7α-Hydroxycholesterol
Based on 3 publication(s) in Google Scholar
7α-Hydroxycholesterol is a cholesterol oxide and can serve as a biomarker for oxidative stress and lipid peroxidation. 7α-Hydroxycholesterol has cytotoxic and pro-inflammatory activities. 7α-Hydroxycholesterol can also inhibit sterol synthesis and reduce the activity of HMG-CoA reductase. 7α-Hydroxycholesterol can be used in the research of diseases such as diabetes and atherosclerosis.
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- Pureté : 99.99%
- CAS No.: 566-26-7
- Formule: C27H46O2
- Masse moléculaire:402.65
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Stockage:
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Activité biologique
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Chemical Information
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Solvant et solubilité
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
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Cholesterol (from animal)ERRα Agonist
Publications Citing Use of MedChemExpress (MCE) 7α-Hydroxycholesterol
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Cell Imaging/Staining
Activité biologique
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| C6 | IC50 |
40 μM
Compound: 4, 7alpha-OHC
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Growth inhibition of rat C6 cells after 24 hrs by trypan blue-based cell counting method
Growth inhibition of rat C6 cells after 24 hrs by trypan blue-based cell counting method
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[PMID: 24211631] |
| HT-29 | IC50 |
15.5 μM
Compound: 5
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Cytotoxicity against human HT-29 cells after 48 hrs by Alamar Blue assay
Cytotoxicity against human HT-29 cells after 48 hrs by Alamar Blue assay
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[PMID: 19473028] |
| HT-29 | IC50 |
15.5 μM
Compound: 5
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Cytotoxicity against human HT-29 cells assessed as cell viability after 48 hrs by alamar blue assay
Cytotoxicity against human HT-29 cells assessed as cell viability after 48 hrs by alamar blue assay
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[PMID: 21797280] |
| HT-29 | IC50 |
15.5 μM
Compound: 7
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Cytotoxicity against human HT-29 cells after 48 hrs by Alamar blue assay
Cytotoxicity against human HT-29 cells after 48 hrs by Alamar blue assay
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[PMID: 20931970] |
In Vitro
7α-Hydroxycholesterol (2.5-160 μM; 24 h) has cytotoxicity against 158N and C6 cells, with IC50 values of approximately 15 μM and 40 μM, respectively[1].
7α-Hydroxycholesterol (8 μg/mL; 2-4 h) significantly reduces the sterol synthesis rate and HMG-CoA reductase activity in primary hepatocytes or L-cell cultures[2].
7α-Hydroxycholesterol (5 µg/mL; 48 h) increases the transcriptional level of TLR6, promotes the expression of CD14, and induces monocytes to produce chemokines such as CCL2, CCL3, and CCL4 in monocytes/macrophages. The mechanism involves the phosphorylation of Akt, Src, ERK1/2, and the p65 subunit[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:THP-1 cells
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Concentration:5 µg/mL
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Incubation Time:48 h
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Result:Significantly increased the mRNA levels of TLR6 and CD14.
Chemical Information
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CAS No. 566-26-7
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Appearance Solid
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Masse moléculaire 402.65
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Formule C27H46O2
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Color White to off-white
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SMILES
CC(C)CCC[C@@H](C)[C@H]1CC[C@@]2([H])[C@]3([H])[C@H](O)C=C4C[C@@H](O)CC[C@]4(C)[C@@]3([H])CC[C@]12C
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Structure Classification
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Initial Source
fish oil, serum
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Publications (3)
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Journal Impact Factor
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Most Recent
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ACS Nano
Immune Modulatory Oxysterols Produced from Cholesterol-Containing Lipid Nanoparticles Regulate Tumor Growth. [Abstract]2026 Mar 13. PMID: 41825961 -
Cell Chem Biol
Transient hydroxycholesterol treatment restrains TCR signaling to promote long-term immunity. [Abstract]2024 May 16;31(5):920-931.e6. PMID: 38759618
7α-Hydroxycholesterol purchased from MedChemExpress. Usage Cited in: Cell Chem Biol. 2024 May 16;31(5):920-931.e6. [Abstract]
Both 2 ng/μL of 7α-Hydroxycholesterol (7a-HC) and 20S-HC significantly inhibited CD69 levels, with 7a-HC showing a more significant effect.
