From 11:00 pm to 12:00 pm EST ( 8:00 pm to 9:00 pm PST ) on January 6th, the website will be under maintenance. We are sorry for the inconvenience. Please arrange your schedule properly.
Cholesterol sulfate sodium is a naturally occurring, orally active cholesterol derivative that is widely distributed in various tissues and body fluids. Cholesterol sulfate sodium acts as a DOCK2 inhibitor, with IC50 values of 2 μM and 2.9 μM against mouse and human targets, respectively. Cholesterol sulfate sodium restricts excessive neutrophil infiltration and alleviates intestinal inflammation and damage. Cholesterol sulfate sodium serves as an activator of protein kinase C (PKC), which promotes squamous cell differentiation and inhibits skin carcinogenesis. Cholesterol sulfate sodium regulates cholesterol homeostasis and cellular metabolism by activating the AMPK-Sirt1 pathway. Cholesterol sulfate sodium can be used in research related to actinic keratitis, ulcerative colitis, skin cancer, and other conditions.
For research use only. We do not sell to patients.
Cholesterol sulfate sodium is a naturally occurring, orally active cholesterol derivative that is widely distributed in various tissues and body fluids. Cholesterol sulfate sodium acts as a DOCK2 inhibitor, with IC50 values of 2 μM and 2.9 μM against mouse and human targets, respectively. Cholesterol sulfate sodium restricts excessive neutrophil infiltration and alleviates intestinal inflammation and damage. Cholesterol sulfate sodium serves as an activator of protein kinase C (PKC), which promotes squamous cell differentiation and inhibits skin carcinogenesis. Cholesterol sulfate sodium regulates cholesterol homeostasis and cellular metabolism by activating the AMPK-Sirt1 pathway. Cholesterol sulfate sodium can be used in research related to actinic keratitis, ulcerative colitis, skin cancer, and other conditions[1][2][3][4][5][6].
In Vitro
Cholesterol sulfate (0.19-150 μM; 20 min-6 h) sodium inhibits chemokine-induced Rac activation in mouse T cells and bone marrow-derived neutrophils, thereby blocking the migration of these cells in vitro[1]. Cholesterol sulfate (12.5 μM; 60 min) sodium potently inhibits phorbol ester (PMA) (HY-18739)-induced reactive oxygen species (ROS) production in mouse bone marrow-derived neutrophils[2]. Cholesterol sulfate sodium is a sulfated cholesterol. At concentrations of 5-100 μM for 24 h, it activates the SREBP2 signaling pathway in a dose-dependent manner in SULT2B1-knockout human colon cancer cell line HT-29, and this activating effect is enhanced upon SLC10A6 overexpression[3]. Cholesterol sulfate (25-50 μM; 6-18 h) sodium promotes the proteolytic activation of SREBP2 in HEK293T cells[3]. Cholesterol sulfate (50 μM; 24 h) sodium upregulates the expression of key cholesterol biosynthesis genes in human colonic epithelial cell lines HT-29, LOVO, SW480, HCT116, SW1116 and NCM460[3]. Cholesterol sulfate (50 μM; 6-48 h) sodium increases the levels of total cholesterol and free cholesterol in HT-29 cells and SULT2B1-knockout HT-29 human colon cancer cells[3]. Cholesterol sulfate (25-50 μM) sodium increases the cell viability of HT-29 human colon cancer cells treated with 25 or 50 μM cholesterol sulfate, as well as SULT2B1-knockout HT-29 human colon cancer cells, and this effect depends on the activation of SREBP2[3]. Cholesterol sulfate (50 μM) sodium increases the level of mature nuclear-localized SREBP2 in HT-29 cells and SULT2B1-knockout HT-29 human colon cancer cells[3]. Cholesterol sulfate (25 μM; 12-48 h) sodium significantly reduces the intracellular total cholesterol level by 20% to 30% in HEK 293T, Huh-7 and MEF cells[4]. Cholesterol sulfate (50 μM; 24 h) sodium significantly reduces intracellular cholesterol levels in Huh-7 cells[4]. Cholesterol sulfate (25 μM; 12 h) sodium inhibits de novo cholesterol synthesis in HEK 293T, Huh-7 and MEF cells[4]. Cholesterol sulfate (25 μM) sodium can partially inhibit LDL-cholesterol uptake by cholesterol-depleted Huh-7 cells switched to FBS-containing medium[4]. Cholesterol sulfate (3.12-25 μM; 5-16 h) sodium reduces the protein expression level of HMGCR in Huh-7 cells at the post-translational level, with an IC50 of 5.6 μM for inhibiting T7-tagged HMGCR after 