(Rac)-T6167923
(Rac)-T6167923 is the racemic form of T6167923 (HY-19744) and acts as a MyD88 inhibitor. (Rac)-T6167923 disrupts MyD88 homodimer formation and blocks MyD88-dependent signaling, thereby inhibiting TLR2/MyD88 downstream NF-κB activation and pro-inflammatory cytokine production. (Rac)-T6167923 modulates macrophage inflammatory responses and polarization states, and reduces the survival rate of Mycobacterium avium subsp. paratuberculosis (MAP) within infected macrophages. (Rac)-T6167923 can be used for research related to inflammatory responses and mycobacterial infections.
For research use only. We do not sell to patients.
- CAS No.: 1090528-71-4
- Formula: C17H20BrN3O3S2
- Molecular Weight:458.39
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
(Rac)-T6167923 (0-20 µg/mL; 30 min preincubation, 24 h infection) decreases iNOS, TNF-α, and IL-8 expression and modulates MMR expression in PMA-differentiated THP-1 macrophages; at 10 μg/mL, TNF-α and IL-8 expression decrease to 1.15-fold and 1.10-fold, respectively, and MMR increases from 0.71-fold with MAP infection alone to 0.92-fold[1].
(Rac)-T6167923 (10 μg/mL; MAP infection; 24 h) reduces iNOS and IL-8 expression to levels comparable to those in uninfected cells in THP-1-derived macrophages, while promoting M2-related MMR expression and increasing IL-10; under combined conditions, IL-10 increases 2.5-fold compared with MAP infection alone[1].
(Rac)-T6167923 (10 μg/mL; MAP infection; 48 h) reduces intracellular MAP survival to 55% at 48 h in THP-1-derived macrophages[1].
(Rac)-T6167923 (1-500 μM; PAM3CSK4 (HY-P1180) 100 ng/mL; 24 h) concentration-dependently inhibits NF-κB activation in RAW-Blue macrophages; at 100 and 500 μM, NF-κB activation is reduced by 40% and 50%, respectively[2].
(Rac)-T6167923 (0.05-200 μM; PAM3CSK4 50 ng/mL; 8 h) decreases IL-6 production in a concentration-dependent manner in RAW 264.7 macrophages; at 100 μM it reduces IL-6 by 89%, and at 150 and 200 μM IL-6 levels decrease by 15-fold and 19-fold, respectively[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:THP-1 macrophages
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Concentration:0, 2.5, 5, 10, 20 µg/mL
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Incubation Time:30 min (preincubation); 24 h (infection)
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Result:Decreased iNOS, TNF-α and IL-8 expression.
At 10 μg/mL, decreased TNF-α and IL-8 expression to 1.15- and 1.10-fold, respectively.
Increased MMR from 0.71-fold with MAP alone to 0.92-fold at 10 μg/mL.
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Cell Line:THP-1 macrophages
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Concentration:10 µg/mL
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Incubation Time:24 h
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Result:Reduced iNOS and IL-8 expression to near uninfected-cell levels.
Increased M2-associated MMR and IL-10.
Increased IL-10 by 2.5-fold versus MAP infection alone under the combined condition.
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Cell Line:RAW 264.7 macrophages
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Concentration:0.05, 50, 100, 150, 200 μM
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Incubation Time:PAM3CSK4 50 ng/mL; 8 h
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Result:Dose-dependently reduced IL-6 production.
Reduced IL-6 by 89% at 100 μM.
Decreased IL-6 levels by 15-fold at 150 μM and by 19-fold at 200 μM.
Chemical Information
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CAS No. 1090528-71-4
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Molecular Weight 458.39
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Formula C17H20BrN3O3S2
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SMILES
O=C(NC(C=1SC=CC1)C)N2CCN(CC2)S(=O)(=O)C=3C=CC=C(Br)C3
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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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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)