THR-β agonist 11
THR-β agonist 11 is an orally active and selective thyroid hormone receptor (THR-β) agonist. THR-β agonist 11 shows potent cholesterol-lowering activity in cholesterol-fed rats. THR-β agonist 11 significantly reduces serum total TG, LDL-cholesterol, liver total TC and TG levels, and alleviates hepatic steatosis, inflammation and fibrosis in HFD-CCl4-induced Metabolic dysfunction-associated steatohepatitis (MASH) model mice. THR-β agonist 11 can be used for the study of metabolic dysfunction-associated steatohepatitis (MASH) and other fibrotic diseases.
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- CAS No.: 3051970-23-8
- Formule: C26H30ClN2O5P
- Masse moléculaire:516.95
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
Parmacokinetics
In Vivo
THR-β agonist 11 (3 mg/kg, p.o., once daily, 6 weeks) significantly reduces serum total TG, LDL-cholesterol, liver total TC and TG levels in HFD-CCl4-induced MASH model C57BL/6J mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male Sprague-Dawley rats were fed a normal chow diet supplemented with 1.5% cholesterol and 0.5% cholic acid (w/w) for 2 weeks to establish the model[1]
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Dosage:0.5 mg/kg
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Administration:p.o., single administration, 24 h
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Result:Achieved a total plasma cholesterol reduction rate of 29.07%.
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Animal Model:4-week-old male C57BL/6J mice were fed a high-fat diet (HFD) for 10 weeks to induce obesity, then intraperitoneally injected with carbon tetrachloride (CCl4) twice a week for 6 weeks to establish the MASH model[1]
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Dosage:3 mg/kg
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Administration:p.o., once daily, 6 weeks
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Result:Reduced serum total TG, LDL-cholesterol, liver total TC and TG levels.
Decreased serum ALT and AST levels by a notable margin.
Alleviated hepatic steatosis, inflammation and fibrosis.
Downregulated the mRNA expression levels of fibrosis markers Tgfb1 and Acta2.
Chemical Information
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CAS No. 3051970-23-8
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Masse moléculaire 516.95
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Formule C26H30ClN2O5P
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SMILES
CC1=CC(OC[P@]2(OCC[C@H](O2)C3=CC=CC(Cl)=C3)=O)=CC(C)=C1CC4=NNC(C(C(C)C)=C4)=O
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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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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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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
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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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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
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)