GPR35 agonist 8
GPR35 agonist 8 is a cross-species, highly potent GPR35 agonist (human EC50: 12 nM; murine EC50: 2 nM). GPR35 agonist 8 reduces lipid accumulation, ameliorates lipid metabolism disorders, alleviates hepatic inflammation and liver fibrosis, and relieves hepatic steatosis. GPR35 agonist 8 can be used for research on metabolic dysfunction-associated fatty liver disease and metabolic dysfunction-associated steatohepatitis.
For research use only. We do not sell to patients.
- Formula: C19H14N4O5
- Molecular Weight:378.34
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
GPR35 agonist 8 (Compound 9f) at 50 μM significantly reduces lipid accumulation in HepG2 cells induced by Oleic acid (HY-N1446)/Palmitic acid (HY-N0830) via a GPR35-dependent mechanism[1].
GPR35 agonist 8 exhibits moderate metabolic stability in human liver microsomes and higher metabolic stability in mouse liver microsomes[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 J (male, 8 weeks old, high-fat diet-induced MASH)[1]
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Dosage:5 mg/kg; 10 mg/kg
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Administration:i.p.; daily; 8 weeks
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Result:Reduced body weight and liver weight compared to high-fat diet control.
Reversed high-fat diet-induced elevations in serum triglycerides, total cholesterol, low-density lipoprotein cholesterol, aspartate aminotransferase, and alanine aminotransferase, and restored reduced high-density lipoprotein cholesterol levels in a concentration-dependent manner.
Significantly reduced hepatic triglycerides and total cholesterol levels.
Reduced hepatic lipid accumulation as shown by Oil Red O staining.
Downregulated lipid synthesis genes (FASN, SREBP-1c, LXR, SCD1, ACC1, CHREBP, HMGCR) and fatty acid uptake gene CD36, while upregulated fatty acid β-oxidation genes (PPARα, CPT1).
Upregulated PPAR-γ and activated the AMPK signaling pathway to improve insulin sensitivity.
Reduced hepatic collagen surface area as shown by Sirius Red staining, and significantly reduced mRNA/protein levels of the fibrosis biomarker α-SMA.
Lowered hepatic malondialdehyde levels (a marker of oxidative stress).
Suppressed mRNA expression of inflammatory markers (TNF-α, ASC, caspase-1, IL-1β).
Chemical Information
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Molecular Weight 378.34
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Formula C19H14N4O5
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SMILES
O=C1OC2=C(C=C(C=C2C=C1C3=NN=NN3)C4=CC=C(C=C4)C(O)=O)OCC
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Fibrosis/Collagen Morphometry
Fibrosis and collagen morphometry is based on the quantitative visualization of fibrillar collagen deposition in tissue sections using histochemical stains such as Sirius Red (Picrosirius Red) or Masson's trichrome, followed by image-based or polarization-enhanced analysis to estimate collagen proportional area as a surrogate of extracellular matrix accumulation during fibrotic remodeling. Sirius Red combined with polarized light microscopy enhances detection of collagen fibers due to birefringence properties, enabling more specific visualization of collagen type I and III fibrils compared to conventional bright-field histology, while whole-section or region-restricted digital morphometry reduces field-selection bias in fibrosis assessment. Alternative quantitative approaches include second harmonic generation (SHG) and two-photon excited fluorescence microscopy, which enable label-free detection of fibrillar collagen and have been validated against histological staining and biochemica
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3T3-L1 preadipocyte-to-adipocyte differentiation
3T3-L1 preadipocytes are induced to differentiate after growth arrest using adipogenic media containing insulin, dexamethasone, and IBMX; differentiation is assessed by lipid-droplet accumulation, triglyceride increase, Oil Red O staining, and adipocyte-marker induction such as PPARγ and C/EBPα.
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Collagen: Sirius Red Staining
Sirius Red or picrosirius red staining is a histochemical method for visualizing collagen-rich extracellular matrix in tissue sections, and collagen fibers are detected as red-stained structures under bright-field microscopy with enhanced birefringence under polarized light. Picrosirius red is useful for assessing total collagen organization, distribution, and fibrosis burden, but polarized color should not be interpreted as a definitive collagen type I versus type III readout because color is affected by fiber orientation, thickness, and packing.
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Connective Tissue: Masson's Trichrome/Collagen Trichrome Staining
Masson’s Trichrome (collagen/trichrome staining) is a histological technique that differentially stains tissue compartments using sequential acidic dyes to distinguish collagen from muscle and cytoplasmic components based on dye affinity and tissue permeability differences, enabling visualization of fibrosis and connective tissue architecture in histological sections. The classical formulation typically uses Weigert's iron hematoxylin for nuclear staining, Biebrich scarlet-acid fuchsin for cytoplasm and muscle, and aniline blue (or light green variants) for collagen, producing a characteristic blue/green collagen signal contrasted against red cytoplasm and dark nuclei. The staining principle relies on selective displacement of smaller dye molecules by larger anionic dyes in collagen-rich regions under controlled acidified conditions, which enhances collagen-specific dye retention. This property makes the method widely used for fibrosis assessment in organs such as heart, liver, lung, a
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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
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Lipid Droplets: Oil Red O/Sudan Dye Lipid Staining
Lipid droplets are intracellular organelles with a neutral-lipid core that stores triacylglycerols and sterol esters, and Oil Red O or Sudan dyes detect these hydrophobic lipid deposits by partitioning into retained lipids in fresh or frozen specimens. Oil Red O stains neutral triglycerides and lipids in frozen tissue sections or air-dried cytologic preparations, while Sudan Black B has also been used as a histochemical fat stain for lipid-rich tissue structures.
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Liver Histomorphometry
Liver histomorphometry is a quantitative histological approach used to measure structural alterations in hepatic tissue, including parenchymal loss, steatosis, fibrosis, and vascular remodeling, by combining stained tissue section analysis with stereological or computerized image-based measurements. Classical morphometric frameworks quantify volume fractions of liver compartments and fibrotic regions using systematic sampling and image analysis, enabling objective comparison of pathological changes across experimental groups. These approaches are widely applied in liver cirrhosis and fibrosis studies to reduce subjectivity in histological scoring and improve reproducibility of tissue evaluation. Recent methodological advances integrate automated image analysis and radiomics-based extraction of histological features from standard liver stains (e. g. , H&E and fibrotic stains), enabling quantitative correlation between morphometric features and fibrosis stages in non-alcoholic fatty live
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)