BP79
Based on 1 Customer Validation
BP79 is a potent TSLP receptor inhibitor. BP79 disrupts TSLP-mediated ternary complex formation, blocks TSLPR-IL7Rα co-localization, binds and stabilizes TSLPR, and inhibits phosphorylated STAT3/6. BP79 suppresses immune cell infiltration, secretion of IL-13, IL-4. BP79 can be used for the research of inflammation diseases, such as atopic dermatitis, allergic asthma, and allergic rhinitis.
For research use only. We do not sell to patients.
- CAS No.: 3104965-33-2
- Formula: C10H8Cl2N2O2
- Molecular Weight:259.09
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Storage:
4°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
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
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[2]|
STAT3 |
STAT6 |
IL-13 |
IL-4 |
In Vitro
BP79 (5-20 µM; 36 h) inhibits TSLP-induced IL-13 (80% inhibition at 20 µM) and IL-4 (60% inhibition at 20 µM) secretion in HuT78 cells in a concentration-dependent manner [1].
BP79 (0.15-20 µM; 36 h) potently inhibits TSLP-induced IL-4 (IC50 = 2.88 µM) and IL-13 (IC50 = 0.97 µM) secretion in primary human CD4+ T cells, with ≥80% inhibition at 10 µM and 20 µM[1].
BP79 (0.15-20 µM; 24 h) shows no significant cytotoxicity at concentrations up to 20 µM in primary human CD4+ T cells, keratinocytes, and fibroblasts, with viability remaining ≥80%[1].
BP79 (20 µM; 1-5 days) abrogates TSLP-mediated hyperproliferation of primary human CD4+ T cells[1].
BP79 (20 µM) inhibits TSLP-induced STAT6 phosphorylation in primary human CD4+ T cells and STAT3 phosphorylation in primary human keratinocytes[1].
BP79 (20 µM; 24 h) inhibits TSLP-induced OX-40L expression and CCL17 secretion in primary human myeloid dendritic cells, and reduces dendritic cell-mediated IL-13 secretion from naive CD4+ T cells[1].
BP79 (20 µM; 10 min) directly interacts with recombinant TSLPR, thermally stabilizing the protein up to 45 °C[1].
BP79 (20 µM; topical; once daily for 4 days) suppresses pro-inflammatory cytokine secretion, restores skin barrier protein expression, inhibits TSLP production, and blocks CD4+ T-cell infiltration in a human atopic diseases multi-organ chip model, with beneficial effects on both skin and lung tissues[1].
BP79 (10 μM) exhibits moderate binding to some kinases, but does not inhibit JAK2/JAK3/TYK2 kinases in the TSLP signaling pathway[2].
BP79 prevents the co-localization of TSLPR and IL-7Rα in primary keratinocytes following TSLP treatment, supporting its targeting of the TSLP signaling pathway[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:HuT78 cells; TSLP-activated primary CD4+ T cells
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Concentration:0.15; 0.3; 0.6; 1.25; 2.5; 5; 10; 20 µM
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Incubation Time:36 h
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Result:Inhibited TSLP-induced IL-13 secretion by 80% and IL-4 secretion by 60% at 20 µM.
Inhibited TSLP-induced IL-13 and IL-4 in a concentration-dependent manner.
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Cell Line:primary human CD4+ T cells, keratinocytes, and fibroblasts
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Concentration:0.15; 0.3; 0.6; 1.25; 2.5; 5; 10; 20 µM
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Incubation Time:24 h
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Result:Showed no significant cytotoxicity at concentrations up to 20 µM in primary human CD4+ T cells, keratinocytes, and fibroblasts.
Exhibited viability remaining ≥80% in all cell lines.
Chemical Information
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CAS No. 3104965-33-2
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Appearance Solid
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Molecular Weight 259.09
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Formula C10H8Cl2N2O2
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Color White to off-white
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SMILES
NC(/C=C\C(NC1=CC(Cl)=C(C=C1)Cl)=O)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (385.97 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 (sealed storage, away from moisture and light). 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 (sealed storage, away from moisture and light). 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)
Protocols
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Multiplex immunofluorescence IHC
Multiplex immunofluorescence IHC detects multiple protein biomarkers in one tissue section by sequential antibody staining, HRP-mediated tyramide fluorophore deposition, heat-mediated antibody stripping, nuclear counterstaining, multispectral imaging, spectral unmixing, and digital cell phenotyping; TSA deposits fluorophore near the antigen so the fluorescence signal remains after primary and secondary antibodies are removed, enabling repeated staining cycles, including with antibodies from the same host species. Classic FFPE tumor immune-profiling applications use panels such as CD3, CD8, CD68/CD163, FOXP3, PD-1, PD-L1, pancytokeratin, Ki67, and DAPI to identify tumor cells, immune-cell subsets, checkpoint-marker expression, co-expression phenotypes, cell density, and spatial relationships in the tumor microenvironment.
