Idescarpin
Based on 1 Customer Validation
Idescarpin is a phenolic glycoside compound isolated from Idesia polycarpa and exhibits an extremely bitter taste. Idescarpin possesses significant anti-inflammatory, antioxidant, and potent anti-adipogenic activities. Idescarpin reduces melanin biosynthesis by inhibiting tyrosinase activity. Idescarpin is applicable to research on obesity and type 2 diabetes, as well as related studies in food and cosmetics.
For research use only. We do not sell to patients.
- Purity : 93.0%
- CAS No.: 188557-53-1
- Formula: C20H24O11
- Molecular Weight:440.40
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Storage:
-20°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
All Endogenous Metabolite Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
PPAR-γ |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| 3T3-L1 | IC50 |
23.2 μM
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Inhibition of adipocyte differentiation in 3T3-L1 preadipocytes assessed by Oil Red O lipid staining quantification after 8-day incubation during differentiation.
Inhibition of adipocyte differentiation in 3T3-L1 preadipocytes assessed by Oil Red O lipid staining quantification after 8-day incubation during differentiation.
|
j.fbio.2025.106228 |
In Vitro
Idescarpin (25-50 μM; 8 days) significantly reduces lipid droplet formation and inhibits preadipocyte-to-adipocyte differentiation in mouse preadipocytes (3T3-L1)[2].
Idescarpin (25-50 μM; 4-8 days) significantly inhibits C/EBPα protein and mRNA expression in mouse preadipocytes (3T3-L1), downregulates the mRNA expression of adipogenesis-related genes (SREBP1c, SCD-1, FAS), but upregulates PPARγ protein and mRNA expression[2].
Idescarpin (2-10 μg/mL; 24 h) is a key substance in the anti-inflammatory activity of defatted Idesia polycarpa extract, showing a negative correlation with inflammatory mediators (NO, iNOS, TNF-α, IL-6, ROS) and a positive correlation with CAT activity in LPS (HY-D1056)-stimulated RAW 264.7 cells[1].
Idescarpin is predicted to activate 7 human bitter taste receptors (hTAS2R1, hTAS2R5, hTAS2R14, hTAS2R16, hTAS2R39, hTAS2R41, hTAS2R43), with activation probabilities ranging from 51.08% to 69.31%.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:3T3-L1 preadipocytes undergoing differentiation
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Concentration:25 μM; 50 μM
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Incubation Time:4 days; 8 days
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Result:Significantly increased the relative induction of PPARγ mRNA on days 4 and 8.
Dramatically suppressed the relative induction of C/EBPa mRNA on days 4 and 8.
Decreased mRNA levels of SREBP1c, SCD-1, and FAS at both concentrations on days 4 and 8.
Slightly reduced aP2 mRNA levels at both concentrations on days 4 and 8.
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Cell Line:3T3-L1 preadipocytes undergoing differentiation
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Concentration:25 μM; 50 μM
-
Incubation Time:4 days; 8 days
-
Result:Increased PPARγ protein levels on days 4 and 8 at 25 μM and 50 μM.
Decreased C/EBPa protein levels on days 4 and 8 at 25 μM and 50 μM.
Chemical Information
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CAS No. 188557-53-1
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Appearance Solid
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Molecular Weight 440.40
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Formula C20H24O11
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Color White to off-white
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SMILES
O=C([C@]1(C(CCC=C1)=O)O)OCC(C=CC=C2O)=C2O[C@@H]3O[C@@H]([C@H]([C@@H]([C@H]3O)O)O)CO
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Structure Classification
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-20°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Protocols
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
References
[2]. Lee M, et al. Anti-adipogenic activity of compounds isolated from Idesia polycarpa on 3T3-L1 cells. Bioorg Med Chem Lett. 2013 Jun 1;23(11):3170-4. [Content Brief]
[3]. Xiang X, et al. Characterization of key bitter compounds in Idesia polycarpa var. vestita Diels fruit by sensory-guided fractionation. Food chemistry. 2024 May 01;439:138103. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keywords
- Idescarpin
- 188557-53-1
- Endogenous Metabolite
- PPAR
- sterol regulatory element binding protein 1c
- fatty acid synthase
- CCAAT/enhancer binding protein α
- interleukin-6
- inducible nitric oxide synthase
- stearoyl-CoA desaturase 1
- RAW 264.7 cells
- peroxisome proliferator-activated receptor γ
- tumor necrosis factor-α
- 3T3-L1 preadipocytes
- Inhibitor
- inhibitor
- inhibit