2. Autophagy PI3K/Akt/mTOR Metabolic Enzyme/Protease
  3. Autophagy mTOR Akt FXR
  4. Typhaneoside

Typhaneoside is an orally bioavailable signal modulator and cellular regulator. Typhaneoside regulates the PI3K/Akt/mTOR autophagy transduction pathway. Typhaneoside promotes the activation of AMP-activated protein kinase and Caspase-3, induces apoptosis, ferroptosis, autophagy, ROS accumulation, and cell cycle arrest at the G2/M phase, and reduces cancer cell viability. Typhaneoside activates the farnesoid X receptor signaling pathway, improves glucose and lipid metabolism, alleviates inflammatory responses, oxidative stress and hepatic lipid accumulation, and exerts hepatoprotective effects. Typhaneoside is applicable to research related to post-myocardial infarction heart failure, acute myeloid leukemia, non-alcoholic fatty liver disease, and neurological disorders.

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Typhaneoside

Typhaneoside Chemical Structure

CAS No. : 104472-68-6

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Solid + Solvent (Highly Recommended)
10 mM * 1 mL in DMSO
ready for reconstitution
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Based on 3 publication(s) in Google Scholar

Other Forms of Typhaneoside:

Typhaneoside Related Antibodies

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Description

Typhaneoside is an orally bioavailable signal modulator and cellular regulator. Typhaneoside regulates the PI3K/Akt/mTOR autophagy transduction pathway. Typhaneoside promotes the activation of AMP-activated protein kinase and Caspase-3, induces apoptosis, ferroptosis, autophagy, ROS accumulation, and cell cycle arrest at the G2/M phase, and reduces cancer cell viability. Typhaneoside activates the farnesoid X receptor signaling pathway, improves glucose and lipid metabolism, alleviates inflammatory responses, oxidative stress and hepatic lipid accumulation, and exerts hepatoprotective effects. Typhaneoside is applicable to research related to post-myocardial infarction heart failure, acute myeloid leukemia, non-alcoholic fatty liver disease, and neurological disorders[1][2][3][4].

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) potently reduces viability of Kas-1, HL60, and NB4 acute myeloid leukemia cells in a time- and dose-dependent manner, with no significant effect on K562 AML cells or normal 293T cells[2].
Typhaneoside (20-40 μM; 24 h) dose-dependently induces apoptosis in Kas-1, HL60, and NB4 acute myeloid leukemia cells, with 40 μM causing the highest apoptosis rates[2].
Typhaneoside (20-40 μM; 24 h) dose-dependently reduces mRNA expression of mitochondrial dysfunction-associated genes (NDUFS3, SDHB, UQCRFS1, TFAM, ClpP) in Kas-1, HL60, and NB4 acute myeloid leukemia cells[2].
Typhaneoside (40 μM; 24 h, with 2 h pre-treatment of NAC or DFO)-induced reactive oxygen species production and apoptosis in Kas-1, HL60, and NB4 acute myeloid leukemia cells are significantly reversed by pretreatment with NAC or DFO[2].
Typhaneoside (40 μM; 24 h, with 2 h pre-treatment of 5 mM NAC) induces upregulation of autophagy-associated proteins (ATG5, ATG7, Beclin 1, LC3) in Kas-1, HL60, and NB4 acute myeloid leukemia cells, which is reversed by pretreatment 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 50 μM after 24 h[3].
Typhaneoside (12.5-50 μM; 24 h) alleviates OAPA-induced lipid accumulation, oxidative stress, inflammation, and abnormal glucose metabolism in HepG2 cells via activation of AKT/GSK3β signaling[3].
Typhaneoside (5-50 μM; 10 min) inhibits 4-aminopyridine-induced glutamate release from rat cerebrocortical synaptosomes in a concentration-dependent manner with an IC50 of 20 μM[4].
Typhaneoside (20 μM; 10 min)-mediated inhibition of 4-aminopyridine-induced glutamate release from rat cerebrocortical synaptosomes targets Ca2+-dependent vesicular exocytosis, rather than Ca2+-independent glutamate transporter reversal[4].
Typhaneoside (20 μM; 10 min) does not alter resting or 4-aminopyridine-induced changes in synaptosomal plasma membrane potential in rat cerebrocortical synaptosomes[4].
Typhaneoside (20 μM; preincubated prior to KCl addition) inhibits KCl-induced glutamate release from rat cerebrocortical synaptosomes[4].
Typhaneoside (20 μM; 10 min)-mediated inhibition of 4-aminopyridine-induced glutamate release from rat cerebrocortical synaptosomes is dependent on N-type (Cav2.2) voltage-dependent Ca2+ channels, and does not involve intracellular Ca2+ release or mitochondrial Na+/Ca2+ exchange[4].
Typhaneoside (20 μM; 10 min)-mediated inhibition of 4-aminopyridine-induced glutamate release from rat cerebrocortical synaptosomes is dependent on the MAPK/ERK signaling pathway, and does not involve PKA or PKC[4].
Typhaneoside (20 μM; 10 min) reduces 4-aminopyridine-induced phosphorylation of ERK1/2 and its presynaptic target synapsin I, but not JNK or p38, in rat cerebrocortical synaptosomes[4].

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

Typhaneoside Related Antibodies

Cell Viability Assay[2]

Cell Line: Kas-1, HL60, NB4, K562, 293T
Concentration: 0-50 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: 20-40 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: 20-40 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, with the 40 mg/kg dose producing the most significant improvements[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: Sprague-Dawley (male, 8 weeks old, 200 ± 20 g, SPF, left anterior descending coronary artery ligation-induced myocardial infarction followed by 4 weeks of routine feeding to establish heart failure)[1]
Dosage: 10 mg/kg; 20 mg/kg; 40 mg/kg
Administration: once daily; 4 weeks
Result: Improved 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, with the 40 mg/kg dose producing the most significant improvements.
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.
Molecular Weight

770.69

Formula

C34H42O20
CAS No.
Appearance

Solid

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
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 : 250 mg/mL (324.38 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 1.2975 mL 6.4877 mL 12.9754 mL
5 mM 0.2595 mL 1.2975 mL 2.5951 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.

  • Molarity Calculator

  • Dilution Calculator

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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 (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.

    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 (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.

    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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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: 99.74%

SDS (393 KB)

COA (262 KB) HNMR (171 KB) LCMS (84 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 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 Related Classifications

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    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:

Typhaneoside104472-68-6AutophagymTORAktFXRMammalian target of RapamycinPKBProtein kinase BNR1H4PI3K/Akt/mTOR autophagy transduction pathwayacute myeloid leukemiafarnesoid X receptortumor necrosis factor alphamatrix metalloproteinase 2interleukin-6matrix metalloproteinase 9cardiomyocyteInhibitorinhibitorinhibit

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