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TPA/Croton Oil Ear Edema and Dermatitis
The TPA (12-O-tetradecanoylphorbol-13-acetate) and croton oil-induced mouse ear edema model is a well-established acute cutaneous inflammation system used to evaluate topical anti-inflammatory activity by measuring edema formation, neutrophil infiltration, vascular permeability, and cytokine-mediated skin responses in vivo. The inflammatory response is triggered by topical application of phorbol esters (TPA) or croton oil constituents, leading to rapid activation of protein kinase C signaling, leukocyte recruitment, and increased vascular permeability, which can be quantified by ear thickness, weight, dye extravasation, and biochemical markers such as myeloperoxidase (MPO) activity and pro-inflammatory mediators in ear tissue homogenates. This model is widely used for screening anti-inflammatory agents, where reductions in edema and inflammatory biomarkers reflect suppression of acute dermal inflammation and immune cell infiltration. Histological evaluation typically confirms epidermal
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Ovalbumin-Induced Allergic Airway Inflammation
Ovalbumin-induced allergic airway inflammation is a mouse model in which systemic sensitization to ovalbumin, usually with aluminum hydroxide adjuvant, is followed by airway ovalbumin challenge to induce allergic airway inflammation, eosinophil recruitment, mucus production, serum antigen-specific IgE, Th2 cytokine responses, and airway hyperresponsiveness to methacholine. The model is used to study allergen-driven airway inflammation and asthma-like immune responses, but it does not reproduce every feature of human asthma. The main readouts are bronchoalveolar lavage fluid cellularity, lung histopathology, airway hyperresponsiveness, serum OVA-specific IgE, and cytokines such as IL-4, IL-5, and IL-13 in bronchoalveolar lavage fluid or lung samples. Eosinophilia and Th2 cytokines reflect allergic type 2 inflammation, while methacholine responsiveness provides a functional airway-reactivity endpoint.
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Multiplex immunohistochemistry
Multiplex immunohistochemistry (mIHC), also known as tyramide dignal amplification (TSA), is an enzymatic detection method that uses horseradish peroxidase (HRP) to perform high-density in-situ labeling of target proteins or nucleic acids.
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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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Research Protocol for Cancer Immunology
Cancer immunology studies how the immune system recognizes, suppresses, edits, or fails to eliminate malignant cells through tumor antigen release, antigen presentation, T-cell priming, immune trafficking, tumor-cell killing, and feedback inhibition in the tumor microenvironment. The cancer-immunity cycle links tumor antigenicity, dendritic-cell priming, CD8+ T-cell infiltration, cytotoxic function, and immune-checkpoint regulation to tumor rejection or immune escape. Immune-checkpoint pathways such as PD-1/PD-L1 and CTLA-4 suppress antitumor T-cell activity and can be therapeutically blocked, but many tumors remain resistant because of poor antigen presentation, weak T-cell infiltration, suppressive myeloid cells, regulatory T cells, and tumor-intrinsic immune-exclusion programs. Unresolved questions include which immune-cell states predict response, how tumor-intrinsic pathways exclude immune cells, how myeloid suppression limits checkpoint blockade, and which combination strategies
Purity & Documentation
References
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 (sealed storage, away from moisture and light). 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 | 3.8597 mL | 19.2983 mL | 38.5966 mL | 96.4916 mL |
| 5 mM | 0.7719 mL | 3.8597 mL | 7.7193 mL | 19.2983 mL | |
| 10 mM | 0.3860 mL | 1.9298 mL | 3.8597 mL | 9.6492 mL | |
| 15 mM | 0.2573 mL | 1.2866 mL | 2.5731 mL | 6.4328 mL | |
| 20 mM | 0.1930 mL | 0.9649 mL | 1.9298 mL | 4.8246 mL | |
| 25 mM | 0.1544 mL | 0.7719 mL | 1.5439 mL | 3.8597 mL | |
| 30 mM | 0.1287 mL | 0.6433 mL | 1.2866 mL | 3.2164 mL | |
| 40 mM | 0.0965 mL | 0.4825 mL | 0.9649 mL | 2.4123 mL | |
| 50 mM | 0.0772 mL | 0.3860 mL | 0.7719 mL | 1.9298 mL | |
| 60 mM | 0.0643 mL | 0.3216 mL | 0.6433 mL | 1.6082 mL | |
| 80 mM | 0.0482 mL | 0.2412 mL | 0.4825 mL | 1.2061 mL | |
| 100 mM | 0.0386 mL | 0.1930 mL | 0.3860 mL | 0.9649 mL |
BP79 Related Classifications
HY-206870 Related Classifications
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