Quin-C7
Based on 1 Customer Validation
Quin-C7 is an orally active FPR2/ALX antagonist. Quin-C7 binds to the orthosteric ligand-binding pocket of FPR2/ALX, modulates receptor activation, and inhibits pro-inflammatory ERK signaling mediated by serum amyloid A (SAA). Quin-C7 reduces pro-inflammatory mediators TNF-α levels, increases anti-inflammatory IL-10, decreases inflammatory neutrophils and pro-inflammatory M1 macrophages, downregulates ERK1/2 phosphorylation, and upregulates JNK1/2/3 phosphorylation. Quin-C7 blocks FPR2/mFpr2 signaling, reduces brain lesion volume. Quin-C7 can be used for the research of inflammatory bowel disease and neuromyelitis optica spectrum disorder.
For research use only. We do not sell to patients.
- Purity : 99.76%
- CAS No.: 871100-12-8
- Formula: C25H25N3O4
- Molecular Weight:431.48
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Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
Biological Activity
Description
IC50 & Target
[1]|
ERK1 |
ERK2 |
JNK1 |
JNK2 |
JNK3 |
IL-10 |
In Vitro
Quin-C7 binds with high affinity to human FPR2/ALX, forming a network of polar and stacking interactions with receptor residues, including a unique hydrogen bond with Q2586.52[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Quin-C7 (16-32 mg/kg; i.g.; daily; 4 days) significantly reduces pathology in NMOSD mice[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6N (male, SPF grade, 7-8 weeks old, body weight 21 g, DSS-induced acute colitis)[1]
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Dosage:0.512 mg/kg; 2.56 mg/kg; 12.8 mg/kg; 64 mg/kg; 320 mg/kg; 16 mg/kg; 160 mg/kg
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Administration:i.g.; daily; 7 days
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Result:Reduced weight loss and decreased Disease Activity Index (DAI) compared to vehicle-treated colitis mice.
Showed an ED50 for symptomatic amelioration (DAI loss) was 2.2110 mg/kg, and ED50 for weight recovery was 1.1430 mg/kg.
Reduced colonic tissue damage, immune cell infiltration, and histopathological scores compared to vehicle-treated colitis mice.
Reversed DSS-induced colon shortening compared to vehicle-treated colitis mice.
Reduced colonic TNF-α levels, increased colonic IL-10 levels, and reduced colonic myeloperoxidase (MPO) and Ly6G levels compared to vehicle-treated colitis mice.
Reduced splenic neutrophil (CD45+ CD11b+ Ly6G+) fractions, reduced colonic neutrophil fractions and median Ly6G fluorescence intensity, and reduced colonic F4/80+ CD86+ (M1 macrophage) cell fractions compared to vehicle-treated colitis mice.
Decreased phosphorylation levels of colonic ERK1/2 and increased phosphorylation levels of colonic JNK1/2/3 compared to vehicle-treated colitis mice.
Showed no significant change in colonic p38 phosphorylation.
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Animal Model:C57BL/6 (8-10 weeks of age; NMOSD induced by intracerebral infusion of AQP4-IgG and human complement)[2]
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Dosage:16 mg/kg; 32 mg/kg
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Administration:i.g.; daily; 4 days
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Result:Significantly reduced loss of AQP4, GFAP, and MBP, and brain lesion volume at 32 mg/kg/day.
Reduced the absolute number of B cells and NK cells in the spleen, and the absolute number of microglia and infiltrating CD4+ T cells in the brain.
Increased the percentage of microglia expressing anti-inflammatory factors IL-10 and TGF-β.
Decreased the percentage of microglia expressing pro-inflammatory factors IL-6 and TNF-α.
Chemical Information
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CAS No. 871100-12-8
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Appearance Solid
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Molecular Weight 431.48
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Formula C25H25N3O4
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Color White to off-white
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SMILES
CCCCOC1=CC=C(C(NN2C(C3=CC=C(C=C3)O)NC4=CC=CC=C4C2=O)=O)C=C1
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (231.76 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 5 mg/mL (11.59 mM); Clear solution
This protocol yields a clear solution of ≥ 5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (50.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocols
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Kinase activity and phosphorylation assays
Kinase activity assays measure the ability of kinases to transfer phosphate groups from ATP to specific substrates, while phosphorylation assays detect the presence and levels of phosphorylated proteins. Common methods include radiolabeled ATP incorporation (e. g. ,), ADP release detection via bioluminescence (e. g. ,[3]), enzyme-linked immunosorbent assays (ELISA) for phospho-specific epitopes (e. g. ,[6]), and microtiter-based formats for high-throughput screening (e. g. ,[8]). The ADP-Glo assay quantifies kinase activity by measuring ADP produced during phosphorylation using a luciferase-based system. Radiometric assays involve autoradiography or scintillation counting after incorporation of 32P-labeled ATP into substrate proteins. ELISA-based approaches rely on phospho-specific antibodies to detect activated kinases in cell lysates or purified samples.
