2. Metabolic Enzyme/Protease
  3. Endogenous Metabolite
  4. Larsucosterol

Larsucosterol (DUR-928), a cholesterol metabolite, is a potent liver X receptor (LXR) antagonist. Larsucosterol as a potent endogenous regulator decreases lipogenesis. Larsucosterol inhibits the cholesterol biosynthesis via decreasing mRNA levels and inhibiting the activation of SREBP-1.

At equivalent molar concentrations, both the salt and free forms of a compound exhibit comparable biological activity. Nevertheless, the salt form (Larsucosterol (trimethylamine)) usually boasts enhanced water solubility and stability.

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Larsucosterol Chemical Structure

Larsucosterol Chemical Structure

CAS No. : 884905-07-1

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Larsucosterol Related Antibodies

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Description

Larsucosterol (DUR-928), a cholesterol metabolite, is a potent liver X receptor (LXR) antagonist. Larsucosterol as a potent endogenous regulator decreases lipogenesis. Larsucosterol inhibits the cholesterol biosynthesis via decreasing mRNA levels and inhibiting the activation of SREBP-1[1][2][3].

In Vitro

Larsucosterol (DUR-928; 0-25 μM; 8 h; HepG2 cells) inhibits cholesterol biosynthesis by decreasing HMG-CoA reductase mRNA levels and decreases free [14C] cholesterol in a dose-dependent manner[1].
Larsucosterol (0-25 μM; 6 h; HepG2 cells) inhibits HMG-CoA reductase expression by inhibition of both SREBP1 activation and expression in hepatocytes[1].
Larsucosterol (0-50 μM; 48 h) increases cell proliferation and decreases apoptosis in macrophages[2].
Larsucosterol (0-25 μM; 48 h; macrophages) inhibits activation of liver oxysterol receptor LXRα[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Larsucosterol Related Antibodies

Cell Proliferation Assay[2]

Cell Line: Macrophages
Concentration: 0, 5, 10, 15, 20, and 25 μM
Incubation Time: 48 hours
Result: Induces cell proliferation and relative cell number after treatment for 48 h were 120% at 25 μM.

Apoptosis Analysis[2]

Cell Line: Macrophages
Concentration: 0, 5, 10, 15, 20, and 25 μM
Incubation Time: 48 hours
Result: Did not significantly affect the numbers of apoptotic or live cells.

Western Blot Analysis[1]

Cell Line: HepG2 cells
Concentration: 0, 3, 6, 12, and 25 μM
Incubation Time: 6 hours
Result: Inhibited the activation of SREBP-1 and SREBP-2, and subsequently inhibit the expression HMG-CoA reductase.

Western Blot Analysis[2]

Cell Line: Macrophages
Concentration: 0, 3, 6, 12, and 25 μM
Incubation Time: 48 hours
Result: Decreased LXRα levels in the nuclei in a does-dependent manner.
In Vivo

Larsucosterol (DUR-928; 25 mg/kg; i.p.; twice in 14 hours; C57BL/6J mice with nonalcoholic fatty liver diseases (NAFLD) model) reduces serum lipid levels in mice fed a high-fat diet[3].
Larsucosterol (25 mg/kg; i.p.; twice in 14 hours; C57BL/6J mice with nonalcoholic fatty liver diseases (NAFLD) model) suppressed the expression of the genes and inhibits ABCA1 expressionde. Larsucosterolcreases nuclear SREBP-1 Protein levels and cytoplasmic FAS and ACC1 protein levels in liver tissue[3].
Larsucosterol (25 mg/kg; i.p.; once every 3 days for 6 weeks; C57BL/6J mice with nonalcoholic fatty liver diseases (NAFLD) model) protects the liver from injury by suppressing hepatic inflammation[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Female C57BL/6J mice with nonalcoholic fatty liver diseases (NAFLD) model[3]
Dosage: 25 mg/kg
Administration: Intraperitoneal injection; once every 3 days for 6 weeks
Result: Decreased plasma cholesterol levels.
Reduced serum alkaline phosphatase, ALT, and AST levels.
Animal Model: Female C57BL/6J mice with nonalcoholic fatty liver diseases (NAFLD) model[3]
Dosage: 25 mg/kg
Administration: Intraperitoneal injection; twice in 14 hours
Result: Decreased plasma TG, CHOL, and HDL-C by 40, 15, and 20%, respectively.
Reduced the mRNA levels of SREBP-1c, ACC1, and FAS by 46, 57, and 49%, respectively.
Suppressed ABCA1 expression.
Suppressed nuclear SREBP-1, cytoplasmic ACC1, and FAS protein levels by 74, 58, and 47%, respectively.
Clinical Trial
Molecular Weight

482.72

Formula

C27H46O5S
CAS No.
SMILES

C[C@@]12[C@](CC[C@]2([H])[C@H](C)CCCC(C)(O)C)([H])[C@@]3([H])[C@@](CC1)([H])[C@@]4(C(C[C@H](CC4)OS(=O)(O)=O)=CC3)C
Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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Larsucosterol Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    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.

Keywords:

Larsucosterol884905-07-1DUR-928DUR928DUR 928Endogenous Metabolitecholesterol metabolitelipogenesismRNASREBP-1cholesterol biosynthesisHepG2 cellsmacrophagesInhibitorinhibitorinhibit

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