7α-Hydroxycholesterol purchased from MedChemExpress. Usage Cited in: Cell Chem Biol. 2024 May 16;31(5):920-931.e6. [Abstract]
Effects of transient 7α-Hydroxycholesterol (7a-HC) treatment on the phosphorylation levels of TCR and downstream molecules in mouse T cells. Mouse naive CD4+ T cells were transiently treated with 2 ng/μL 7a-HC for 20 min and then stimulated with 5 ng/μL α-CD3ε and 5 ng/μL α-CD28.
7α-Hydroxycholesterol purchased from MedChemExpress. Usage Cited in: Cell Chem Biol. 2024 May 16;31(5):920-931.e6. [Abstract]
Naive mouse CD8+ T cells were subjected to transient treatments with 10 ng/μL cholesterol, 2 ng/μL 7α-Hydroxycholesterol (7a-HC) for 20 min, or left untreated (n = 7). Then the plasma membrane was labeled by octadecyl rhodamine B (R18). Data were shown by the representative images during recovery (left panel) and kinetics curves (right panel). Statistical analysis was performed with the 20 s time points of the three conditions.
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Vet Microbiol
Identification and evaluation of Nordihydroguaiaretic acid (NDGA) as an active traditional Chinese medicine compound inhibiting the 3C-like protease of feline infectious peritonitis virus. [Abstract]2025 Sep 15:310:110730. PMID: 40976146
Solvant et solubilité
In Vitro:
DMSO : 50 mg/mL (124.18 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 (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.
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: 10 mg/mL (24.84 mM); Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 10 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 (100.0 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: 10 mg/mL (24.84 mM); Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 10 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 (100.0 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 (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.
Protocole
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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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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
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Ferroptosis Solutions
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
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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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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
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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.
Pureté et documentation
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Fiche technique (277 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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Instruction de manipulation (2659 KB)
Références
[1]. Nury T, et al. Improved synthesis and in vitro evaluation of the cytotoxic profile of oxysterols oxidized at C4 (4α- and 4β-hydroxycholesterol) and C7 (7-ketocholesterol, 7α- and 7β-hydroxycholesterol) on cells of the central nervous system. Eur J Med Chem. 2013;70:558-67. [Content Brief]
[2]. Kandutsch AA, et al. Inhibition of sterol synthesis in cultured mouse cells by 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, and 7-ketocholesterol. J Biol Chem. 1973 Dec 25;248(24):8408-17. [Content Brief]
[3]. Son Y, et al. Glucocorticoids Impair the 7α-Hydroxycholesterol-Enhanced Innate Immune Response. Immune Netw. 2023 Oct 19;23(5):e40. [Content Brief]
[4]. Ferderbar S, et al. Cholesterol oxides as biomarkers of oxidative stress in type 1 and type 2 diabetes mellitus. Diabetes Metab Res Rev. 2007 Jan;23(1):35-42. [Content Brief]
[5]. Kitano S, et al. Oxidative status of human low density lipoprotein isolated by anion-exchange high-performance liquid chromatography--assessment by total hydroxyoctadecadienoic acid, 7-hydroxycholesterol, and 8-iso-prostaglandin F(2alpha). Anal Chim Acta. 2007 Feb 28;585(1):86-93. [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 | 2.4835 mL | 12.4177 mL | 24.8355 mL | 62.0887 mL |
| 5 mM | 0.4967 mL | 2.4835 mL | 4.9671 mL | 12.4177 mL | |
| 10 mM | 0.2484 mL | 1.2418 mL | 2.4835 mL | 6.2089 mL | |
| 15 mM | 0.1656 mL | 0.8278 mL | 1.6557 mL | 4.1392 mL | |
| 20 mM | 0.1242 mL | 0.6209 mL | 1.2418 mL | 3.1044 mL | |
| 25 mM | 0.0993 mL | 0.4967 mL | 0.9934 mL | 2.4835 mL | |
| 30 mM | 0.0828 mL | 0.4139 mL | 0.8278 mL | 2.0696 mL | |
| 40 mM | 0.0621 mL | 0.3104 mL | 0.6209 mL | 1.5522 mL | |
| 50 mM | 0.0497 mL | 0.2484 mL | 0.4967 mL | 1.2418 mL | |
| 60 mM | 0.0414 mL | 0.2070 mL | 0.4139 mL | 1.0348 mL | |
| 80 mM | 0.0310 mL | 0.1552 mL | 0.3104 mL | 0.7761 mL | |
| 100 mM | 0.0248 mL | 0.1242 mL | 0.2484 mL | 0.6209 mL |
7α-Hydroxycholesterol Related Classifications
HY-N7264 Related Classifications
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