Tenacissoside H
Based on 1 publication(s) in Google Scholar
Tenacissoside H (Tenacissimoside C) is a compound found in Caulis Marsdeniae Tenacissimae. Tenacissoside H shows anti-inflammation, anti-tumor and neuroprotective effects. Tenacissoside H inhibits PI3K/Akt and NF-κB signaling pathway. Tenacissoside H inhibits cancer cells proliferation, S phase arrest, and inhibits tumor growyh in mice. Tenacissoside H promotes neurological recovery of ischemia-reperfusion injury in mice by inhibiting inflammation and apoptosis. Tenacissoside H can be used for the research of cancer, inflammation and neurological diseases, such as esophageal cancer and cerebral ischemia.
For research use only. We do not sell to patients.
- Purity : 99.89%
- CAS No.: 191729-45-0
- Formula: C42H66O14
- Molecular Weight:794.97
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Storage:
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)
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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
Publications Citing Use of MedChemExpress (MCE) Tenacissoside H
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Biological Activity
Description
In Vitro
Tenacissoside H (2-10 mg/mL; 24-48 h) potently inhibits human esophageal carcinoma EC9706 cell proliferation in a time- and dose-dependent manner, with IC50 values of 9.81 mg/mL at 24 h and 6.45 mg/mL at 48 h[1].
Tenacissoside H (10 mg/mL; 24 h) blocks human esophageal carcinoma EC9706 cells from entering the S phase from the G1 phase, significantly reducing the percentage of cells in the S phase to 12.82% relative to the blank control group[1].
Tenacissoside H (10 mg/mL; 1-7 days) downregulates PI3K and NF-κB p65 mRNA expression in human esophageal carcinoma EC9706 cells[1].
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:human esophageal carcinoma EC9706 cells
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Concentration:2, 4, 6, 8, 10 mg/mL
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Incubation Time:24 h; 48 h
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Result:Significantly inhibited EC9706 cell proliferation in a time- and dose-dependent manner.
Reduced cell proliferation by 52.65% at 10 mg⋅mL-1 after 24 h incubation.
Reduced cell proliferation by 64.79% at 10 mg⋅mL-1 after 48 h incubation.
Exhibited an IC50 of 9.81 mg/mL for 24 h incubation.
Exhibited an IC50 of 6.45 mg/mL for 48 h incubation.
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Cell Line:human esophageal carcinoma EC9706 cells
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Concentration:10 mg/mL
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Incubation Time:24 h
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Result:Significantly reduced the percentage of EC9706 cells in the S phase to 12.82%.
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Cell Line:human esophageal carcinoma EC9706 cells
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Concentration:10 mg/mL
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Incubation Time:1, 3, 5, 7 day
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Result:Reduced PI3K mRNA expression over time, with significant differences relative to the blank control group at day 5 and day 7.
Decreased NF-κB p65 mRNA expression from day 3 onward, with significant differences relative to the blank control group at day 5 and day 7.
In Vivo
Tenacissoside H (20-80 mg/kg; i.p.; daily; 5 consecutive days 30 minutes before operation) dose-dependently protects male C57BL/6 mice against cerebral ischemia-reperfusion injury, with the 80 mg/kg dose producing the most significant improvements in neurological function, reduction in brain damage, and modulation of inflammatory and oxidative stress pathways via the TrkB signaling axis[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Balb/c nude mice (male and female, 6 weeks old, 18-22 g, subcutaneous inoculation of EC9706 cells)[1]
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Dosage:100 mg/kg
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Administration:i.p.; twice weekly; 14 days
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Result:Reduced tumor volume.
Reduced PCNA positive cell ratio to 53.02%.
Downregulated PI3K, Akt, p-Akt and NF-κB protein expression.
Induced large areas of tumor necrosis.
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Animal Model:C57BL/6 (male, 22-25 g, cerebral ischemia-reperfusion injury model via middle cerebral artery occlusion thread embolization with 2h ischemia followed by reperfusion)[2]
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Dosage:20 mg/kg; 40 mg/kg; 80 mg/kg
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Administration:i.p.; daily; 5 consecutive days
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Result:Reduced modified Neurological Severity Score (mNSS).
Reduced apoptotic cell and Caspase3-positive cells.
Reduced cerebral MDA, SOD, GSH-PX, BDNF levels.
Reduced TNF-α, IL-1β, IL-6 levels, increased IL-4, IL-10, TGF-β levels.
Reduced iNOS relative expression, increased Arg1 relative expression, reduced Iba1-positive microglia.
Increased Nrf2 relative expression, reduced p-NF-κB relative expression, increased TrkB relative expression, increased PPARγ relative expression.
