a mitochondrion-mediated pathway, activating caspase-9 and caspase-3, cleaving PARP, increasing Bax protein expression, decreasing Bcl-2 protein expression, and elevating the Bax/Bcl-2 ratio^[2].
Macranthoside B (15 μM; 48 h) treatment of SKGT-4 AEG cells alters the expression of 1800+ genes, upregulating pathways related to oxidoreductase activity, ferroptosis, and autophagy^[3].
Macranthoside B (10-15 μM; 48 h) induces concentration-dependent accumulation of lipid reactive oxygen species in SKGT-4 and OE-19 AEG cells, with significant increases at 10 μM and 15 μM^[3].
Macranthoside B (0-15 μM; 0-48 h) downregulates GPX4 protein levels in SKGT-4 and OE-19 AEG cells in both concentration- and time-dependent manners, reducing levels to as low as 0.1 and 0.5 of control, respectively^[3].
Macranthoside B (0-15 μM; 0-48 h) upregulates NCOA4 and FTH1 protein levels in SKGT-4 and OE-19 AEG cells in both concentration- and time-dependent manners, activating NCOA4-mediated ferritinophagy^[3].
Macranthoside B (0-15 μM; 48 h) inhibits NRF2 in SKGT-4 and OE-19 AEG cells, downregulating NRF2 protein levels and its downstream target genes HERC2 and VAMP8, disrupting iron homeostasis^[3].
Macranthoside B (48 h) disrupts iron homeostasis in SKGT-4 and OE-19 AEG cells, significantly increasing intracellular Fe²⁺ levels^[3].
Macranthoside B enhances Paclitaxel (HY-B0015)-mediated apoptosis in human cervical adenocarcinoma HeLa cells via ROS overgeneration and activation of the MAPKs/JNK pathway^[4].

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

Cell Viability Assay^[1]

Cell Line:

Human ovarian carcinoma A2780 cells, human embryonic lung fibroblast HFL1 cells
Concentration:

1.25 μM, 2.5 μM, 5 μM, 1 μM, 20 μM
Incubation Time:

24 h, 48 h, 72 h
Result:

Inhibited A2780 cell viability in a concentration- and time-dependent manner, with IC₅₀ values of 14.66 μM (24 h), 11.23 μM (48 h), 7.52 μM (72 h).
Exhibited IC₅₀ values of 59.58 μM (24 h), 42.34 μM (48 h), 38.44 μM (72 h) in HFL1 cells, showing greater cytotoxicity toward tumor cells than normal cells.

Western Blot Analysis^[1]

Cell Line:

human ovarian carcinoma A2780 cells
Concentration:

5 μM, 10 μM, 20 μM (48 h incubation); 10 μM (48 h incubation with inhibitor pretreatment or beclin 1 siRNA transfection)
Incubation Time:

48 h
Result:

Increased levels of cleaved caspase-3, cleaved caspase-9, cleaved PARP, and LC3-II in a concentration-dependent manner at 5, 10, 20 μM for 48 h (cleaved caspase-3 levels relative to β-actin: 4.4, 20.0, 24.7; cleaved caspase-9: 10.5, 14.9, 23.5; cleaved PARP: 2.2, 3.4, 4.7; LC3-II: 3.4, 12.4, 24.9).
Decreased levels of cleaved caspase-3 (from 10.0 to 8.5), cleaved caspase-9 (from 2.0 to 1.8), cleaved PARP (from 1.0 to 0.5), and LC3-II (from 1.0 to 0.23) when cells were pretreated with 5 mM 3-methyladenine prior to 10 μM treatment.
Decreased LC3-II levels (from 1.0 to 0.19) and cleaved PARP levels (from 1.0 to 0.05) when cells were transfected with beclin 1 siRNA prior to 10 μM treatment.
Decreased levels of cleaved caspase-3 (from 2.1 to 0.2), cleaved caspase-9 (from 6.5 to 2.7), cleaved PARP (from 4.8 to 1.9), but increased LC3-II levels (from 2.0 to 3.8) when cells were pretreated with 10 μM Z-VAD-FMK prior to 10 μM treatment.
Decreased levels of cleaved caspase-3 (from 2.2 to 0.8), cleaved caspase-9 (from 1.7 to 1.5), cleaved PARP (from 1.6 to 0.7), and LC3-II (from 5.0 to 2.5) when cells were pretreated with 5 mM NAC prior to 10 μM treatment.
Decreased levels of cleaved caspase-3 (from 1.8 to 0.7) and LC3-II (from 1.6 to 0.7) when cells were pretreated with 10 μM Compound C prior to 10 μM treatment.

