2. Metabolic Enzyme/Protease NF-κB Immunology/Inflammation Apoptosis
  3. TrxR Reactive Oxygen Species (ROS) Apoptosis
  4. TrxR-IN-4

TrxR-IN-4 is a thioredoxin reductase (TrxR) inhibitor with a rat IC50 of 0.37 μM. TrxR-IN-4 inhibits TrxR activity, elevates reactive oxygen species (ROS) and induces apoptosis. TrxR-IN-4 mediates endoplasmic reticulum stress and induces mitochondrial dysfunction. TrxR-IN-4 can be used for the research of hepatocellular carcinoma.

For research use only. We do not sell to patients.

TrxR-IN-4

TrxR-IN-4 Chemical Structure

CAS No. : 2414906-32-2

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TrxR-IN-4 Related Antibodies

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Description

TrxR-IN-4 is a thioredoxin reductase (TrxR) inhibitor with a rat IC50 of 0.37 μM. TrxR-IN-4 inhibits TrxR activity, elevates reactive oxygen species (ROS) and induces apoptosis. TrxR-IN-4 mediates endoplasmic reticulum stress and induces mitochondrial dysfunction. TrxR-IN-4 can be used for the research of hepatocellular carcinoma[1].

In Vitro

TrxR-IN-4 (Compound 1b) (0.125-2 μM) potently inhibits purified rat liver TrxR with an IC50 of 0.37 μM[1].
TrxR-IN-4 (72 h) potently inhibits the proliferation of HepG2, SMMC-7721, and Hep3B human hepatocellular carcinoma cells with IC50 values of 5.40 μM, 10.05 μM, and 10.89 μM respectively, shows lower potency against MCF-7 and HT-29 cancer cells, and exhibits selective toxicity toward tumor cells over normal LO2 liver cells[1].
TrxR-IN-4 (0.5-10 μM; 24 h) inhibits intracellular TrxR activity in HepG2 human hepatocellular carcinoma cells with an IC50 of 6.51 μM, and dose-dependently reduces TrxR mRNA and protein expression[1].
TrxR-IN-4 (2.5-10 μM; 24-72 h) induces G2/M phase cell cycle arrest in HepG2 human hepatocellular carcinoma cells after 72 h of treatment, and reduces the expression of Cyclin A and CDK2 proteins at 10 μM after 24 h of treatment[1].
TrxR-IN-4 (2.5-10 μM; 24-72 h) dose-dependently induces apoptosis in HepG2 human hepatocellular carcinoma cells after 72 h of treatment, and upregulates pro-apoptotic proteins AIF, cytochrome c, and cleaved-PARP/PARP after 24 h of treatment[1].
TrxR-IN-4 (2.5-10 μM; 24 h) dose-dependently elevates reactive oxygen species levels, increases ROS-endoplasmic reticulum colocalization, and activates endoplasmic reticulum stress via upregulation of CHOP and Calnexin in HepG2 human hepatocellular carcinoma cells[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

TrxR-IN-4 Related Antibodies

Real Time qPCR[1]

Cell Line: HepG2
Concentration: 2.5 μM; 5 μM; 10 μM
Incubation Time: 24 h
Result: Dose-dependently reduced TrxR mRNA expression.

Western Blot Analysis[1]

Cell Line: HepG2
Concentration: 2.5 μM; 5 μM; 10 μM
Incubation Time: 24 h
Result: Dose-dependently reduced TrxR protein expression.

Immunofluorescence[1]

Cell Line: HepG2
Concentration: 2.5 μM; 5 μM; 10 μM
Incubation Time: 24 h
Result: Dose-dependently reduced TrxR protein expression.

Apoptosis Analysis[1]

Cell Line: HepG2
Concentration: 2.5 μM; 5 μM; 10 μM
Incubation Time: 24 h
Result: Elevated intracellular ROS levels.
Dose-dependently increased cell death.

Cell Cycle Analysis[1]

Cell Line: HepG2
Concentration: 2.5 μM; 5 μM; 10 μM
Incubation Time: 72 h
Result: Dose-dependently increased the proportion of HepG2 cells accumulated in the G2/M phase.

Western Blot Analysis[1]

Cell Line: HepG2
Concentration: 2.5 μM; 5 μM; 10 μM
Incubation Time: 24 h
Result: Significantly reduced the expression of G2/M phase-related proteins Cyclin A and CDK2 at 10 μM.
Upregulated the expression of pro-apoptotic proteins AIF, cytochrome c, and cleaved-PARP/PARP.
Upregulated the expression of CHOP and Calnexin.
In Vivo

TrxR-IN-4 (Compound 1b) (20 mg/kg; i.p.; daily; 2 weeks) significantly improves CCl4-induced liver damage in mice by down-regulating TrxR expression and reducing inflammation and collagen accumulation[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: ICR (male, 4-week-old, 18-22 g, chronic liver injury induced by CCl4 injection)[1]
Dosage: 20 mg/kg
Administration: i.p.; daily; 2 weeks
Result: Significantly ameliorated liver tissue morphological changes observed via H&E staining.
Reduced collagen accumulation in liver tissue detected by Masson's and Sirius red staining.
Decreased serum levels of liver injury factors ALT, AST, and LDH compared to the CCl4 model group.
Reduced NFκB expression, decreased TNFα and IL-1b levels to suppress inflammatory cell infiltration.
Significantly lowered TrxR expression and serum TrxR levels in CCl4-injured liver tissue.
Showed no toxicity in mouse hearts, spleens, lungs, or kidneys at this dose.
Molecular Weight

796.40

Formula

C28H20AuF8N2O2P
CAS No.
SMILES

FC(C=C1)=CC=C1[C@@H]2[N]3=CC(C=CC=C4)=C4[O-][Au+3]35[O-]C6=CC=CC=C6C=[N]5[C@H]2C7=CC=C(F)C=C7.F[P-](F)(F)(F)(F)F
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Purity & Documentation
References
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TrxR-IN-4 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

TrxR-IN-42414906-32-2TrxRReactive Oxygen Species (ROS)ApoptosisThioredoxin ReductaseHep3Bmitochondrial dysfunctionHepG2hepatocellular carcinoma cellsSMMC-7721LO2 liver cellscalf thymus DNAreactive oxygen speciesendoplasmic reticulum stressthioredoxin reductaseInhibitorinhibitorinhibit

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