Cholesterol sulfate
Cholesterol sulfate is a naturally occurring, orally active cholesterol derivative that is widely distributed in various tissues and body fluids. Cholesterol sulfate acts as a DOCK2 inhibitor, with IC50 values of 2 μM and 2.9 μM against mouse and human targets, respectively. Cholesterol sulfate restricts excessive neutrophil infiltration and alleviates intestinal inflammation and damage. Cholesterol sulfate serves as an activator of protein kinase C (PKC), which promotes squamous cell differentiation and inhibits skin carcinogenesis. Cholesterol sulfate regulates cholesterol homeostasis and cellular metabolism by activating the AMPK-Sirt1 pathway. Cholesterol sulfate can be used in research related to actinic keratitis, ulcerative colitis, skin cancer, and other conditions.
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- CAS 番号: 1256-86-6
- 分子式: C27H46O4S
- 分子量:466.72
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保管条件:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
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生物活性
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化学情報
- 純度とドキュメンテーション
- 参考文献
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Help & FAQs
生物活性
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Human Endogenous Metabolite |
DOCK2 2 μM (IC50) |
Cholesterol sulfate (0.19-150 μM; 20 min-6 h) 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) potently inhibits phorbol ester (PMA) (HY-18739)-induced reactive oxygen species (ROS) production in mouse bone marrow-derived neutrophils[2].
Cholesterol sulfate 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) promotes the proteolytic activation of SREBP2 in HEK293T cells[3].
Cholesterol sulfate (50 μM; 24 h) 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) 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) 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) 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) 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) significantly reduces intracellular cholesterol levels in Huh-7 cells[4].
Cholesterol sulfate (25 μM; 12 h) inhibits de novo cholesterol synthesis in HEK 293T, Huh-7 and MEF cells[4].
Cholesterol sulfate (25 μM) 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) 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) 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) 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) 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) 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) inhibits LDLR endocytosis in Huh-7 cells, resulting in the accumulation of LDLR on the cell surface[4].
Cholesterol sulfate (25 μM; 8 h) partially inhibits the upregulation of SREBP2 target genes in cholesterol-depleted Huh-7 cells[4].
Cholesterol sulfate (25 μM) 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) 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) 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) 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) 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) 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 induces squamous differentiation of normal human keratinocytes by inhibiting cell growth and upregulating the expression and activity of TGase 1[6].
Cholesterol sulfate 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.
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Cell Line:HT-29, LOVO, SW480, HCT116, SW1116, NCM460 human colon epithelial cell lines
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Concentration:50 μM
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Incubation Time:24 h
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Result:Increased mRNA levels of HMGCS1, DHCR7, FDFT1, and CYP51A1 significantly in all tested human colon epithelial cell lines.
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Cell Line:Huh-7 cells, Huh-7 cells stably expressing T7-tagged HMGCR
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Concentration:12.5 μM, 25 μM (endogenous HMGCR); 3.12 μM, 6.25 μM, 12.5 μM, 25 μM (T7-tagged HMGCR)
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Incubation Time:16 h (endogenous HMGCR); 5 h (T7-tagged HMGCR)
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Result:Reduced endogenous HMGCR protein levels in a dose-dependent manner.
Reduced T7-tagged HMGCR protein levels, with an estimated IC50 of 5.6 μM.
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Cell Line:Huh-7 cells stably expressing T7-tagged HMGCR
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Concentration:12.5 μM, 25 μM (with 20 μM MG132); 25 μM (mutant analysis)
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Incubation Time:5 h
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Result: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.
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Cell Line:HEK 293T cells
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Concentration:25 μM
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Incubation Time:8 h
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Result: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.
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Cell Line:Huh-7 cells
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Concentration:12.5 μM, 25 μM
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Incubation Time:5 h (after 16 h lovastatin pretreatment)
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Result:Abolished statin-induced accumulation of HMGCR protein, reducing it even beyond control levels in a dose-dependent manner.
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Cell Line:Huh-7 cells
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Concentration:25 μM
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Incubation Time:4 h, 24 h
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Result:Did not alter total LDLR expression, but significantly increased cell surface LDLR levels compared to controls.