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Western Blot
Western blotting (WB) is a commonly used experimental method in molecular biology, biochemistry, and immunogenetics for identifying and quantifying target proteins. It combines gel electrophoresis with immunoassay, enabling researchers to analyze protein expression, post-translational modifications, and molecular weight.
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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
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Protocol for Kinase activity and phosphorylation assays
Kinase activity assays measure transfer of phosphate from ATP to a protein or peptide substrate, generating phosphorylated substrate, ADP, or incorporated radiolabeled phosphate as the readout; phosphorylation assays measure site-specific phosphorylation in cells or tissues as a proxy for kinase-pathway activation, inhibition, or substrate regulation. Phosphorylation can be detected by phospho-specific Western blot, immunoprecipitation kinase assay, phospho-immunofluorescence, phospho-flow cytometry, luminescent ADP detection, radiolabeled ATP incorporation, or reporter-based pathway assays, and these readouts can be applied to cancer cells, primary neurons, mouse tumors, organoids, inflammatory macrophages, ferroptosis studies, and mitophagy studies when the kinase target is biologically relevant.
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Amyloid: Congo Red Amyloid Staining
Congo red amyloid staining is a histochemical method used to detect extracellular amyloid deposits in tissue sections based on the affinity of Congo red dye for β-pleated sheet-rich protein aggregates. When bound to amyloid, Congo red produces characteristic apple-green birefringence under polarized light microscopy, which is widely regarded as a diagnostic feature of amyloid deposition in histopathology. The diagnostic principle relies on the combination of dye binding (congophilia) and optical anisotropy under polarized illumination, which distinguishes amyloid from most non-amyloid eosinophilic extracellular deposits in routine histological evaluation. Amyloid identification by Congo red staining remains a cornerstone in diagnostic pathology despite the availability of adjunct methods such as immunohistochemistry and mass spectrometry, particularly because of its ability to localize deposits directly within tissue architecture. The specificity of Congo red-positive deposits is incre
Purity & Documentation
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Data Sheet (279 KB)
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SDS (254 KB)
- English - EN (254 KB)
- Français - FR (254 KB)
- Deutsch - DE (254 KB)
- Norwegian - NO (254 KB)
- Español - ES (254 KB)
- Swedish - SV (254 KB)
- Italian - IT (254 KB)
- Korean - KR (254 KB)
- Portuguese - PT (254 KB)
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Handling Instructions (2659 KB)
References
[1]. Yang WS, et al. Oral FPR2/ALX modulators tune myeloid cell activity to ameliorate mucosal inflammation in inflammatory bowel disease. Acta Pharmacol Sin. 2025;46(7):1958-1973. [Content Brief]
[2]. Qi C, et al. Targeting formyl peptide receptor 2 to suppress neuroinflammation in neuromyelitis optica spectrum disorder. Theranostics. 2025;15(10):4495-4506. Published 2025 Mar 19. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 2.3176 mL | 11.5880 mL | 23.1760 mL | 57.9401 mL |
| 5 mM | 0.4635 mL | 2.3176 mL | 4.6352 mL | 11.5880 mL | |
| 10 mM | 0.2318 mL | 1.1588 mL | 2.3176 mL | 5.7940 mL | |
| 15 mM | 0.1545 mL | 0.7725 mL | 1.5451 mL | 3.8627 mL | |
| 20 mM | 0.1159 mL | 0.5794 mL | 1.1588 mL | 2.8970 mL | |
| 25 mM | 0.0927 mL | 0.4635 mL | 0.9270 mL | 2.3176 mL | |
| 30 mM | 0.0773 mL | 0.3863 mL | 0.7725 mL | 1.9313 mL | |
| 40 mM | 0.0579 mL | 0.2897 mL | 0.5794 mL | 1.4485 mL | |
| 50 mM | 0.0464 mL | 0.2318 mL | 0.4635 mL | 1.1588 mL | |
| 60 mM | 0.0386 mL | 0.1931 mL | 0.3863 mL | 0.9657 mL | |
| 80 mM | 0.0290 mL | 0.1449 mL | 0.2897 mL | 0.7243 mL | |
| 100 mM | 0.0232 mL | 0.1159 mL | 0.2318 mL | 0.5794 mL |