Cycloartenyl ferulate
Based on 1 publication(s) in Google Scholar
Cycloartenyl ferulate (Cycloartenol ferulate; Cycloartenol ferulic acid ester) is a derivative of γ-oryzanol (HY-B2194) with multiple biological activities including antioxidant, anti-inflammatory, and anti-tumor properties. Cycloartenyl ferulate selectively binds to IFNγR1 (binding affinity Kd = 0.5 μM) to activate the canonical JAK1/2-STAT1 signaling pathway. Cycloartenyl ferulate inhibits paraquat (PQ)-triggered apoptosis and ROS in HK2 cells. Cycloartenyl ferulate enhances the activation and cytolytic activity of natural killer (NK) cells by upregulating the expression of NK cell activation receptors (NKG2D, NKp30, NKp44) and the release of cytotoxic molecules and cytokine IFNγ. Cycloartenyl ferulate exerts anti-cancer effects in tumor mice models. Cycloartenyl ferulate can be used for the study of cancer and allergic inflammation intervention.
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- Reinheit : 99.15%
- CAS. Nr.: 21238-33-5
- Formel: C40H58O4
- Molecular Weight:602.89
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Speicherung:
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Publications Citing Use of MedChemExpress (MCE) Cycloartenyl ferulate
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Biologische Aktivität
Beschreibung
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| MCF7 | IC50 |
80 μM
Compound: 4
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Cytotoxicity against human MCF7 cells after 72 hrs by MTT assay
Cytotoxicity against human MCF7 cells after 72 hrs by MTT assay
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[PMID: 15679326] |
| Raji | IC50 |
15.9 nM
Compound: 17
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Inhibition of TPA-induced Epstein-Barr virus early antigen activation in Raji cells after 48 hrs
Inhibition of TPA-induced Epstein-Barr virus early antigen activation in Raji cells after 48 hrs
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[PMID: 17503850] |
In Vitro
Cycloartenyl ferulate (0-10 μM, 72 h) enhances cytolytic activity of NK92 cells against K562, A2058, A549 cancer cells in a dose-dependent manner, upregulates CD107a expression, activates receptors (NKG2D, NKp30, NKp44) and increases granzyme B, perforin, IFNγ release without impairing cell viability[1].
Cycloartenyl ferulate (0-10 μM, 24 h) activates NK cells via the IFNγR-JAK1/2-STAT1-dependent signaling pathway[1].
Cycloartenyl ferulate (20-80 μM, 24 h) significantly reverses the decrease in HK-2 cell viability induced by paraquat (PQ)[2].
Cycloartenyl ferulate (20-80 μM, 24 h) significantly reduces the proportion of HK-2 cells in sub-G1 phase, decreases DNA fragmentation and chromatin condensation, inhibits phosphatidylserine externalization, and reverses the apoptotic characteristics of cells caused by paraquat[2].
Cycloartenyl ferulate (20-80 μM, 0-120 min) dose-dependently and time-dependently inhibits the production of intracellular ROS and superoxide in HK-2 cells induced by PQ[2].
Cycloartenyl ferulate (80 μM, 24 h) reverses the inhibition of Nrf2 and its downstream effectors HO1 and NQO1 expression in HK-2 cells by PQ[2].
Cycloartenyl ferulate (60 min) inhibits degranulation of DNP-IgE-sensitized RBL-2H3 mast cells stimulated with DNP-HSA in a concentration-dependent manner[3].
Cycloartenyl ferulate (1-30 μM, 60 min) decreases the detected concentration of IgE by ELISA in a concentration-dependent manner[3].
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:NK92 cells
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Concentration:0, 0.1, 1, 10 μM
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Incubation Time:24 h
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Result:Upregulated p-JAK1/p-JAK2/p-STAT1 without affecting p-JAK3/p-STAT3/p-STAT5/p-mTOR/p-AKT/p-ERK.
Promoted IFNγR1/IFNγR2 dimer formation in NK92 cells.
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Cell Line:HK-2 cells
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Concentration:20, 40, 80 μM
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Incubation Time:24 h
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Result:Inhibited the increase in caspase-3, -8, and -9 activities induced by PQ.
Inhibited the up-regulation of Bax protein and down-regulation of Bcl-2 protein caused by PQ.
In Vivo
Cycloartenyl ferulate (12.5-50 mg/kg, i.g., once daily, 21 days) reduces dose-dependent formation of lung melanoma nodules in C57BL/6J mice[1].
