UM-232
UM-232 is a highly selective covalent STING antagonist with an EC50 of 6.20 μM in STING R232-expressing THP-1 cells. UM-232 covalently targets C292 and C309 cysteines of STING, blocks STING oligomerization and inhibits downstream TBK1/IRF3 activation and proinflammatory cytokine transcription. UM-232 has low off-target reactivity and good hepatic stability, serving as a chemical probe for STING-driven autoimmune and inflammatory diseases including Aicardi-Goutières syndrome (AGS), Systemic Lupus Erythematosus (SLE) and Amyotrophic Lateral Sclerosis (ALS).
For research use only. We do not sell to patients.
- Formula: C29H35ClN6O2
- Molecular Weight:535.08
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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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
In Vitro
UM-232 (1 h) exhibits minimal toxicity at concentrations below 40 μM in THP1 Dual cells[1].
UM-232 covalently engages C292 and C309 residues of STING in HEK293T cells[1].
UM-232 (2.5-5 μM; 1 h) inhibits diABZI (diABZI STING agonist-1) (HY-112921A)-triggered transcription of Ifnb, Il6, and Cxcl10 in a dose-dependent manner in BMDMs[1].
UM-232 (5 μM; 1 h) inhibits STING activation and downstream signaling in vitro in BMDMs[1].
UM-232 (5 μM; 15 min) possesses favorable metabolic stability in human liver microsomes and superior stability relative to control compound in mouse liver microsomes[1].
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:HEK293T cells
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Concentration:5 μM
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Incubation Time:1 h
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Result:Covalently bound wild-type STING.
Produced drastically weakened labeling signals on STING with C292A or C309 mutations.
Markedly reduced the levels of phospho-IRF3 and phospho-TBK1 after treatment.
Blocked STING oligomerization.
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Cell Line:Bone marrow-derived macrophages (BMDMs)
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Concentration:2.5 μM, 5 μM
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Incubation Time:1 h
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Result:Suppressed diABZI-induced transcription of Ifnb, Il6, and Cxcl10 in a dose-dependent manner.
Chemical Information
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Molecular Weight 535.08
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Formula C29H35ClN6O2
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SMILES
CC(Cl)C(NCCC[C@H](N1N=NC(C2=CC=C(C3=CC=CC=C3)C=C2)=C1)C(N(CC4)CCC54COC5)=O)=N
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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)
UM-232 Related Classifications
HY-184593 Related Classifications
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