JNJ-27390467
JNJ-27390467 is a potent, orally active, and selective tryptase inhibitor (human β-tryptase IC50 = 3.6 nM, Ki = 3.7 nM). JNJ-27390467 exhibits excellent selectivity over trypsin of ~5000-fold. JNJ-27390467 shows effects in animal models of airway inflammation. JNJ-27390467 can be used for allergic asthma research.
For research use only. We do not sell to patients.
- CAS No.: 1025795-12-3
- Formula: C33H30N2O5
- Molecular Weight:534.60
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
human β-tryptase 3.6 nM (IC50) |
human β-tryptase 3.7 nM (Ki) |
Chemical Information
-
CAS No. 1025795-12-3
-
Molecular Weight 534.60
-
Formula C33H30N2O5
-
SMILES
NCC1=CC=C(OCC23CCN(C(C4=CC=C(C#CC5=CC=CC=C5)O4)=O)CC3)C2=C1.OC(C6=CC=CC=C6)=O
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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.
-
Ovalbumin-Induced Allergic Airway Inflammation
Ovalbumin-induced allergic airway inflammation is a mouse model in which systemic sensitization to ovalbumin, usually with aluminum hydroxide adjuvant, is followed by airway ovalbumin challenge to induce allergic airway inflammation, eosinophil recruitment, mucus production, serum antigen-specific IgE, Th2 cytokine responses, and airway hyperresponsiveness to methacholine. The model is used to study allergen-driven airway inflammation and asthma-like immune responses, but it does not reproduce every feature of human asthma. The main readouts are bronchoalveolar lavage fluid cellularity, lung histopathology, airway hyperresponsiveness, serum OVA-specific IgE, and cytokines such as IL-4, IL-5, and IL-13 in bronchoalveolar lavage fluid or lung samples. Eosinophilia and Th2 cytokines reflect allergic type 2 inflammation, while methacholine responsiveness provides a functional airway-reactivity endpoint.
-
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)