R-03201195
Based on 1 publication(s) in Google Scholar
R-03201195 is an efficient and selective p38 MAP kinase inhibitor with an IC50 for p38α of 0.7 nM. R-03201195 has inhibitory activity against TNF-α in THP-1 cells and against IL-1β in human whole blood, with IC50 values of 0.25 and 0.57 nM respectively. R-03201195 can be used for inflammatory diseases such as rheumatoid arthritis.
For research use only. We do not sell to patients.
- CAS No.: 249936-55-8
- Formula: C19H18FN3O4
- Molecular Weight:371.36
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) R-03201195
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Biological Activity
Description
IC50 & Target
[1]|
p38 MAP kinase |
IL-1β |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| THP-1 | IC50 |
0.25 μM
Compound: 63
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Inhibition of LPS-induced TNFalpha production in THP1 cells
Inhibition of LPS-induced TNFalpha production in THP1 cells
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[PMID: 16509574] |
| THP-1 | IC50 |
250 nM
Compound: Ro-3201195
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Inhibition of p38alpha-induced TNFalpha production in human THP1 cells
Inhibition of p38alpha-induced TNFalpha production in human THP1 cells
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[PMID: 18539026] |
Chemical Information
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CAS No. 249936-55-8
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Molecular Weight 371.36
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Formula C19H18FN3O4
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SMILES
OC[C@H](O)COC1=CC=CC(C(C2=C(N)N(C3=CC=C(F)C=C3)N=C2)=O)=C1
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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.
Publications (1)
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Journal Impact Factor
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Most Recent
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Front Med (Lausanne)
Wogonoside alleviates hyperosmotic stress-induced inflammation and apoptosis in human corneal epithelial cells via PI3K/AKT signaling. [Abstract]2026 May 4:13:1828021. PMID: 42210954
Protocols
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Collagen-Induced Arthritis
Collagen-induced arthritis (CIA) is an autoimmune murine model of rheumatoid arthritis in which immunization with type II collagen (CII) emulsified in an adjuvant induces a T cell- and autoantibody-driven inflammatory arthritis characterized by synovial hyperplasia, immune cell infiltration, and joint destruction. The model typically relies on genetically susceptible mouse strains (e. g. , DBA/1) and reproduces key features of human rheumatoid arthritis, including anti-collagen immune responses and progressive joint inflammation. Disease onset generally occurs within ~3-4 weeks after immunization, depending on antigen/adjuvant combinations and protocol variation. The immunopathology is driven by adaptive immune activation against CII, leading to systemic and local joint inflammation mediated by pro-inflammatory cytokines and effector immune cells, making CIA a standard preclinical platform for evaluating immunomodulatory and anti-arthritic interventions.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)