SPH7050
SPH7050 is an orally active LANCL2 agonist with a Kd of 3.73 μM. SPH7050 inhibits PGE2 production. SPH7050 attenuates the disease activity index and colonic inflammation in TNBS-induced colitis in mice. SPH7050 can be used for research on inflammatory bowel disease.
For research use only. We do not sell to patients.
- Formula: C31H24N8O2
- Molecular Weight:540.57
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
LANCL2 3.73 μM (Kd) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| BMDM | IC50 |
0.85 μM
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Inhibition of PGE2 production in bone marrow-derived macrophages stimulated with lipopolysaccharide (LPS) for 17 hours, measured by ELISA.
Inhibition of PGE2 production in bone marrow-derived macrophages stimulated with lipopolysaccharide (LPS) for 17 hours, measured by ELISA.
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42623744 |
In Vitro
SPH7050 (0.78-50 μM) binds LANCL2 with a KD of 3.73 μM[1].
SPH7050 inhibits PGE2 production in BMDMs with an IC50 of 0.85 μM[1].
SPH7050 (2-10 μM; 90 min) exhibits extremely low permeability in Caco-2 cells with Papp AP-BL values below or at the 1 × 10-6 cm/s threshold, indicating limited transepithelial transport[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
| Species | Dose | Route | Cmax | Plasma Concentration |
|---|---|---|---|---|
| Mice[1] | 8 mg/kg | p.o. | 6.900 ng/mL | 6.900 (0.5 h) ng/mL |
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c (female, 8-10 weeks old, 18-20 g, TNBS-induced colitis)[1]
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Dosage:12.5, 25, and 50 mg/kg
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Administration:p.o.; BID; Day -1 to Day 5
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Result:Attenuated body weight loss in a dose-dependent manner, with the 50 mg/kg group recovering nearly to baseline by Day 6.
Reduced Disease Activity Index scores dose-dependently, outperforming BT-11 at equal doses and matching mesalazine in efficacy.
Alleviated diarrhea and hematochezia.
Increased colon length and reduced colon weight and weight-to-length ratio relative to vehicle in a dose-dependent manner, with the 50 mg/kg group approaching sham values.
At 50 mg/kg (BID), was superior to BT-11 at the same dose and comparable to mesalazine (100 mg/kg, QD) across all intestinal parameters.
Chemical Information
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Molecular Weight 540.57
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Formula C31H24N8O2
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SMILES
O=C(N[C@H]1[C@]2([H])CN(C(C3=NC(C4=NC5=CC=CC=C5N4)=CC=C3)=O)C[C@]12[H])C6=NC(C7=NC8=CC=CC=C8N7)=CC=C6
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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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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.
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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)
SPH7050 Related Classifications
HY-189377 Related Classifications
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