SAR113945
SAR113945 is a highly selective IKK-β inhibitor with an IC50 value of 0.4 nM. SAR113945 blocks the canonical NFκB signaling pathway. SAR113945 alleviates hyperalgesia to heat and mechanical stimuli, and exerts effects in a zymosan-induced knee joint inflammation model. SAR113945 is applicable to research related to symptomatic knee osteoarthritis.
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- CAS. Nr.: 869796-50-9
- Formel: C28H25N7O3
- Molecular Weight:507.55
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
- Protokoll
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
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Biologische Aktivität
Beschreibung
IC50 & Target
[1]|
IKK-β |
In Vitro
SAR113945 potently inhibits the native IKK complex purified from HeLa cell extracts, with an IC50 of 0.018 μM[1].
SAR113945 (10 μM) exhibits high kinase specificity. In a kinome panel comprising 62 kinases, it only inhibits mixed lineage kinase 1 (MLK1) by 59% at a concentration of 10 μM[1].
SAR113945 (10 μM) exhibits high receptor and enzyme specificity, acting solely as an antagonist of the adenosine A3 receptor, with an IC50 of 0.89 μM in a screening panel comprising 106 targets[1].
SAR113945 (Compound 1) inhibits IKK-β with an IC50 of 0.4 nM[3].
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:Lewis rats (male)[1]
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Dosage:0.01 mg per joint; 0.1 mg per joint; 1 mg per joint; 10 mg per joint
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Administration:intra-articular; single dose
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Result:Produced a maximum pain reduction of 88% at the highest dose of 10 mg per joint.
Was well tolerated.
Chemical Information
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CAS. Nr. 869796-50-9
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Molecular Weight 507.55
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Formel C28H25N7O3
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SMILES
N(C[C@H](NC(=O)C=1C=C2C(=CC1)NC(=C2)C3=NC(NC)=NC=C3)C(O)=O)(C4=CC=CC=C4)C5=CC=CC=N5
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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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Collagen-Induced Arthritis
Collagen-induced arthritis (CIA) is an autoimmune murine model of rheumatoid arthritis in which immunization with type II collagen (CII) emulsified in an adjuvant induces a T cell- and autoantibody-driven inflammatory arthritis characterized by synovial hyperplasia, immune cell infiltration, and joint destruction. The model typically relies on genetically susceptible mouse strains (e. g. , DBA/1) and reproduces key features of human rheumatoid arthritis, including anti-collagen immune responses and progressive joint inflammation. Disease onset generally occurs within ~3-4 weeks after immunization, depending on antigen/adjuvant combinations and protocol variation. The immunopathology is driven by adaptive immune activation against CII, leading to systemic and local joint inflammation mediated by pro-inflammatory cytokines and effector immune cells, making CIA a standard preclinical platform for evaluating immunomodulatory and anti-arthritic interventions.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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
[1]. Grothe K, et al. IκB kinase inhibition as a potential treatment of osteoarthritis - results of a clinical proof-of-concept study. Osteoarthritis Cartilage. 2017 Jan;25(1):46-52. [Content Brief]
[2]. Liu D, et al. Small molecule inhibitors of osteoarthritis: Current development and future perspective. Frontiers in physiology. 2023;14:1156913. [Content Brief]
[3]. Noha SM, et al. Discovery of a novel IKK-β inhibitor by ligand-based virtual screening techniques. Bioorganic & medicinal chemistry letters. 2011 Jan 01;21(1):577-83. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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