YS-01
YS-01 is an inhibitor of pendrin (SLC26A4) with pulmonary protective activity. YS-01 inhibits pendrin-mediated anion exchange activity, reduces pendrin expression, and suppresses the activation of NF-κB and the production of proinflammatory cytokines. YS-01 alleviates lipopolysaccharide-induced and ventilator-induced lung injury. YS-01 attenuates ovalbumin-induced airway hyperresponsiveness, inflammatory infiltration, epithelial thickening and goblet cell hyperplasia, and reduces eosinophil and neutrophil counts. YS-01 decreases MUC5AC transcription levels induced by IL-4, reverses the reduction of airway surface liquid volume, and inhibits the increase of apical SCN− concentration in epithelial cells. YS-01 can be used in studies related to lung injury and allergic asthma.
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- No. CAS: 312724-83-7
- Fòrmula: C18H17NO2S
- Peso molecular:311.40
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Almacenamiento:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Actividad biológica
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Chemical Information
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Help & FAQs
Actividad biológica
YS-01 potently inhibits pendrin-mediated Cl−/SCN− exchange activity in pendrin-transfected human alveolar epithelial cells, with an IC50 of 4.7 μM; it significantly inhibits LPS-induced increase in apical SCN− concentration in human nasal epithelial cells[1].
YS-01 (0-100 μM; 10 minutes at 37°C) potently and selectively inhibits human and mouse pendrin-mediated anion exchange across multiple anion pairs in CHO-K1 cells, and shows no activity against a variety of related ion channels and transporters at relevant concentrations[3].
YS-01 (0-100 μM) inhibits IL-4-induced pendrin-mediated Cl−/HCO3− exchange activity in primary human nasal epithelial cells in a dose-dependent manner, with significant inhibition observed at concentrations as low as 3 μM[3].
YS-01 (30 μM; 24-48 h) reduces the functional expression of IL-4-induced pendrin protein levels in primary human nasal epithelial cells (without affecting mRNA levels) and exerts no effect on related ion channels[3].
YS-01 (30 μM; 30 min) inhibits IL-4-induced transepithelial SCN− transport in primary human nasal epithelial cells cultured at an air-liquid interface[3].
YS-01 reduces IL-4-induced MUC5AC expression and IL-4/IL-13-induced goblet cell hyperplasia in primary human nasal epithelial cells; it rescues the reduction of airway surface liquid volume induced by IL-4 and IL-13 in primary human nasal epithelial cells expressing wild-type pendrin[3].
YS-01 inhibits IL-4-induced activation of NF-κB in primary human nasal epithelial cells[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:primary human nasal epithelial cells
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Concentration:30 μM
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Incubation Time:24 h, 48 h
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Result:Reduced IL-4-induced pendrin functional expression at the protein level (not mRNA) in primary human nasal epithelial cells after 24 or 48 hours of treatment, without affecting related ion channels.
YS-01 (10 mg/kg; i.p.; single dose) significantly attenuates lung inflammation and injury in supine HTV-ventilated pendrin wild-type 129SVEV mice, including reducing TNF-α and MIP-2 levels by 83% and 81% respectively[2].
YS-01 (10 mg/kg; i.p.) significantly reduces OVA-induced airway hyperresponsiveness, airway inflammation, and goblet cell hyperplasia in a murine allergic asthma model without affecting OVA-specific IgE levels[3].
YS-01 provides therapeutic benefits by reducing airway hyperresponsiveness and goblet cell hyperplasia in mice with established allergic asthma[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (male, 8-10 weeks old, 20-24 g, intranasal LPS-induced acute lung injury)[1]
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Dosage:10 mg/kg (pre-treatment; post-treatment)
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Administration:i.p.; single dose (1 hour before LPS instillation for pre-treatment); two doses (6 and 12 hours after LPS instillation for post-treatment)
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Result:Reduced LPS-evoked pulmonary damage by lowering BALF cell count, protein content and lung injury scores.
Inhibited NF-κB signaling, downregulated pendrin expression and decreased pulmonary pro-inflammatory cytokine production (IL-1β, MIP-2, IL-6, TNF-α) upon LPS stimulation.
Abolished such pulmonary protective effects following co-administration with intranasal NaSCN, with all injury indicators returning to the levels of the LPS-alone group.
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Animal Model:129SVEV mice (pendrin wild-type, weight 20-25 g, age 6-8 weeks)[2]
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Dosage:10 mg/kg
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Administration:i.p.; single dose
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Result:Decreased total cell numbers in BALF and alleviated lung injury.
Dropped lung TNF‑α and MIP‑2 contents to 1.03 pg/mL and 110.28 pg/mL respectively, corresponding to 83% and 81% reductions.
Downregulated pendrin expression within lung tissues.
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Animal Model:BALB/c (8-week-old, sex-matched, OVA-sensitized and challenged allergic asthma model)[3]
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Dosage:10 mg/kg
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Administration:i.p.; 12 hours before each intranasal OVA challenge; 3 total doses
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Result:Mitigated OVA-triggered airway hyperresponsiveness against gradient methacholine stimulation.
Lessened eosinophil and neutrophil infiltration in BALF.
Relieved airway inflammatory infiltration, epithelial thickening and goblet cell hyperplasia, accompanied by decreased peribronchial inflammation scores.
Exerted no obvious influence on serum OVA-specific IgE concentrations.
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Animal Model:NF-kB luciferase-dTomato reporter (8-week-old, OVA-sensitized and challenged allergic asthma model)[3]
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Dosage:10 mg/kg
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Administration:i.p.; 12 hours before each intranasal OVA challenge; 3 total doses
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Result:Inhibited pulmonary NF-κB activation in OVA-challenged mice.
Co-administration with NaSCN abolished this inhibitory action against NF-κB activation.
Chemical Information
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No. CAS 312724-83-7
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Peso molecular 311.40
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Fòrmula C18H17NO2S
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SMILES
CC(C)(C)C1=CC=C(C2=N/C(C(O2)=O)=C/C3=CC=CS3)C=C1
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
Referencias
[1]. Lee EH, et al. Inhibition of Pendrin by a small molecule reduces Lipopolysaccharide-induced acute Lung Injury. Theranostics. 2020;10(22):9913-9922. [Content Brief]
[2]. Choi JS, et al. Pendrin inhibition is associated with protective effect of prone positioning in a ventilator-induced lung injury mouse model. Scientific reports. 2025 Nov 20;15(1):40926. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
YS-01 Related Classifications
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