Mogrol

SKU: orb1297164

Description

Mogrol, the bioactive aglycone of mogrosides, acts as a signaling modulator by suppressing ERK1/2 and STAT3 pathways while activating AMPK, which concurrently reduces CREB activity. This mechanism supports its research utility in metabolic and inflammation studies, applicable in both cellular and animal models.

Research Area

Epigenetics & Chromatin, Signal Transduction, Stem Cell & Developmental Biology

Key Properties

• CAS Number: 88930-15-8
• MW: 476.73
• Purity: 99.95% (May vary between batches)
• Formula: C₃₀H₅₂O₄
• SMILES: [H][C@@]12CC[C@H](O)C(C)(C)C1=CC[C@@]1([H])[C@]3(C)CC[C@H]([C@H](C)CC[C@@H](O)C(C)(C)O)[C@@]3(C)C[C@@H](O)[C@@]21C
• Target: AMPK,STAT,ERK
• Solubility: DMSO:110 mg/mL (230.74 mM);10% DMSO+40% PEG300+5% Tween 80+45% Saline:4 mg/mL (8.39 mM)

Bioactivity

• In Vitro:
  Mogrol, but not mogrosides, suppressed triglyceride accumulation by affecting early (days 0 2) and late (days 4 8), but not middle (days 2 4), differentiation stages. At the late stage, mogrol increased AMP-activated protein kinase (AMPK) phosphorylation and reduced glycerol-3-phosphate dehydrogenase activity. At the early stage, mogrol promoted AMPK phosphorylation, inhibited the induction of CCAAT/enhancer-binding protein β (C/EBPβ; a master regulator of adipogenesis), and reduced 3T3-L1 cell contents (e.g., clonal expansion). In addition, mogrol, but not the AMPK activator AICAR, suppressed the phosphorylation and activity of the cAMP response element-binding protein (CREB), which regulates C/EBPβ expression. Mogrol suppressed adipogenesis by reducing CREB activation in the initial stage of cell differentiation and by activating AMPK signaling in both the early and late stages of this process.
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Storage & Handling

• Storage: -20°C
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

Extracellular signal regulated kinases, ERK2, ERK, ERK1, Inhibitor, Mogrol, inhibit, STAT, STAT3

Compound Identifiers

PubChem CID

14525327