Cat. No.: HY-N0712

Typhaneoside

4 Cited Publications

Customer Review

Based on 4 publication(s) in Google Scholar

Typhaneoside is an orally active activator of PI3K/Akt/mTOR and farnesoid X receptor. Typhaneoside promotes the activation of AMPK and Caspase-3, induces apoptosis, ferroptosis, autophagy, ROS accumulation, cell cycle arrest at the G₂/M phase, and reduces cancer cell viability. Typhaneoside improves glucose and lipid metabolism, alleviates inflammatory responses, oxidative stress and hepatic lipid accumulation, and exerts hepatoprotective effects. Typhaneoside can be used in research related to heart failure after myocardial infarction, acute myeloid leukemia, non-alcoholic fatty liver disease and neurological disorders.

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

Purity: 99.74%
CAS No.: 104472-68-6
Formula: C₃₄H₄₂O₂₀
Molecular Weight:770.69

Storage:

4°C, protect from light

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

Typhaneoside Chemical Structure

CAS No.: 104472-68-6

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Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Publications (4)
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

All mTOR Isoforms :

All Akt Isoforms :

All PI3K Isoforms :

All Calcium Channel Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
N9	IC₅₀	>100 μM Compound: 10	Antineuroinflammatory activity in mouse N9 cells assessed as inhibition of LPS-induced nitric oxide production after 24 hrs by Griess assay Antineuroinflammatory activity in mouse N9 cells assessed as inhibition of LPS-induced nitric oxide production after 24 hrs by Griess assay	[PMID: 28073678]
Raji	IC₅₀	592 molar ratio Compound: 12	Inhibition of TPA-induced EBV-early antigen activation in human Raji cells relative to TPA Inhibition of TPA-induced EBV-early antigen activation in human Raji cells relative to TPA	[PMID: 17190444]

In Vitro

Typhaneoside (0-50 μM; 12-48 h) significantly reduces the viability of Kas-1, HL60 and NB4 acute myeloid leukemia cells in a time- and dose-dependent manner, while exerts no significant effect on K562 acute myeloid leukemia cells or normal 293T cells^[2].
Typhaneoside (20-40 μM; 24 h) induces apoptosis in Kas-1, HL60 and NB4 acute myeloid leukemia cells in a dose-dependent manner, with the highest apoptosis rate induced by treatment at 40 μM^[2].
Typhaneoside (20-40 μM; 24 h) dose-dependently reduces the mRNA expression levels of genes associated with mitochondrial dysfunction (NDUFS3, SDHB, UQCRFS1, TFAM, ClpP) in Kas-1, HL60 and NB4 acute myeloid leukemia cells^[2].
The effects of typhaneoside (40 μM; 24 h) on inducing reactive oxygen species production and apoptosis in Kas-1, HL60 and NB4 acute myeloid leukemia cells are significantly reversed by pre-treatment with NAC or DFO^[2].
Typhaneoside (40 μM; 24 h) upregulates autophagy-related proteins (ATG5, ATG7, Beclin 1, LC3) in Kas-1, HL60, and NB4 acute myeloid leukemia cells, and this effect is reversed by pre-treatment with 5 mM NAC for 2 h^[2].
Typhaneoside (12.5-50 μM; 24 h) activates FXR-dependent BSEP promoter activity in HEK293T cells, with significant activation observed at the concentration of 50 μM after 24 h^[3].
Typhaneoside (12.5-50 μM; 24 h) alleviates OAPA-induced lipid accumulation, oxidative stress, inflammatory response and glucose metabolism disorder in HepG2 cells by activating the AKT/GSK3β signaling pathway^[3].
Typhaneoside (5-50 μM; 10 min) concentration-dependently inhibits 4-aminopyridine (HY-B0604)-induced glutamate release from rat cerebral cortical synaptosomes, with an IC₅₀ of 20 μM^[4].
Typhaneoside (20 μM; 10 min)-mediated inhibition of 4-aminopyridine-induced glutamate release from rat cerebral cortex synaptosomes targets Ca²⁺-dependent vesicular exocytosis, rather than reverse transport via Ca²⁺-independent glutamate transporters^[4].
Typhaneoside (20 μM) inhibits KCl-induced glutamate release from rat cerebral cortex synaptosomes^[4].
Typhaneoside (20 μM; 10 min)-mediated inhibition of 4-aminopyridine-induced glutamate release from rat cerebral cortex synaptosomes depends on N-type (Ca_v2.2) voltage-dependent Ca²⁺ channels, and does not involve intracellular Ca²⁺ release or mitochondrial Na⁺/Ca²⁺ exchange^[4].
The inhibitory effect of Typhaneoside (20 μM; 10 min) on 4-aminopyridine-induced glutamate release from rat cerebral cortex synaptosomes depends on the MAPK/ERK signaling pathway, and does not involve PKA or PKC^[4].
Typhaneoside (20 μM; 10 min) reduces the phosphorylation levels of 4-aminopyridine-induced ERK1/2 and its presynaptic target synapsin I in rat cerebral cortex synaptosomes, but exerts no such effect on JNK or p38^[4].

