PRDX1-IN-4
PRDX1-IN-4 is a PRDX1 inhibitor with an IC50 of 122 nM against human targets and high subtype selectivity. PRDX1-IN-4 covalently binds to PRDX1 to promote ROS accumulation. PRDX1-IN-4 inhibits NLRP3 inflammasome activation, blocks hepatic stellate cell activation and reduces collagen deposition. PRDX1-IN-4 induces apoptosis in activated hepatic stellate cells. PRDX1-IN-4 has good safety profile, with no significant body weight loss or hepatotoxicity observed in mice at a dose of 20 mg/kg. PRDX1-IN-4 ameliorates CCl4-induced liver injury and liver fibrosis in mice at a dose of 1 mg/kg. PRDX1-IN-4 can be used for the research of liver fibrosis.
For research use only. We do not sell to patients.
- Formula: C33H45BrN2O5
- Molecular Weight:629.62
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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
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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NLRP3 |
PRDX1-IN-4 (derivative 5) (0.1-2 μM; 48 h treatment) dose-dependently reduces the protein expression levels of α-SMA and COL1A1 in TGF-β1-induced activated LX-2 cells[1].
PRDX1-IN-4 (0.1-2 μM; 48 h treatment) dose-dependently increases TGF-β1-induced intracellular ROS levels in activated LX-2 cells, with ROS positive rates reaching 18.0%, 26.4% and 34.7% at concentrations of 0.1, 1 and 2 μM, respectively[1].
PRDX1-IN-4 (0.1-1 μM; 48 h treatment) dose-dependently upregulates the expression of pro-apoptotic proteins Bax, Cyt c, and activated Caspase-3, and downregulates the expression of anti-apoptotic protein Bcl-2 and pro-Caspase-3 in TGF-β1-induced activated LX-2 cells[1].
PRDX1-IN-4 (0.5 μM; 6 h) exerts no significant effect on the viability of THP-M cells, and its NLRP3 inhibitory activity is not derived from cytotoxicity[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:THP-1-derived macrophages (induced by 100 ng/mL PMA overnight)
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Concentration:0.5 μM
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Incubation Time:6 h
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Result:Showed no significant effect on the viability of THP-M cells, indicating that its NLRP3 inhibitory activity was not attributed to cytotoxicity.
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Cell Line:THP-1-derived macrophages (induced by 100 ng/mL PMA overnight)
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Concentration:0.01 μM, 0.1 μM, 1 μM, 10 μM
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Incubation Time:Pretreated for 0.5 h, then stimulated with 10 μM Nigericin for 1 h, 5 mM ATP for 1 h, or 200 μg/mL MSU for 4 h
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Result:Dose-dependently reduced the levels of cleaved caspase-1 p20 and mature IL-1β in the supernatants, and inhibited ASC oligomerization in the pellets. It did not consistently affect the expression of pro-IL-1β, pro-caspase-1, total ASC, or NLRP3 in the cell lysates.
PRDX1-IN-4 (1 mg/kg; intraperitoneal injection; once daily for 4 consecutive weeks, starting from the 3rd week of modeling) significantly ameliorates CCl4-induced liver injury and fibrosis in the CCl4-induced hepatic fibrosis model of male C57BL/6 mice. It reduces the liver/body weight ratio, serum ALT and AST levels, and collagen fiber deposition, downregulates the expressions of α-SMA and COL1A1 in liver tissues, and inhibits NLRP3 inflammasome activation. No mouse death is observed, and its safety is superior to that of celastrol at the same dose[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male C57BL/6 mice, housed under SPF conditions, acclimatized for 1 week; hepatic fibrosis model established by intraperitoneal injection of CCl4 (1 mL/kg, diluted 1:8 in corn oil) twice weekly for 6 consecutive weeks[1]
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Dosage:1 mg/kg
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Administration:intraperitoneal injection once daily for 4 weeks
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Result:Significantly normalized the liver/body weight ratio and reduced the serum levels of ALT and AST, indicating improved liver function. H&E staining showed that derivative 5 alleviated CCl4-induced hemorrhagic necrosis and inflammatory cell infiltration in the liver.
Markedly reduced collagen fiber deposition in the fibrotic liver.
Downregulated the protein expression of α-SMA and COL1A1, and decreased the levels of IL-1β and cleaved caspase-1 without altering the total expression of NLRP3.
Chemical Information
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Molecular Weight 629.62
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Formula C33H45BrN2O5
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SMILES
C[C@@H](C(OC)=O)NC(N[C@@](CC[C@]1(C)CC[C@]2(C)C3=CC=C4C(C)=C5O)(C)C[C@@]1([H])[C@]2(C)C[C@@](Br)([H])[C@@]3(C)C4=CC5=O)=O
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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)
PRDX1-IN-4 Related Classifications
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