Vexicitinib
Vexicitinib (Vexicitinibum) is a SYK and JAK2 inhibitor with IC50 values both less than 10 nM. Vexicitinib exhibits anti-inflammatory and immunosuppressive effects. Vexicitinib can be used in tumor-related research.
For research use only. We do not sell to patients.
- CAS No.: 2230362-69-1
- Formula: C22H27N7O4S
- Molecular Weight:485.56
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[2]|
JAK2 <10 nM (IC50) |
Syk <10 nM (IC50) |
In Vitro
Vexicitinib (Compound C10R) potently inhibits purified SYK protein kinase activity with an IC50 of <10 nM[2].
Vexicitinib potently inhibits purified JAK2 protein kinase activity with an IC50 of <10 nM[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
| Species | Dose | Route | Tmax | T1/2 | Cmax | AUC0-24 |
|---|---|---|---|---|---|---|
| Mice[2] | 5 mg/kg | p.o. | 0.5 h | 2.41 h | 451.36 ng/mL | 1243.51 ng/mL·h |
Chemical Information
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CAS No. 2230362-69-1
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Molecular Weight 485.56
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Formula C22H27N7O4S
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SMILES
O=S(N1C[C@@]2([H])N(CC1)C3=CC=C(NC4=NC=C(C(N)=O)C(NC5CC5)=N4)C=C3OC2)(C6CC6)=O
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Synonyms
Vexicitinibum
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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)