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

Cell Viability Assay^[2]

Cell Line:

Kas-1, HL60, NB4, K562, 293T
Concentration:

0, 10, 20, 30, 40 and 50 μM
Incubation Time:

12 h, 24 h, 48 h
Result:

Reduced cell viability of Kas-1, HL60, and NB4 cells in a time- and dose-dependent manner.
Showed no significant effect on cell viability of K562 or 293T cells.

Cell Cycle Analysis^[2]

Cell Line:

Kas-1, HL60, NB4
Concentration:

20, 30 and 40 μM
Incubation Time:

24 h
Result:

Dose-dependently arrested Kas-1, HL60, and NB4 cells at the G2/M phase.
Decreased G1/G0 phase cell percentage in a dose-dependent manner for all three cell lines.
Decreased S phase cell percentage in a dose-dependent manner for all three cell lines.

Western Blot Analysis^[2]

Cell Line:

Kas-1, HL60, NB4
Concentration:

20, 30 and 40 μM
Incubation Time:

24 h
Result:

Dose-dependently reduced protein expression of Cyclin B1 and p-Cdc2 in Kas-1, HL60, and NB4 cells.
Dose-dependently enhanced protein expression of p53 and p27 in Kas-1, HL60, and NB4 cells.\nDose-dependently reduced protein expression of anti-apoptotic Bcl-2 in Kas-1, HL60, and NB4 cells.
Dose-dependently increased protein expression of pro-apoptotic Bax and cleaved Caspase-3 in Kas-1, HL60, and NB4 cells.\nDose-dependently increased protein expression of p-AMPK in Kas-1, HL60, and NB4 cells.
Dose-dependently decreased protein expression of p-mTOR in Kas-1, HL60, and NB4 cells.\nDose-dependently increased protein expression of ATG5, ATG7, Beclin 1, and LC3 in Kas-1, HL60, and NB4 cells.

Western Blot Analysis^[2]

Cell Line:

Kas-1, HL60, NB4
Concentration:

40 μM
Incubation Time:

24 h (with 2 h pre-treatment of 5 mM NAC)
Result:

Induced upregulation of ATG5, ATG7, Beclin 1, and LC3 protein expression that was reversed by pretreatment with 5 mM NAC in Kas-1, HL60, and NB4 cells.

In Vivo

Typhaneoside (10-40 mg/kg; once daily; 4 weeks) improves cardiac function, normalizes hemodynamic parameters, reduces pro-inflammatory and cardiac remodeling biomarkers, and inhibits excessive autophagy via activation of the PI3K/Akt/mTOR pathway in a dose-dependent manner in rats with heart failure post-myocardial infarction^[1].
Typhaneoside (10-30 mg/kg; i.p.; daily; 30 days) dose-dependently suppresses AML tumor growth in BALB/c nude mice, with the 30 mg/kg dose achieving the greatest tumor volume reduction and the highest 30-day survival rate of ~50%, while showing no overt tissue toxicity^[2].
Typhaneoside (30 mg/kg; i.p.; daily; 30 days) causes no overt tissue toxicity in healthy BALB/c nude mice^[2].
Typhaneoside (15-60 mg/kg/day; p.o.; daily; 8 weeks) dose-dependently alleviates HFD-induced NAFLD in male C57BL/6 mice by activating FXR signaling, reducing body and adipose tissue weight, improving lipid and glucose homeostasis, mitigating liver injury, oxidative stress and inflammation, and enhancing BAT thermogenesis and energy expenditure^[3].