Chemical Information
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CAS No. 191729-45-0
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Appearance Solid
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Molecular Weight 794.97
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Formula C42H66O14
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Color White to off-white
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SMILES
C[C@@]([C@@H]([C@@H](OC(C(C)CC)=O)[C@]1([H])[C@]23C)OC(C)=O)([C@@H]4C(C)=O)[C@]5(CC4)[C@@]1(CC[C@@]2([H])C[C@@H](O[C@@](O[C@H](C)[C@H]6O[C@@](O[C@H](C)[C@@H](O)[C@H]7OC)([H])[C@@H]7O)([H])C[C@H]6OC)CC3)O5
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Synonyms
Tenacissimoside 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
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)
Publications (1)
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Journal Impact Factor
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Most Recent
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Clin Exp Pharmacol Physiol
Tenacissoside H promotes neurological recovery of cerebral ischaemia/reperfusion injury in mice by modulating inflammation and oxidative stress via TrkB pathway. [Abstract]2021 May;48(5):757-769. PMID: 32799328
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (125.79 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, 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.
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.
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: 5 mg/mL (6.29 mM); Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 5 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (50.0 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: ≥ 2.5 mg/mL (3.14 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
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. * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
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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EdU Incorporation Assay (Click Chemistry-Based DNA Synthesis Measurement)
The EdU incorporation assay measures DNA synthesis by adding the thymidine analog 5-ethynyl-2′-deoxyuridine to cells or tissues, where it is incorporated into newly synthesized DNA during S phase. Incorporated EdU is detected by copper-catalyzed azide-alkyne cycloaddition, in which a fluorescent azide covalently reacts with the ethynyl group on EdU, allowing S-phase cells to be detected by fluorescence microscopy, flow cytometry, or high-content imaging. EdU detection does not require DNA denaturation or anti-BrdU antibody access, which preserves sample structure and improves compatibility with immunostaining and multiparameter cytometry compared with BrdU-based detection. EdU can be cytotoxic in a cell-type- and exposure-dependent manner, so pulse duration, concentration, and continuous-labeling designs should be validated for each cell type.
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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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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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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
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Data Sheet (285 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]. Jia YS, et al. Antitumor Activity of Tenacissoside H on Esophageal Cancer through Arresting Cell Cycle and Regulating PI3K/Akt-NF-κB Transduction Cascade. Evid Based Complement Alternat Med. 2015;2015:464937. [Content Brief]
[2]. Zhang R, et al. Tenacissoside H promotes neurological recovery of cerebral ischaemia/reperfusion injury in mice by modulating inflammation and oxidative stress via TrkB pathway. Clin Exp Pharmacol Physiol. 2021 May;48(5):757-769. [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, 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.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 1.2579 mL | 6.2895 mL | 12.5791 mL | 31.4477 mL |
| 5 mM | 0.2516 mL | 1.2579 mL | 2.5158 mL | 6.2895 mL | |
| 10 mM | 0.1258 mL | 0.6290 mL | 1.2579 mL | 3.1448 mL | |
| 15 mM | 0.0839 mL | 0.4193 mL | 0.8386 mL | 2.0965 mL | |
| 20 mM | 0.0629 mL | 0.3145 mL | 0.6290 mL | 1.5724 mL | |
| 25 mM | 0.0503 mL | 0.2516 mL | 0.5032 mL | 1.2579 mL | |
| 30 mM | 0.0419 mL | 0.2097 mL | 0.4193 mL | 1.0483 mL | |
| 40 mM | 0.0314 mL | 0.1572 mL | 0.3145 mL | 0.7862 mL | |
| 50 mM | 0.0252 mL | 0.1258 mL | 0.2516 mL | 0.6290 mL | |
| 60 mM | 0.0210 mL | 0.1048 mL | 0.2097 mL | 0.5241 mL | |
| 80 mM | 0.0157 mL | 0.0786 mL | 0.1572 mL | 0.3931 mL | |
| 100 mM | 0.0126 mL | 0.0629 mL | 0.1258 mL | 0.3145 mL |
Tenacissoside H Related Classifications
HY-N0670 Related Classifications
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Keywords
- Tenacissoside H
- 191729-45-0
- Tenacissimoside C
- PI3K
- Akt
- NF-κB
- Apoptosis
- male C57BL/6 mice
- necrosis
- apoptosis
- nude mice
- TrkB signaling pathway
- esophageal cancer
- human esophageal carcinoma EC9706 cell
- cerebral ischemia/reperfusion-induced acute brain injury
- cell cycle arrest
- PI3K/Akt-NF-κB cascade
- Inhibitor
- inhibitor
- inhibit