Iptocigistat
Iptocigistat (Iptocigistatum) is a cyclic GMP-AMP synthase (cGAS) inhibitor. Iptocigistat prevents excessive immune responses. Iptocigistat can be used to study inflammation-related autoimmune diseases.
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- CAS. Nr.: 3047739-67-0
- Formel: C18H22N6O6S
- Molecular Weight:450.47
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
Beschreibung
In Vitro
Iptocigistat (Compound 10) inhibits the activity of human guanylate-adenylate cyclase in a cell-free Kinase-Glo assay, with an IC50 ranging from ≥0.005 μM to <0.02 μM[1].
Iptocigistat inhibits the activity of human guanylate-adenylate synthase in cell-free LCMS assays, with an IC50 of ≥0.005 μM and <0.02 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS. Nr. 3047739-67-0
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Molecular Weight 450.47
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Formel C18H22N6O6S
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SMILES
O=C1OC(C(NC2=NN=C(N3N=CC=C3C)S2)=O)=CC(NC(COC)COC)=C1OC
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Synonyms
Iptocigistatum; VENT-03
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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
Reinheit & Dokumentation
Verweise
Calculators
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