NPC-18915 free base
NPC-18915 free base is a neutrophil activation inhibitor. NPC-18915 free base inhibits CD11b/CD18-mediated neutrophil adhesion. NPC-18915 free base induces shedding of L-selectin on the neutrophil surface, thereby reducing endothelial cell adhesion. NPC-18915 free base inhibits calcium ionophore-induced LTB4 synthesis in neutrophils. NPC-18915 free base reduces the severity of TNBS-induced acute and recurrent colitis in rat experiments. NPC-18915 free base can be used in studies related to colitis.
For research use only. We do not sell to patients.
- CAS No.: 179487-75-3
- Formula: C23H16O3
- Molecular Weight:340.37
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Biological Activity
Description
IC50 & Target
[1]|
LTB4 |
In Vitro
NPC-18915 (0.001-100 μg/mL; 10 min pre-incubation, 30 min post-stimulation) free base almost completely eliminates calcium ionophore-induced LTB4 synthesis in rat peritoneal neutrophils at concentrations of 10 μg/mL and 100 μg/mL, while no such effect is observed at lower concentrations[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
NPC-18915 (10 mg/kg; i.p.; 1 hour before each subcutaneous injection of TNBS; for 3 consecutive days) free base reduces colon damage and granulocyte infiltration in male Wistar rats with recurrent TNBS-induced colitis, and restores all indicators to the levels of non-recurrent rats[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar (male, 200-225 g, acute colitis induced by intracolonic TNBS instillation)[1]
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Dosage:0.2 mg/kg (pre-induction); 2 mg/kg (pre-induction); 10 mg/kg (pre-induction); 10 mg/kg (post-induction)
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Administration:i.p.; every 12 h; 4 days (pre-induction); i.p.; every 12 h; 4 days (post-induction starting 48 h after induction)
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Result:Reduced colonic damage scores significantly at 2 mg/kg and 10 mg/kg pre-induction doses.
Reduced diarrhea incidence to 4 of 8 rats at 10 mg/kg pre-induction dose.
Reduced colon wall thickness to 1.76 mm at 2 mg/kg pre-induction dose.
Reduced colon wall thickness to 2.25 mm at 10 mg/kg pre-induction dose.
Did not significantly affect colonic myeloperoxidase activity at any pre-induction dose.
Did not significantly affect colonic damage scores, diarrhea incidence, adhesion formation, colon wall thickness, or myeloperoxidase activity at 10 mg/kg post-induction dose.
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Animal Model:Wistar (male, 200-225 g, reactivated colitis induced by subcutaneous TNBS 6 weeks after initial intracolonic TNBS-induced acute colitis)[1]
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Dosage:10 mg/kg
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Administration:i.p.; 1 h before each subcutaneous TNBS injection; over 3 days
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Result:Reduced colonic macroscopic damage scores significantly to levels not different from non-reactivated rats.
Reduced histological damage scores significantly to levels not different from non-reactivated rats.
Reduced myeloperoxidase activity significantly to levels not different from non-reactivated rats.
Chemical Information
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CAS No. 179487-75-3
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Molecular Weight 340.37
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Formula C23H16O3
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SMILES
OC(C(C=C1)=CC=C1/C=C/C2=C(C=CC=C2)C3=CC4=CC=CC=C4O3)=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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Human pluripotent stem cell neural induction and neuron differentiation
Human pluripotent stem cell neural induction can be achieved by blocking BMP and TGFβ/Activin/Nodal SMAD signaling, which suppresses non-neural differentiation and promotes early neuroectodermal identity; the expected readout is loss of pluripotency markers such as OCT4 and induction of neural markers such as PAX6, followed by neural progenitor and neuron marker acquisition during differentiation. This protocol uses dual-SMAD neural induction as the core induction method, followed by cortical neuron differentiation as a representative neuron differentiation model; published cortical protocols describe generation of cortical progenitors, temporally ordered cortical projection neurons, action-potential firing, synaptogenesis, and neural network formation over an approximately 80-day process.
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DSS-Induced Colitis
Dextran sulfate sodium (DSS)-induced colitis is generated by administering DSS in mouse drinking water, producing epithelial injury, barrier disruption, weight loss, diarrhea, fecal blood, colon shortening, histologic mucosal damage, and inflammatory mediator changes; the model is mainly used to study acute or chronic intestinal inflammation resembling selected features of ulcerative colitis. DSS injury is interpreted through clinical and tissue readouts rather than a single molecular endpoint: daily body weight, stool consistency, and bleeding are combined into a disease activity index, while colon length, histology, cytokines, myeloperoxidase activity, intestinal permeability, and tight-junction markers provide complementary measures of inflammation and barrier damage.
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TNBS-Induced Colitis
TNBS-induced colitis is produced by intrarectal delivery of 2,4,6-trinitrobenzene sulfonic acid in ethanol, where ethanol disrupts the mucosal barrier and TNBS haptenates colonic proteins, generating immune-mediated colonic inflammation with weight loss, diarrhea, ulceration, transmural injury, inflammatory-cell infiltration, and cytokine responses. The model is used as an experimental intestinal inflammation model with Crohn’s disease–like features, especially when Th1-type responses, IL-12–dependent inflammation, chronic relapsing inflammation, or fibrosis-related endpoints are studied.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
NPC-18915 free base Related Classifications
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