Florensocatib hydrate
Florensocatib hydrate (HSK31858 hydrate) is a potent reversible dipeptidyl peptidase 1 (DPP1) inhibitor with an IC50 of 1.6 nM against DPP1. Florensocatib hydrate inhibits DPP1 and thereby reduces DPP1-dependent maturation and activation of neutrophil serine proteases (NSPs). Florensocatib hydrate can be used in studies of bronchiectasis and neutrophilic inflammation.
For research use only. We do not sell to patients.
- CAS No.: 2971064-13-6
- Formula: C23H25FN4O5
- Molecular Weight:456.47
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[2]|
DPP1 1.6 nM (IC50) |
In Vitro
Florensocatib hydrate (HSK31858 hydrate) exhibits high inhibitory potency against neutrophil serine protease activity in vitro[1].
Florensocatib hydrate (30 min) potently inhibits the activity of recombinant human DPP1 enzyme, with an IC50 value of 1.6 nM[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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CAS No. 2971064-13-6
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Molecular Weight 456.47
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Formula C23H25FN4O5
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SMILES
CN1C2=CC(C3=CC(F)=C(C=C3)C[C@@H](C#N)NC([C@@H]4CNCCCO4)=O)=CC=C2OC1=O.O
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Synonyms
HSK31858 hydrate
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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)