GPR43 agonist 1
GPR43 agonist 1 is a selective, orally active GPR43 agonist. GPR43 agonist 1 downregulates the activity of NF-κB. GPR43 agonist 1 can be used in studies of acute colitis.
For research use only. We do not sell to patients.
- Formula: C19H22FN5O3S
- Molecular Weight:419.47
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
GPR43 |
In Vitro
GPR43 agonist 1 (Compound 187) selectively inhibits cAMP production in HEK293-hGPR43 cells, with an EC50 value of 16 nM[1].
GPR43 agonist 1 is a potent positive allosteric agonist that induces Ca2+ influx in HEK293-hGPR43 cells, with enhanced potency in the presence of acetic acid[1].
GPR43 agonist 1 (treated for 25 min, incubated for 1 h) acts as a partial positive allosteric agonist, which induces the GPR43-β-arrestin 2 interaction in HEK293-hGPR43 cells, with enhanced activity in the presence of acetate[1].
GPR43 agonist 1 (pretreated for 20 min and co-incubated with 10 ng/mL TNF-α for 6 h) potently inhibits TNF-α-induced NF-κB activity in HEK293-hGPR43 cells, with an EC50 of 19 nM[1].
GPR43 agonist 1 reverses TNF-α-induced IκBα degradation in HEK293-hGPR43 cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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 (female, 6 weeks old post-acclimation)[1]
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Dosage:30 mg/kg
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Administration:p.o.; daily; 8 days
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Result:Reduced myeloperoxidase (MPO) staining in colon tissue compared to vehicle-treated DSS-induced colitis mice.
Showed no significant change in colon length relative to vehicle-treated mice.
Reported no significant reductions in body weight loss score, rectal bleeding score, stool consistency score, or daily activity index relative to vehicle-treated mice.
Chemical Information
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Molecular Weight 419.47
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Formula C19H22FN5O3S
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SMILES
NC1=C(S(=O)(C2=CC=CC=C2F)=O)C3=NC(C)=NC(N4C[C@@H](C)O[C@@H](C)C4)=C3N1
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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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DSS-Induced Colitis
Dextran sulfate sodium (DSS)-induced colitis is generated by administering DSS in mouse drinking water, producing epithelial injury, barrier disruption, weight loss, diarrhea, fecal blood, colon shortening, histologic mucosal damage, and inflammatory mediator changes; the model is mainly used to study acute or chronic intestinal inflammation resembling selected features of ulcerative colitis. DSS injury is interpreted through clinical and tissue readouts rather than a single molecular endpoint: daily body weight, stool consistency, and bleeding are combined into a disease activity index, while colon length, histology, cytokines, myeloperoxidase activity, intestinal permeability, and tight-junction markers provide complementary measures of inflammation and barrier damage.
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TNBS-Induced Colitis
TNBS-induced colitis is produced by intrarectal delivery of 2,4,6-trinitrobenzene sulfonic acid in ethanol, where ethanol disrupts the mucosal barrier and TNBS haptenates colonic proteins, generating immune-mediated colonic inflammation with weight loss, diarrhea, ulceration, transmural injury, inflammatory-cell infiltration, and cytokine responses. The model is used as an experimental intestinal inflammation model with Crohn’s disease–like features, especially when Th1-type responses, IL-12–dependent inflammation, chronic relapsing inflammation, or fibrosis-related endpoints are studied.
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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
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
GPR43 agonist 1 Related Classifications
HY-184925 Related Classifications
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