Cycloartenyl ferulate (50 mg/kg, i.g., once daily, 19 days) combined with anti-PD1 antibody inhibits tumor growth more effectively than alone in C57BL/6J mice harboring Lewis cells[1].
Cycloartenyl ferulate (0-30 μM, intradermal injection, 60 min) attenuates DNP-HSA-induced passive cutaneous anaphylaxis reaction in 8-week-old male Sprague-Dawley rats[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:RMA/RMAS cells (1 × 106) were intraperitoneally injected into 6-8-week-old female C57BL/6J mice (18-20 g)[1]
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Dosage:12.5, 25, 50 mg/kg
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Administration:i.g., once daily for 3 days
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Result:Enhanced the clearance of MHC-I-deficient RMAS cells in a dose-dependent manner.
Induced significant elimination of MHC-I-normal RMA cells at the dose of 50 mg/kg.
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Animal Model:B16-F10 melanoma cells (2 × 105) were intravenously injected into 6-8-week-old female C57BL/6J mice (18-20 g) to establish a pulmonary metastasis model[1]
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Dosage:12.5, 25, 50 mg/kg
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Administration:i.g., once daily, 21 days
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Result:Reduced the formation of lung melanoma nodules in a dose-dependent manner.
Increased the percentages of splenic CD3- NK1.1+ (Pan-NK) and CD3- NKp46+ (activated NK) cells.
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Animal Model:Lewis lung cancer cells (2 × 106) were subcutaneously implanted into the right flanks of 6-8-week-old female C57BL/6J mice (18-20 g)[1]
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Dosage:50 mg/kg combined with anti-PD1 antibody (0.2 mg, i.p. every 3 days)
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Administration:i.g., once daily, 19 days
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Result:Inhibited Lewis lung tumor growth.
Reduced the populations of myeloid-derived suppressor cells (MDSCs, CD45+ CD11B+ LY6G+) and Foxp3+ Regulatory T cells (Tregs, CD3+CD4+CD25+Foxp3+) in the spleen and tumor tissue.
Increased the infiltration of NK cells (NK1.1+) and CD8+ T cells in tumor tissue.
Promoted the release of granzyme B.
Chemical Information
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CAS. Nr. 21238-33-5
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Appearance Solid
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Molecular Weight 602.89
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Formel C40H58O4
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Color White to off-white
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SMILES
C[C@]12[C@@]3([H])[C@@]4(CC[C@@]1([C@@](CC2)([H])[C@H](C)CC/C=C(C)\C)C)[C@@]5([C@](CC3)([H])C(C)([C@H](CC5)OC(/C=C/C6=CC(OC)=C(C=C6)O)=O)C)C4
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Synonyms
Cycloartenol ferulate; Cycloartenol ferulic acid ester
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Structure Classification
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Initial Source
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Publications (1)
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Journal Impact Factor
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Most Recent
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J Biol Chem
Cycloartenyl ferulate improves natural killer (NK) cell immunity against cancer by binding to IFNγ receptor 1. [Abstract]2023 Aug;299(8):104990. PMID: 37392850
Lösungsmittel & Löslichkeit
In Vitro:
DMSO : 5 mg/mL (8.29 mM; ultrasonic and warming and heat to 60°C; 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 (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.
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.
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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.
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 (protect from 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.
Protokoll
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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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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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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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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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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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.
Reinheit & Dokumentation
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Data Sheet (280 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)
Verweise
[1]. Li M, et al. Cycloartenyl ferulate improves natural killer (NK) cell immunity against cancer by binding to IFNγ receptor 1. J Biol Chem. 2023 Aug;299(8):104990. [Content Brief]
[2]. Guang-Liang Hong, et al. The reversal of paraquat-induced mitochondria-mediated apoptosis by cycloartenyl ferulate, the important role of Nrf2 pathway. Exp Cell Res. 2013 Nov 1;319(18):2845-55. [Content Brief]
[3]. T Oka, et al. Cycloartenyl ferulate, a component of rice bran oil-derived gamma-oryzanol, attenuates mast cell degranulation.Phytomedicine. 2010 Feb;17(2):152-6. [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 (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 | 1.6587 mL | 8.2934 mL | 16.5868 mL | 41.4669 mL |
| 5 mM | 0.3317 mL | 1.6587 mL | 3.3174 mL | 8.2934 mL |