| Field | Specification |
|---|---|
| Target | |
| CAS no. | |
| Applications | |
| Source | Marine — Marine algae |
| Molecular weight | |
| Molecular formula | C29H48O2 |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Saringosterol is an orally active steroid isolated from Sargassum muticum that acts as an LXR agonist. It can lower cholesterol levels and suppress the mRNA and protein expression of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT enhancer-binding protein α (C/EBPα), and it has been reported to have anti-obesity, anti-atherosclerosis, anti-Mycobacterium tuberculosis, and anti-depressant activities[1][2][3][4]. It is supplied as a white to off-white solid (C29H48O2, MW 428.69).
Physical & Chemical Properties
| CAS Number | 6901-60-6 |
|---|---|
| Molecular Formula | C29H48O2 |
| Molecular Weight | 428.69 g/mol |
| Appearance | Solid |
| Color | White to off-white |
| Structure Classification | Steroids |
| SMILES | C[C@@]12[C@](CC[C@]2([H])[C@H](C)CCC(C=C)(O)C(C)C)([H])[C@@]3([H])[C@@](CC1)([H])[C@@]4(C(C[C@H](CC4)O)=CC3)C |
| Target | PPARγ |
| Signaling Pathway | Metabolic Enzyme/Protease; Vitamin D Related/Nuclear Receptor; Anti-infection; Cell Cycle/DNA Damage |
| Initial Source | Marine — Marine algae |
| Storage | Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 6 months; -20°C, 1 month. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
[4]. Jin H G, et al. Antidepressant-like effects of saringosterol, a sterol from Sargassum fusiforme by performing in vivo behavioral tests[J]. Medicinal Chemistry Research, 2017, 26(5): 909-915.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
Saringosterol (12.5-200 μM; 24 h) does not lower the viability of 3T3-L1 cells[1]. In 3T3-L1 preadipocytes, Saringosterol (50-200 μM; 8 days) dose-dependently inhibits lipid and triglyceride accumulation, and 200 μM brings accumulation down to 26.6% of that in control differentiated cells[1]. In 3T3-L1 adipocytes, Saringosterol (50-200 μM; 24 h) increases glycerol release in a dose-dependent manner, with a statistically significant elevation at 200 μM[1]. Saringosterol (100-200 μM; 8 days) significantly lowers PPARγ and C/EBPα expression at both the mRNA and protein levels in 3T3-L1 cells[1]. In 3T3-L1 cells, Saringosterol (100-200 μM; 8 days) significantly decreases mRNA expression of the adipogenic marker genes (aP2, adiponectin, resistin, and FAS)[1]. In RAW264.7 macrophage-derived foam cells, Saringosterol (20 μM; 24 h) raises mRNA expression of the LXR-regulated cholesterol transport/uptake genes (ABCA1, ABCG1, and IDOL) and lowers cellular cholesterol content[2]. Saringosterol displays antitubercular activity with an MIC of 0.25 μg/mL[3]. Against Vero cells, Saringosterol shows no appreciable toxicity, with an IC50 above 128 μg/mL[3].
Real Time qPCR[1]
| Cell Line | MDI-induced 3T3-L1 cells |
|---|---|
| Concentration | 100, 200 μM |
| Incubation Time | 8 days (from initiation of differentiation) |
| Result | Significantly inhibited mRNA expression of PPARγ and C/EBPα, with both concentrations showing statistically significant inhibition. Significantly inhibited mRNA expression of aP2, adiponectin, resistin, and FAS, with both concentrations showing statistically significant inhibition. |
Western Blot Analysis[1]
| Cell Line | MDI-induced 3T3-L1 cells |
|---|---|
| Concentration | 100, 200 μM |
| Incubation Time | 8 days (from initiation of differentiation) |
| Result | Significantly inhibited protein expression of PPARγ and C/EBPα, with both concentrations showing statistically significant inhibition. |
In Vivo
In ApoE−/− mice, Saringosterol (50 mg/kg, p.o., once daily for 2 weeks) lowers atherosclerotic plaque burden, improves lipid profiles in serum and liver, and modulates LXR-regulated cholesterol metabolism genes, without inducing hepatic lipogenesis[2]. In mouse behavioral despair models, Saringosterol (10-30 mg/kg, i.p., as a single dose 30 min prior to testing; 30 mg/kg, p.o., once daily for 7 days) produces significant, dose-dependent antidepressant-like effects[4].
| Animal Model | ApoE−/− mice with a high-fat die with (8-week-old)[2] |
|---|---|
| Dosage | 50 mg/kg |
| Administration | p.o.; daily; 2 weeks |
| Result | Reduced atherosclerotic plaque burden, with en face aortic plaque area (percentage of total aortic area) and aortic root cross-sectional plaque area significantly lower than control mice. Significantly decreased serum total cholesterol, low-density lipoprotein cholesterol, and triglyceride levels; significantly increased serum high-density lipoprotein cholesterol levels. No significant change in liver total cholesterol levels; significantly reduced liver triglyceride levels compared to control mice. Attenuated hepatic steatosis, with reduced liver weight and liver weight-to-body weight ratio compared to control mice; no upregulation of hepatic lipogenic genes (SREBP-1c, ACC, FASN, SCD1, chREBP). Upregulated mRNA levels of cholesterol efflux transporters ABCA1 and ABCG1, and LDLR-degrading protein IDOL in peritoneal macrophages. Upregulated hepatic mRNA levels of cholesterol catabolism enzyme CYP7A1, cholesterol efflux transporters ABCG5 and ABCG8, and HDL-cholesterol influx receptor SR-B1. Downregulated intestinal mRNA levels of cholesterol absorption transporter NPC1L1; upregulated intestinal mRNA levels of cholesterol efflux transporters ABCG5, ABCG8, and ABCA1. |
| Animal Model | ICR (male, 20-22 g)[4] |
|---|---|
| Dosage | 10 mg/kg; 20 mg/kg; 30 mg/kg (single dose; behavioral tests); 30 mg/kg (neurotransmitter analysis) |
| Administration | i.p (10-30 mg/kg); p.o.; daily for 7 days (30 mg/kg) |
| Result | Reduced immobility time in forced swim test and tail suspension test. Did not significantly alter locomotor activity in open-field test at all tested doses. Increased brain serotonin (5-HT) levels, 5-hydroxyindoleacetic acid (5-HIAA) levels and noradrenaline (NE) levels. Showed no significant effect on brain dopamine (DA) levels. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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