PI3Kγ inhibitor 4
PI3Kγ inhibitor 4 is a potent, selective and orally active inhibitor of PI3Kγ, with an IC50 of 40 nM. PI3Kγ inhibitor 4 shows ∼7, 43, and 18-fold selectivity for PI3Kγ over the α, β, and δ isoforms, respectively. PI3Kγ inhibitor 4 can be used for the research of airway inflammation.
For research use only. We do not sell to patients.
- CAS No.: 1821038-80-5
- Formula: C20H24N4O4S
- Molecular Weight:416.49
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
PI3Kγ 40 nM (IC50) |
PI3Kα 300 nM (IC50) |
In Vitro
PI3Kγ inhibitor 4 inhibits PI3Kγ and PI3Kα in U937 cells, with IC50s of 120 nM and 6250 nM, respectively[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
PI3Kγ inhibitor 4 (a single p.o.) exhibits high oral bioavailability (72, 94 and 122%) and Cmax (1.53, 12.2 and 25.2 μM) following oral administration (10, 100 and 300 mg/kg) in rats[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 1821038-80-5
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Molecular Weight 416.49
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Formula C20H24N4O4S
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SMILES
O=S(C1=CC=C(C)C(C2=CC(C3=CN=C(C)O3)=C(N)N=C2)=C1)(NCC(C)(O)C)=O
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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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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
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)