5 h of treatment[4]. Cholesterol sulfate (12.5-25 μM; 5 h,) sodium promotes ubiquitination and proteasomal degradation of wild-type HMGCR in Huh-7 cells, and this process depends on Lys89 and Lys248 of HMGCR[4]. Cholesterol sulfate (25 μM; 8 h) sodium promotes the interaction between INSIG1 and HMGCR in HEK 293T cells, a process that mediates the ubiquitination and degradation of HMGCR[4]. Cholesterol sulfate (25 μM; 8 h) sodium promotes the interaction between INSIG1 and SCAP in HEK 293T cells, thereby inhibiting the translocation of SREBP2 to the Golgi apparatus; this interaction depends on the L343 and V355 residues of SCAP, but not on I348[4]. Cholesterol sulfate (25 μM; 4-24 h) sodium reduces LDL-cholesterol uptake in Huh-7 cells through two mechanisms: a secondary effect of cholesterol depletion, and direct inhibition of clathrin-mediated endocytosis[4]. Cholesterol sulfate (25 μM; 4-24 h) sodium inhibits LDLR endocytosis in Huh-7 cells, resulting in the accumulation of LDLR on the cell surface[4]. Cholesterol sulfate (25 μM; 8 h) sodium partially inhibits the upregulation of SREBP2 target genes in cholesterol-depleted Huh-7 cells[4]. Cholesterol sulfate (25 μM) sodium inhibits the proteolytic processing of SREBP2 in cholesterol-depleted Huh-7 cells and reduces the level of the active nuclear form of SREBP2[4]. Cholesterol sulfate (20-40 μM; 2-4 days) sodium inhibits RANKL-induced osteoclast differentiation and NFATc1 pathway activation in mouse bone marrow macrophages (BMMs) without reducing cell viability; treatment with 30 μM for 2 days suppresses the expression of NFATc1 and its target genes, and this inhibitory effect persists for up to 4 days[5]. Cholesterol sulfate (30 μM; 2-4 days) sodium inhibits RANKL-induced osteoclast differentiation in a RORα-independent manner, as it exerts comparable inhibitory effects on osteoclast formation and NFATc1 expression in bone marrow macrophages (BMMs) from wild-type (WT) and RORα-deficient mice[5]. Cholesterol sulfate (30 μM; 0.5-24 h) sodium activates the AMPK-Sirt1 axis in a RORα-independent manner, thereby inhibiting NF-κB activity in mouse bone marrow-derived macrophages (BMMs) and RAW264.7 cells[5]. Cholesterol sulfate (30 μM; 10 h-8 days) sodium induces caspase-dependent apoptosis in differentiated murine osteoclasts, disrupts their actin ring structure, and inhibits bone resorptive activity[5]. Cholesterol sulfate (30 μM; 12 h-4 days) sodium induces apoptosis of mouse osteoclasts via AMPK-dependent NF-κB inhibition, thereby reducing the production of IL-1β; treatment with IL-1β reverses the aforementioned pro-apoptotic and inhibitory effects without altering the activation level of AMPK[5]. Cholesterol sulfate sodium induces squamous differentiation of normal human keratinocytes by inhibiting cell growth and upregulating the expression and activity of TGase 1[6]. Cholesterol sulfate sodium induces granular cell differentiation in mouse basal keratinocytes and regulates the expression of differentiation markers[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Abolished CS-induced HMGCR reduction when co-treated with MG132. Increased polyubiquitination of HMGCR. Reduced protein levels of wild-type HMGCR but not K89R/K248R double mutant HMGCR.
Induced the interaction between INSIG1 and HMGCR, albeit with less potency than 25-HC. Induced the interaction between INSIG1 and wild-type SCAP, albeit with less potency than 25-HC. Mutations at L343A or V355A significantly reduced SCAP retention in the presence of CS. The I348F mutation did not reduce CS-induced SCAP-INSIG1 binding.
3-4 days (osteoclast differentiation assay); 2 days (NFATc1 protein/ mRNA expression); 3 days (cell viability assay)
Result:
Inhibited RANKL-induced osteoclast differentiation in a dose-dependent manner. Showed no effect on BMM cell viability at all tested concentrations. Strongly inhibited RANKL-induced NFATc1 protein expression, with suppression sustained for 4 days. Inhibited the transcription of Nfatc1 and its target genes Acp5, Ctsk, and Mmp9.
4 days (osteoclast differentiation assay); 2 days (protein expression analysis)
Result:
Inhibited RANKL-induced osteoclast formation and NFATc1 protein expression in cKO BMMs to the same extent as in WT BMMs.