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

Animal Model:

BALB/c nude (4-week-old male; AML model via subcutaneous injection of 1×10⁷ HL60 cells, tumor grown to 50 mm³ before treatment)^[2]
Dosage:

10 mg/kg; 20 mg/kg; 30 mg/kg
Administration:

i.p.; daily; 30 days
Result:

Significantly reduced mean tumor volume to ~1000 mm³ (10 mg/kg), ~800 mm³ (20 mg/kg), and ~500 mm³ (30 mg/kg) at day 30 compared to controls.
Improved 30-day survival rate to ~20% (10 mg/kg), ~30% (20 mg/kg), and ~50% (30 mg/kg) in a dose-dependent manner.
Significantly reduced white blood cell counts in a dose-dependent manner compared to controls.

Animal Model:

C57BL/6 (male, 8-week-old, 20-22 g, SPF, HFD-induced NAFLD)^[3]
Dosage:

15 mg/kg/day; 30 mg/kg/day; 60 mg/kg/day
Administration:

p.o.; daily; 8 weeks
Result:

Reduced HFD-induced body weight gain in a dose-dependent manner, with a significant decrease in area under the curve for body weight across all doses.
Dose-dependently reduced liver weight,
Dose-dependently reversed HFD-induced serum and hepatic lipid abnormalities: decreased serum triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and free fatty acid (FFA) levels; increased serum high-density lipoprotein cholesterol (HDL-C) levels; decreased hepatic TG levels.
Dose-dependently reversed HFD-induced liver injury, oxidative stress, and inflammation: decreased serum and hepatic AST, ALT, and MDA levels; increased serum and hepatic SOD levels; suppressed HFD-induced upregulation of proinflammatory mRNA (IL-6, IL-1β, NF-κB, TNF-α) in liver and WAT.
Dose-dependently upregulated mRNA expression of FXR, SHP, BSEP, and TGR5 in liver, and increased hepatic FXR protein expression detected by immunofluorescence.

Chemical Information

CAS No. 104472-68-6
Appearance Solid
Molecular Weight 770.69
Formula C₃₄H₄₂O₂₀
Color Light yellow to yellow
SMILES

O=C1C(O[C@H](O[C@H](CO[C@H](O[C@@H](C)[C@H](O)[C@H]2O)[C@@H]2O)[C@@H](O)[C@@H]3O)[C@@H]3O[C@@](O[C@@H](C)[C@H](O)[C@H]4O)([H])[C@@H]4O)=C(C5=CC(OC)=C(O)C=C5)OC6=CC(O)=CC(O)=C16
Structure Classification
- Flavonoids
- Flavonols
- Phenols
- Polyphenols
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)

Publications (4)

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Journal Impact Factor

Microbiome

Desulfovibrio vulgaris interacts with novel gut epithelial immune receptor LRRC19 and exacerbates colitis. [Abstract]

2024 Jan 3;12(1):4. PMID: 38172943
Food Chem

Effects of sun drying combined with baking processes on the flavor quality of Chongqing Tuocha raw tea. [Abstract]

2025 Dec 30:497:146992. PMID: 41285060
Food Chem

Flavonoid-mediated metabolic underpinning quality variation in red bud-sport pear mutants. [Abstract]

2025 May 31:489:144992. PMID: 40466530
Ind Crops Prod

2026 May 8;246:123392.

Solvent & Solubility

In Vitro:

DMSO : 250 mg/mL (324.38 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

1.2975 mL

6.4877 mL

12.9754 mL

5 mM

0.2595 mL

1.2975 mL

2.5951 mL

10 mM

0.1298 mL

0.6488 mL

1.2975 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 (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.

Molarity Calculator

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

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

Dilution Calculator

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

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In Vivo:

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

Stock Solution Working Solution

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 (2.70 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.

Protocol 2

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

Solubility: ≥ 2.08 mg/mL (2.70 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.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.08 mg/mL (2.70 mM); Clear solution

This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
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

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (296 KB)
SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 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)
Handling Instructions (2659 KB)

References

[1]. Zhang X, et al. Effect of typhaneoside on ventricular remodeling and regulation of PI3K/Akt/mTOR pathway. Wirkung von Typhaneosid auf ventrikuläres Remodeling und Regulierung des PI3K/Akt/mTOR-Signalwegs. Herz. 2020;45(Suppl 1):113-122. [Content Brief]

[2]. Zhu HY, et al. Typhaneoside prevents acute myeloid leukemia (AML) through suppressing proliferation and inducing ferroptosis associated with autophagy. Biochem Biophys Res Commun. 2019;516(4):1265-1271. [Content Brief]

