2. GPCR/G Protein Immunology/Inflammation Autophagy Metabolic Enzyme/Protease NF-κB Apoptosis
  3. CXCR Autophagy NOD-like Receptor (NLR) Reactive Oxygen Species (ROS) Apoptosis
  4. CXCR2-IN-3

CXCR2-IN-3 is a CXCR2 inhibitor with an IC50 of 11.37 μM. CXCR2-IN-3 mediates CXCR2-Ca2+ signalling inhibition halted autophagic flux, subsequently facilitating ROS-mediated apoptotic cell death. CXCR2-IN-3 suppresses the CXCR2-NLRP3 canonical pathway, suppressing pre-tumorigenic markers. CXCR2-IN-3 causes autophagy-dependent cell death in polyploid giant cancer cells (PGCCs). CXCR2-IN-3 can be used for the research of oral squamous cell carcinoma (OSCC).

For research use only. We do not sell to patients.

CXCR2-IN-3

CXCR2-IN-3 Chemical Structure

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CXCR2-IN-3 Related Antibodies

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CXCR CXCR1 CXCR2 CXCR3 CXCR4 CXCR7 CXCR6

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NLRP3 NLRP1 NOD1 NOD2

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Description

CXCR2-IN-3 is a CXCR2 inhibitor with an IC50 of 11.37 μM. CXCR2-IN-3 mediates CXCR2-Ca2+ signalling inhibition halted autophagic flux, subsequently facilitating ROS-mediated apoptotic cell death. CXCR2-IN-3 suppresses the CXCR2-NLRP3 canonical pathway, suppressing pre-tumorigenic markers. CXCR2-IN-3 causes autophagy-dependent cell death in polyploid giant cancer cells (PGCCs). CXCR2-IN-3 can be used for the research of oral squamous cell carcinoma (OSCC)[1].

IC50 & Target[1]

125I-IL-8-CXCR2

11.37 μM (IC50)

NLRP3

 

In Vitro

CXCR2-IN-3 (compound 5) shows potent ROS scavenging activity in RAW 264.7 macrophages[1].
In combination of 5-Fluorouracil (HY-90006), CXCR2-IN-3 is strikingly showing significant cytotoxicity in CAL27 cells with the LD50 of 48.00 μM[1].
CXCR2-IN-3 (25-100 μM) inhibits the migration as well as reduce the clonogenic potency of the CAL27 cells[1].
CXCR2-IN-3 decreases IL-8 expression in both CAL27 and LPS stimulated CAL27 cells. CXCR2-IN-3 reduces the Ca2+ level in the CAL27[1].
CXCR2-IN-3 (10-50 μM) induces autophagy in a dose-dependent manner, as evidenced through higher LC3 puncta formation in the CAL27 cells. CXCR2-IN-3 reduces the autophagosome-lysosome fusion initiated by Rapamycin (HY-10219)[1].
CXCR2-IN-3 shows dependent autophagic flux inhibition fuels anti-inflammatory response in the oral cancer cells via downregulating the canonical CXCR2-NLRP3 signalling cascade[1].
CXCR2-IN-3 (5 μM, 50 μM; 21 days, 24 h) primes oral cancer cells and enhances chemo-sensitization in CAL27[1].
CXCR2-IN-3 (5-50 μM; 24-72 h) induces autophagy-dependent cell death in PGCCs (CDDP-resistant oral cancer cells) and reduces autophagic flux and triggers autophagy-mediated apoptotic cell death in CAL27[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

CXCR2-IN-3 Related Antibodies
Parmacokinetics
Species Dose Route Note AUC Cmax Tmax T1/2
Rat[1] 17.5 mg/kg p.o. 文献审核 39.14 ng·h/mL 5.07 ng/mL 0.33 h 18.67 h
Molecular Weight

469.34

Formula

C21H13F6N3O3
SMILES

O=C1C(C(NC2=CC3=C(NC=C3)C=C2)=C1NC4=CC=C(C(C(F)(F)F)(O)C(F)(F)F)C=C4)=O
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Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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CXCR2-IN-3 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

CXCR2-IN-3CXCRAutophagyNOD-like Receptor (NLR)Reactive Oxygen Species (ROS)ApoptosisCXC chemokine receptorsC-X-C motif chemokine receptorsCXCR2,Polyploid giant cancer cells (PGCC),Oral squamous Cell carcinoma (OSCC)Inhibitorinhibitorinhibit

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