Western Blot Analysis^[1]

Cell Line:

human ovarian carcinoma A2780 cells
Concentration:

5 μM, 10 μM, 20 μM (48 h incubation); 10 μM (48 h incubation with inhibitor pretreatment)
Incubation Time:

48 h
Result:

Increased p-AMPK levels relative to β-actin (13.0, 18.9, 23.9) and decreased p-mTOR (0.9, 0.8, 0.6) and p-P70S6K (0.6, 0.4, 0.1) levels in a concentration-dependent manner at 5, 10, 20 μM for 48 h.
Decreased p-AMPK (from 2.4 to 1.1), p-mTOR (from 0.4 to 0.9), and p-P70S6K (from 0.5 to 1.0) levels when cells were pretreated with 5 mM NAC prior to 10 μM treatment.
Decreased p-AMPK (from 5.1 to 0.3), p-mTOR (from 0.3 to 0.9), and p-P70S6K (from 0.4 to 0.6) levels when cells were pretreated with 10 μM Compound C prior to 10 μM treatment.

Cell Viability Assay^[2]

Cell Line:

human hepatoma HepG2, human gastric cancer MGC-803, human mammary adenocarcinoma MCF-7, human colonic carcinoma SW1116, human glioblastoma U251, rat glioma C6, mouse melanoma B16F1, mouse melanoma B16F10
Concentration:

2.55-80 μM; 4.25-48 μM (HepG2 cells)
Incubation Time:

48 h
Result:

Inhibited HepG2 cell viability with inhibitory rates of 2.58%, 23.21%, 55.89%, 86.55%, and 98.14% at concentrations of 4.25, 7.08, 14.75, 23.04, and 48 μM respectively, with an IC₅₀ of 10 μM.
Inhibited viability of all tested cell lines with IC₅₀ values: MGC-803 (16 μM), MCF-7 (12 μM), SW1116 (14 μM), U251 (18 μM), C6 (14 μM), B16F1 (15 μM), and B16F10 (16 μM).

Apoptosis Analysis^[2]

Cell Line:

Human hepatoma HepG2
Concentration:

40 μM
Incubation Time:

4 h
Result:

Increased the percentage of early apoptotic cells to 39.02% and the percentage of late apoptotic/necrotic cells to 13.45%, compared to control cells.

Western Blot Analysis^[2]

Cell Line:

human hepatoma HepG2
Concentration:

30 μM, 40 μM
Incubation Time:

4 h
Result:

Increased cleaved PARP levels in a concentration-dependent manner.
Decreased procaspase-9 expression significantly, decreased procaspase-3 expression slightly, and increased levels of activated caspase-3 p17 and p12 subunits.
Increased Bax protein levels by 82% and 113% at 30 μM and 40 μM respectively, decreased Bcl-2 protein levels slightly, resulting in a notable increase in the Bax/Bcl-2 ratio.

Cell Viability Assay^[3]

Cell Line:

normal gastric epithelial cell line (NGEC), adenocarcinoma of the esophagogastric junction (AEG) cell lines SKGT-4, OE-19, OE-33
Concentration:

0, 5, 10, 20, 30, 40 μM
Incubation Time:

24 h; 48 h
Result:

Inhibited AEG cell viability in a concentration-dependent manner, with normal NGEC cells showing lower sensitivity.
Exhibited 24 h IC₅₀ values of 9.51 μM (SKGT-4), 12.70 μM (OE-19), 10.98 μM (OE-33), and 22.80 μM (NGEC).
Exhibited 48 h IC₅₀ values of 8.59 μM (SKGT-4), 8.47 μM (OE-19), 4.74 μM (OE-33), and 11.69 μM (NGEC).

Cell Proliferation Assay^[3]

Cell Line:

adenocarcinoma of the esophagogastric junction (AEG) cell lines SKGT-4, OE-19
Concentration:

0, 8, 10 μM
Incubation Time:

24 h, followed by 15-20 days of drug-free growth
Result:

Reduced the number of colonies in SKGT-4 and OE-19 cells in a concentration-dependent manner.
Caused statistically significant decreases (***p < 0.001) at both 8 μM and 10 μM compared to the control.

Cell Proliferation Assay^[3]

Cell Line:

adenocarcinoma of the esophagogastric junction (AEG) cell lines SKGT-4, OE-19
Concentration:

0, 10, 15 μM
Incubation Time:

48 h
Result:

Reduced the EDU-positive cell rate in SKGT-4 and OE-19 cells in a concentration-dependent manner.
Caused statistically significant decreases (**p < 0.01, ***p < 0.001) at 10 μM and 15 μM compared to the control.

Western Blot Analysis^[3]

Cell Line:

adenocarcinoma of the esophagogastric junction (AEG) cell lines SKGT-4, OE-19
Concentration:

0, 5, 10, 15 μM
Incubation Time:

0, 12, 24, 36, 48 h
Result:

Reduced GPX4 protein levels in SKGT-4 and OE-19 cells in both concentration- and time-dependent manners.
Reduced GPX4 levels to 0.1 of control at 15 μM, and to 0.3 of control after 48 h in SKGT-4 cells.
Reduced GPX4 levels to 0.8 of control at 15 μM, and to 0.5 of control after 48 h in OE-19 cells.\nUpregulated NCOA4 and FTH1 protein levels in SKGT-4 and OE-19 cells in both concentration- and time-dependent manners.
Increased NCOA4 levels to 1.09 of control at 15 μM and 1.1 of control after 48 h; increased FTH1 levels to 1.1 of control at 15 μM and 1.3 of control after 48 h in SKGT-4 cells.
Increased NCOA4 levels to 2.5 of control at 15 μM and 1.1 of control after 48 h; increased FTH1 levels to 1.1 of control at 15 μM and 1.4 of control after 48 h in OE-19 cells.