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Cell Line:Huh-7 cells
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Concentration:25 μM
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Incubation Time:8 h (after 16 h cholesterol depletion with lovastatin)
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Result:Partially attenuated the cholesterol depletion-induced increase in SREBP2 target gene transcripts (SREBF2, HMGCS1, HMGCR, SQLE, LDLR).
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Cell Line:Mouse bone marrow-derived macrophages (BMMs)
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Concentration:20, 30 and 40 μM (osteoclast differentiation assay, 3-4 days); 30 μM (NFATc1 protein/ mRNA expression, 2 days)
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Incubation Time:3-4 days (osteoclast differentiation assay); 2 days (NFATc1 protein/ mRNA expression); 3 days (cell viability assay)
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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.
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Cell Line:Wild-type (WT) and myeloid-specific RORα conditional knockout (cKO) mouse bone marrow-derived macrophages (BMMs)
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Concentration:30 μM (osteoclast differentiation assay, 4 days); 30 μM (protein expression analysis, 2 days)
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Incubation Time:4 days (osteoclast differentiation assay); 2 days (protein expression analysis)
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Result:Inhibited RANKL-induced osteoclast formation and NFATc1 protein expression in cKO BMMs to the same extent as in WT BMMs.
Cholesterol sulfate (8 μg/μL; topical; three times daily; for 3 days) 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) 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) 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)) 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) 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) 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.
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Animal Model:C57BL/6 background Sult2b1−/− (age- and sex-matched littermates)[1]
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Dosage:8 μg/μL
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Administration:topical (eye drop); 6 total doses (1 pre-UV, 5 at 4-hour intervals)
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Result:Significantly reduced the number of inflammatory cells in the anterior chamber compared to vehicle-treated controls.
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Animal Model:C57BL/6 background Sult2b1−/− (age- and sex-matched littermates)[1]
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Dosage:8 μg/μL
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Administration:topical (eye drop); three times daily at 4-hour intervals; days 10, 11, 12
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Result:Significantly reduced the number of inflammatory cells in the conjunctiva compared to vehicle-treated controls.
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Animal Model:C57BL/6J (male, 9-12 weeks old, indomethacin-induced small intestinal ulceration)[2]
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Dosage:200 mg/kg
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Administration:p.o.; three times at 4-hour intervals
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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.
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Animal Model:C57BL/6 (female, 8-week-old; postmenopausal osteoporosis model via ovariectomy)[5]
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Dosage:20 mg/kg
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Administration:intraperitoneal; six times weekly; 3 weeks
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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.
化学情報
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CAS 番号 1256-86-6
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性状 Solid
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分子量 466.72
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分子式 C27H46O4S
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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])CC=C4C[C@@H](OS(=O)(O)=O)CC[C@]4(C)[C@@]3([H])CC[C@]12C
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Structure Classification
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Initial Source
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
純度とドキュメンテーション
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取扱説明書 (2659 KB)
参考文献
[1]. Sakurai T, et al. Cholesterol sulfate is a DOCK2 inhibitor that mediates tissue-specific immune evasion in the eye. Sci Signal. 2018;11(541):eaao4874. Published 2018 Jul 31. [Content Brief]
[2]. Morino K, et al. Cholesterol sulfate limits neutrophil recruitment and gut inflammation during mucosal injury. Front Immunol. 2023;14:1131146. Published 2023 Mar 17. [Content Brief]
[4]. Nam LB, et al. Cholesterol sulfate as a negative regulator of cellular cholesterol homeostasis. Mol Cells. 2025;48(6):100209. [Content Brief]
[5]. Park JH, et al. Cholesterol sulfate inhibits osteoclast differentiation and survival by regulating the AMPK-Sirt1-NF-κB pathway. J Cell Physiol. 2023;238(9):2063-2075. [Content Brief]
[6]. Kuroki T, et al. Cholesterol sulfate, an activator of protein kinase C mediating squamous cell differentiation: a review. Mutat Res. 2000;462(2-3):189-195. [Content Brief]
Calculators
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Cholesterol sulfate 関連分類
HY-111355 関連分類
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