CX-Se13
CX-Se13 is an orally active pulmonary fibrosis inhibitor with anti-inflammatory and antioxidant activities. CX-Se13 regulates the Keap1/Nrf2/HO-1/NQO1, YAP/TAZ-TEAD, NF-κB p65 and TGF-β/Smads signaling pathways. CX-Se13 activates the cellular antioxidant defense system, restores redox balance, alleviates inflammatory responses, reduces collagen deposition, decreases pro-inflammatory cytokine levels and inhibits pathological progression. CX-Se13 can be used in studies related to pulmonary fibrosis.
For research use only. We do not sell to patients.
- Formula: C29H38N4O4Se
- Molecular Weight:585.60
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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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Biological Activity
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YAP/TAZ-TEAD |
Smad3 |
p65 |
IL-1β |
IL-6 |
TNF-α |
CX-Se13 (compound E13) exhibits anti-inflammatory, antioxidant and antifibrotic activities, with an NO IC50 of 3.4 μM, an ROS inhibition rate of 93.4%, an α-SMA inhibition rate of 85.4%, and a cytotoxicity IC50 >100 μM[1].
CX-Se13 (1.25-20.0 μM) inhibits LPS-induced production of proinflammatory cytokines in RAW264.7 macrophages in vitro in a concentration-dependent manner[1].
CX-Se13 (10.0 μM) ameliorates TGF-β1-induced oxidative stress in MRC-5 fibroblasts by reducing ROS and MDA levels and increasing SOD levels[1].
CX-Se13 (0.625-40 μM; 24-72 h) inhibits TGF-β1-induced proliferation of MRC-5 fibroblasts in a time-dependent manner, with its IC50 value decreasing from 3.4 μM at 24 h to 0.9 μM at 72 h[1].
CX-Se13 (2.5-10.0 μM; 24 h) inhibits TGF-β1-induced migration of MRC-5 fibroblasts [1].
CX-Se13 (2.5-10.0 μM) reduces the expression of fibrosis markers in TGF-β1-induced MRC-5 fibroblasts in a concentration-dependent manner in vitro, and its antifibrotic activity is superior to that of PFD at equivalent doses; it activates the TGF-β1-induced Keap1/Nrf2/HO-1 pathway in MRC-5 fibroblasts and restores cellular redox balance[1].
CX-Se13 exhibits moderate permeability in Caco-2 cells, with a Papp value of 1.8 × 10-6 cm/s[1].
CX-Se13 directly binds to intracellular ROCK2 in living cells[1].
CX-Se13 (2.5-10.0 μM) dose-dependently inhibits the TGF-β1-induced NF-κB p65/IκBα pathway in MRC-5 fibroblasts in vitro. It also inhibits the TGF-β1/Smad pathway and reduces the expression of proteins related to collagen deposition, as well as suppresses the YAP/TAZ-TEAD pathway, thereby inhibiting fibroblast activation and extracellular matrix deposition[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:TGF-β1-stimulated MRC-5 fibroblasts
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Concentration:0.625, 1.25, 2.5, 5, 10, 20, 40 μM
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Incubation Time:24 h, 48 h, 72 h
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Result:Inhibited TGF-β1-induced MRC-5 cell proliferation with IC50 values of 3.4 μM (24 h), 2.6 μM (48 h), and 0.9 μM (72 h), showing a time-dependent reduction in required drug dosage.
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Cell Line:TGF-β1-stimulated MRC-5 fibroblasts
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Concentration:2.5, 5, 10 μM
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Incubation Time:24 h
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Result:Effectively reversed TGF-β1-induced abnormal migration of MRC-5 cells, with inhibitory effects comparable to positive control pirfenidone (PFD) at the same dose.
CX-Se13 (10-40 mg/kg; intragastric administration once daily for 14 consecutive days starting from day 7 of modeling) dose-dependently ameliorates systemic and respiratory abnormalities in mice with bleomycin (HY-108345)-induced pulmonary fibrosis, alleviates pulmonary hemorrhage, alveolar injury, collagen deposition and inflammatory infiltration, and downregulates fibrosis markers and inflammatory cytokines; it also activates the Nrf2 antioxidant pathway and inhibits the pro-inflammatory and pro-fibrotic NF-κB, TGF-β/Smad, and YAP/TAZ pathways[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:ICR mice[1]
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Dosage:500 mg/kg
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Administration:p.o.; daily; 5 days
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Result:Observed no mortality, toxic symptoms, lethargy, or significant body weight loss over a 12-day experimental cycle.
Detected no obvious histopathological changes in heart, liver, spleen, lung, or kidney tissues via H&E staining.
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Animal Model:Male C57BL/6 mice were intratracheally instilled with Bleomycin (2 mg/kg) to construct pulmonary fibrosis model, Pirfenidone (HY-B0673) (100 mg/kg) was set as positive control[1]
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Dosage:10, 20, 40 mg/kg
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Administration:Intragastric administration; once daily for 14 days starting from day 7 after modeling
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Result:Alleviated weight loss, lethargy and dyspnea in a dose-dependent manner, restored lung elasticity and reduced pulmonary hemorrhagic foci and fibrous scars.
Relieved alveolar destruction, alveolar septal thickening and inflammatory infiltration observed in H&E staining; lowered collagen fiber deposition displayed by Masson staining.
Downregulated the expression of α-SMA, Collagen I, Collagen III and Fibronectin in lung tissues, and decreased serum hydroxyproline content.
Reduced concentrations of TNF-α, IL-1β and IL-6 in serum and bronchoalveolar lavage fluid (BALF).
Activated Keap1/Nrf2/HO-1/NQO1 signaling axis, inhibited phosphorylation of NF-κB p65/IκBα, blocked TGF-β/Smad2/3 pathway activation and suppressed YAP/TAZ-TEAD4 fibrotic signaling in lung tissues.
Chemical Information
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Molecular Weight 585.60
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Formula C29H38N4O4Se
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SMILES
O=C(NC1CCC(OC)CC1)C2=CC3=CC(C4=CN(C5CCN(C(OC(C)(C)C)=O)CC5)N=C4)=CC=C3[Se]2
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
CX-Se13 Related Classifications
HY-187219 Related Classifications
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