In Vivo

Macranthoside B (5 mg/kg; intravenous injection; once every 2 days; for 14 consecutive days) exhibits in vivo anti-tumor activity in the HepG2 xenograft mouse tumor model, with a tumor growth inhibition rate of 53.29%^[2].

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

Animal Model:

Athymic BALB/cA nude mice (female, 35-40 days old, 18-22 g, subcutaneous implantation of HepG2 cells)^[2]
Dosage:

5 mg/kg
Administration:

i.v.; every two days; 14 days
Result:

Achieved 53.29% inhibition of tumor growth compared to vehicle control.
Significantly reduced relative tumor volume.
Lowered excised tumor weights compared to vehicle control.

Chemical Information

CAS No. 146100-02-9
Appearance Solid
Masse moléculaire 1075.24
Formule C₅₃H₈₆O₂₂
Color White to off-white
SMILES

C[C@@]12C([C@@]3([H])[C@](C(O)=O)(CCC(C)(C)C3)CC2)=CC[C@@]4([H])[C@]1(CC[C@]5([H])[C@@]4(CC[C@H](O[C@@]6([H])[C@@H]([C@H]([C@@H](O)CO6)O)O[C@@]7([H])[C@@H]([C@@H]([C@@H](O)[C@H](C)O7)O[C@]8([H])O[C@@H]([C@@H](O[C@]9([H])O[C@@H]([C@@H](O)[C@H](O)[C@H]9O)CO)[C@H](O)[C@H]8O)CO)O)[C@@]5(C)CO)C)C
Structure Classification
- Terpenoids
- Other Terpenoids
Initial Source
Livraison

Room temperature in continental US; may vary elsewhere.
Stockage

4°C, sealed storage, away from moisture and light

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

Solvant et solubilité

In Vitro:

DMSO : 100 mg/mL (93.00 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

0.9300 mL

4.6501 mL

9.3002 mL

5 mM

0.1860 mL

0.9300 mL

1.8600 mL

10 mM

0.0930 mL

0.4650 mL

0.9300 mL

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 (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Calculateur de molarité

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

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

Calculateur de dilution

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

Concentration _(start) Concentration _(start)

Volume _(start) Volume _(start)

Concentration _(final) Concentration _(final)

Volume _(final) Volume _(final)

Pureté et documentation

Select Batch:

Pureté: 99.98%

Assay: 99.98%

ee.: 99.98%

Fiche technique (298 KB)
SDS (252 KB)
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- Español - ES (252 KB)
- Swedish - SV (252 KB)
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- Portuguese - PT (252 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Instruction de manipulation (2659 KB)

Références

[1]. Shan Y, et al. Macranthoside B Induces Apoptosis and Autophagy Via Reactive Oxygen Species Accumulation in Human Ovarian Cancer A2780 Cells. Nutrition and cancer. 2016;68(2):280-9. [Content Brief]

[2]. Wang J, et al. Macranthoside B, a hederagenin saponin extracted from Lonicera macranthoides and its anti-tumor activities in vitro and in vivo. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association. 2009 Jul;47(7):1716-21. [Content Brief]

[3]. Wang L, et al. Macranthoside B Suppresses the Growth of Adenocarcinoma of Esophagogastric Junction by Regulating Iron Homeostasis and Ferroptosis through NRF2 Inhibition. Current cancer drug targets. 2025;25(8):1013-1027. [Content Brief]

[4]. Li M, et al. Macranthoside B Enhances Paclitaxel-induced Human Cervical Cancer Cell Apoptosis Through ROS-JNK Pathway. Anticancer research. 2025 Jul;45(7):2859-2870. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	0.9300 mL	4.6501 mL	9.3002 mL	23.2506 mL
	5 mM	0.1860 mL	0.9300 mL	1.8600 mL	4.6501 mL
	10 mM	0.0930 mL	0.4650 mL	0.9300 mL	2.3251 mL
	15 mM	0.0620 mL	0.3100 mL	0.6200 mL	1.5500 mL
	20 mM	0.0465 mL	0.2325 mL	0.4650 mL	1.1625 mL
	25 mM	0.0372 mL	0.1860 mL	0.3720 mL	0.9300 mL
	30 mM	0.0310 mL	0.1550 mL	0.3100 mL	0.7750 mL
	40 mM	0.0233 mL	0.1163 mL	0.2325 mL	0.5813 mL
	50 mM	0.0186 mL	0.0930 mL	0.1860 mL	0.4650 mL
	60 mM	0.0155 mL	0.0775 mL	0.1550 mL	0.3875 mL
	80 mM	0.0116 mL	0.0581 mL	0.1163 mL	0.2906 mL

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Macranthoside B

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