[3]. Zheng Y, et al. Hepatoprotective effect of Typhaneoside on non-alcoholic fatty liver disease via farnesoid X receptor in vivo and in vitro. Biomed Pharmacother. 2023;164:114957. [Content Brief]

[4]. Chiu KM, et al. Typhaneoside Suppresses Glutamate Release Through Inhibition of Voltage-Dependent Calcium Entry in Rat Cerebrocortical Nerve Terminals. Chem Res Toxicol. 2021;34(5):1286-1295. [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	1.2975 mL	6.4877 mL	12.9754 mL	32.4385 mL
	5 mM	0.2595 mL	1.2975 mL	2.5951 mL	6.4877 mL
	10 mM	0.1298 mL	0.6488 mL	1.2975 mL	3.2438 mL
	15 mM	0.0865 mL	0.4325 mL	0.8650 mL	2.1626 mL
	20 mM	0.0649 mL	0.3244 mL	0.6488 mL	1.6219 mL
	25 mM	0.0519 mL	0.2595 mL	0.5190 mL	1.2975 mL
	30 mM	0.0433 mL	0.2163 mL	0.4325 mL	1.0813 mL
	40 mM	0.0324 mL	0.1622 mL	0.3244 mL	0.8110 mL
	50 mM	0.0260 mL	0.1298 mL	0.2595 mL	0.6488 mL
	60 mM	0.0216 mL	0.1081 mL	0.2163 mL	0.5406 mL
	80 mM	0.0162 mL	0.0811 mL	0.1622 mL	0.4055 mL
	100 mM	0.0130 mL	0.0649 mL	0.1298 mL	0.3244 mL

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Typhaneoside

Apoptosis Compound Library

Immunology/Inflammation Compound Library

Membrane Transporter/Ion Channel Compound Library

Metabolism/Protease Compound Library

Neuronal Signaling Compound Library

NF-κB Signaling Compound Library

PI3K/Akt/mTOR Compound Library

Stem Cell Signaling Compound Library

Natural Product Library

Anti-Cancer Compound Library

Autophagy Compound Library

Anti-Aging Compound Library

Antioxidant Compound Library

Reprogramming Compound Library

Glycoside Compound Library

Oxygen Sensing Compound Library

Anti-Cardiovascular Disease Compound Library

Ferroptosis Compound Library

Phenols Library

Glycolysis Compound Library

Cytoskeleton Compound Library

Orally Active Compound Library

Glutamine Metabolism Compound Library

Traditional Chinese Medicine Active Compound Library

Flavonoids Library

Neuroprotective Compound Library

Anti-Pancreatic Cancer Compound Library

Anti-Blood Cancer Compound Library

Anti-Cancer Metabolism Compound Library

Anti-Parkinson's Disease Compound Library

Neurodegenerative Disease-related Compound Library

Angiogenesis-Related Compound Library

Glucose Metabolism Compound Library

Food-Sourced Compound Library

Anti-Cancer Natural Product Library

Antidepressant Compound Library

Anti-inflammatory Traditional Chinese Medicine Active Compound Library

Plant-Sourced Natural Product Library

Nuclear Receptor Compound Library

Pain-Related Compound Library

Mitochondrial Protection Compound Library

Metabolic Enzyme Compound Library

Membrane Protein-targeted Compound Library

Membrane Receptor-targeted Compound Library

Cell Death Library

Ion Channel Compound Library

Anti-Hematopathy Compound Library

Multi-Target Compound Library

Radioprotector Library

Bioactive Compound Library Max

MCE Bioactive Compound Library

Natural Product Library Plus

Natural Product and Natural Product-Like Compound Library

Bioactive Compound Library

PBCRBS Traditional Chinese Medicine Compound Library

Protein Kinase Compound Library

Non-Alcoholic Fatty Liver Disease (NAFLD) Compound Library

Cell Proliferation Compound Library

High-Throughput Bioactive Compound Library

High-Throughput Natural Product Library

Diarrhea-Related Traditional Chinese Medicine Active Compound Library

Mongolian Medicine Compound Library

Natural Product Diversity Scaffold Library

Lactylation Compound Library

Mass Spectrometry Natural Product Library

Publications Citing Use of MedChemExpress (MCE) Typhaneoside

All mTOR Isoforms

All Akt Isoforms

All PI3K Isoforms

All Calcium Channel Isoforms

Biological Activity

Chemical Information

Publications (4)

Solvent & Solubility

Purity & Documentation

References

Help & FAQs

Complete Stock Solution Preparation Table

Typhaneoside Related Classifications