In Vivo
Cholesterol sulfate (8 μg/μL; topical; 6 total doses) sodium suppresses inflammatory cell infiltration in the anterior chamber of UV-induced photokeratitis models in Sult2b1−/− mice[1]. Cholesterol sulfate (8 μg/μL; topical; three times daily; for 3 days) sodium suppresses inflammatory cell infiltration in the conjunctiva of experimental allergic conjunctivitis models in Sult2b1−/− mice[1]. Cholesterol sulfate (200 mg/kg; p.o.; three times at 4-hour intervals) sodium ameliorates Indomethacin (HY-14397)-induced small intestinal ulceration and reduces neutrophil infiltration into ulcerative lesions in Sult2b1-/- mice[2]. Cholesterol sulfate (0.004%; dietary supplementation; continued for 6 days) sodium alleviates 2.5% DSS-induced acute ulcerative colitis in Sult2b1ΔIEC mice by reducing disease severity markers and promoting colonic epithelial cell proliferation[3]. Cholesterol sulfate (20 mg/kg; subcutaneous (calvarial); 2 doses (Days 0 and 2)) sodium inhibits LPS-induced bone destruction and osteoclast formation in male C57BL/6 mice, reducing bone cavity formation by ~6-fold and TRAP-positive osteoclasts by ~24-fold[5]. Cholesterol sulfate (20 mg/kg; intraperitoneal; six times weekly; 3 weeks) sodium protects against ovariectomy-induced bone loss in female C57BL/6 mice, restoring key bone density parameters and increasing osteoclast apoptosis to ~55% of TRAP-positive cells[5]. Cholesterol sulfate (400 µg; topical; weekly; 19 weeks) sodium inhibits skin tumor promotion in mice, reducing tumor incidence by 56%, tumor number per mouse by 81%, and tumor size by 60% at 20 weeks[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
C57BL/6 background Sult2b1−/− (age- and sex-matched littermates)[1]
Dosage:
8 μg/μL
Administration:
topical (eye drop); 6 total doses (1 pre-UV, 5 at 4-hour intervals)
Result:
Significantly reduced the number of inflammatory cells in the anterior chamber compared to vehicle-treated controls.
Animal Model:
C57BL/6 background Sult2b1−/− (age- and sex-matched littermates)[1]
Dosage:
8 μg/μL
Administration:
topical (eye drop); three times daily at 4-hour intervals; days 10, 11, 12
Result:
Significantly reduced the number of inflammatory cells in the conjunctiva compared to vehicle-treated controls.
Animal Model:
C57BL/6J (male, 9-12 weeks old, indomethacin-induced small intestinal ulceration)[2]
Dosage:
200 mg/kg
Administration:
p.o.; three times at 4-hour intervals
Result:
Reduced the number of small intestinal ulcers in Sult2b1-/- mice to levels comparable to Sult2b1+/+ mice. Reduced the total ulcer area in Sult2b1-/- mice to levels matching Sult2b1+/+ mice. Suppressed the increase in absolute neutrophil counts in ulcerative lesions of Sult2b1-/- mice, bringing neutrophil numbers close to those in Sult2b1+/+ mice.
Animal Model:
C57BL/6 (female, 8-week-old; postmenopausal osteoporosis model via ovariectomy)[5]
Dosage:
20 mg/kg
Administration:
intraperitoneal; six times weekly; 3 weeks
Result:
Restored ovariectomy-induced reductions in bone mineral density, trabecular number, bone surface density, and bone volume density. Reduced ovariectomy-induced increases in trabecular separation. Reduced ovariectomy-induced increases in TRAP-positive osteoclasts by ~2-fold. Increased the percentage of caspase 3-positive TRAP-positive cells to ~55% (compared to ~35% in ovariectomized controls). Had no effect on bone mineral apposition rate.
Room temperature in continental US; may vary elsewhere.
Storage
-20°C, stored under nitrogen, away from moisture
*In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen, away from moisture)
Solvent & Solubility
In Vitro:
DMSO : 10 mg/mL (20.46 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)
H2O : < 0.1 mg/mL (insoluble)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
2.0462 mL
10.2312 mL
20.4625 mL
5 mM
0.4092 mL
2.0462 mL
4.0925 mL
10 mM
0.2046 mL
1.0231 mL
2.0462 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 (stored under nitrogen, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
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.
This protocol yields a clear solution of ≥ 1 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (10.0 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.
Protocol 2
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 1 mg/mL (2.05 mM); Clear solution
This protocol yields a clear solution of ≥ 1 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (10.0 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.
Protocol 3
Add each solvent one by one: 10% DMSO 90% Corn Oil
Solubility: ≥ 1 mg/mL (2.05 mM); Clear solution
This protocol yields a clear solution of ≥ 1 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 μLDMSO stock solution (10.0 mg/mL) to 900 μLCorn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
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 (stored under nitrogen, away from moisture)
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.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
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.
*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 (stored under nitrogen, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Optional Solvent
ConcentrationSolventMass
1 mg
5 mg
10 mg
25 mg
DMSO
1 mM
2.0462 mL
10.2312 mL
20.4625 mL
51.1561 mL
5 mM
0.4092 mL
2.0462 mL
4.0925 mL
10.2312 mL
10 mM
0.2046 mL
1.0231 mL
2.0462 mL
5.1156 mL
15 mM
0.1364 mL
0.6821 mL
1.3642 mL
3.4104 mL
20 mM
0.1023 mL
0.5116 mL
1.0231 mL
2.5578 mL
Cholesteryl sulfate sodium Related Classifications
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.
MedChemExpress values your privacy and your trust is important to us. We use cookies to enhance your website experience. Some cookies are necessary to run the website.
Privacy and Cookie Policy
Powered by Bioz
