RIP1 kinase inhibitor 9
RIP1 kinase inhibitor 9 (compound SY-1) is a selective RIP kinase inhibitor. RIP1 kinase inhibitor 9 effectively suppresses the central inflammatory response induced by epilepsy. RIP1 kinase inhibitor 9 inhibits Z-VAD-FMK (HY-16658B)-induced necroptosis in HT-29 cells with an EC50 of 7.04 nM.
For research use only. We do not sell to patients.
- CAS No.: 3040025-57-5
- Formula: C25H21N3O3
- Molecular Weight:411.45
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HT-29 | CC50 |
>100 μM
Compound: SY1
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Cytotoxicity against human HT-29 cells
Cytotoxicity against human HT-29 cells
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[PMID: 38484677] |
| HT-29 | EC50 |
7.04 nM
Compound: SY1
|
Anti-necroptosis activity against human HT-29 cell assessed as inhibition of TSZ-induced necroptosis by chemiluminescence assay
Anti-necroptosis activity against human HT-29 cell assessed as inhibition of TSZ-induced necroptosis by chemiluminescence assay
|
[PMID: 38484677] |
In Vitro
RIP1 kinase inhibitor 9 (10 nM, 4 h) effectively prevents the phosphorylation of both RIP1 and RIP3, hinders necrosome formation[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 3040025-57-5
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Molecular Weight 411.45
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Formula C25H21N3O3
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SMILES
CN1C([C@H](COC2=CC=CC=C21)NC(C3=CC4=C(NC=C4C5=CC=CC=C5)C=C3)=O)=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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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)