TrxR-IN-3
TrxR-IN-3 is a thioredoxin reductase (TrxR) inhibitor with an IC50 of 0.12 µM in MDA-MB-231 cells. TrxR-IN-3 inhibits TrxR enzyme activity and suppresses TrxR protein expression. TrxR-IN-3 induces reactive oxygen species (ROS) accumulation, apoptosis, and autophagy. TrxR-IN-3 modulates apoptosis-related proteins by decreasing anti-apoptotic protein levels and increasing caspase cleavage. TrxR-IN-3 modulates autophagy-related proteins by increasing autophagy markers and reducing autophagy substrate proteins. TrxR-IN-3 can be used for breast cancer research.
For research use only. We do not sell to patients.
- CAS No.: 2445565-58-0
- Formula: C14H11F3O2
- Molecular Weight:268.23
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
TrxR 0.12 μM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| MDA-MB-231 | IC50 |
0.59 μM
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Antiproliferative activity against human MDA-MB-231 cells assessed as viability reduction incubated 72 hrs by SRB assay.
Antiproliferative activity against human MDA-MB-231 cells assessed as viability reduction incubated 72 hrs by SRB assay.
|
32736231 |
| MCF7 | IC50 |
1.04 μM
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Antiproliferative activity against human MCF-7 cells assessed as viability reduction incubated 72 hrs by SRB assay.
Antiproliferative activity against human MCF-7 cells assessed as viability reduction incubated 72 hrs by SRB assay.
|
32736231 |
| A549 | IC50 |
0.44 μM
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Antiproliferative activity against human A549 cells assessed as viability reduction incubated 72 hrs by SRB assay.
Antiproliferative activity against human A549 cells assessed as viability reduction incubated 72 hrs by SRB assay.
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32736231 |
| KB | IC50 |
0.53 μM
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Antiproliferative activity against human KB cells assessed as viability reduction incubated 72 hrs by SRB assay.
Antiproliferative activity against human KB cells assessed as viability reduction incubated 72 hrs by SRB assay.
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32736231 |
| KB-V1 | IC50 |
0.84 μM
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Antiproliferative activity against human KB-VIN cells assessed as viability reduction incubated 72 hrs by SRB assay.
Antiproliferative activity against human KB-VIN cells assessed as viability reduction incubated 72 hrs by SRB assay.
|
32736231 |
In Vitro
TrxR-IN-3 inhibits purified TrxR enzyme in the DTNB assay[1].
TrxR-IN-3 (compound 2c) (72 h) inhibits MDA-MB-231 breast cancer cell proliferation with an IC50 of 0.59 µM[1].
TrxR-IN-3 (0.01-5.0 µM; 72 h) inhibits TrxR activity in MDA-MB-231 cells with an IC50 of 0.12 µM[1].
TrxR-IN-3 (0.2-1.8 µM; 72 h) inhibits TrxR1 protein expression in MDA-MB-231 cells after 72 h[1].
TrxR-IN-3 (0.2-1.8 µM; 72 h) regulates apoptosis-related proteins in MDA-MB-231 cells[1].
TrxR-IN-3 (0.2-1.8 µM; 72 h) induced apoptosis in MDA-MB-231 cells, with apoptotic cells reaching 56.8% at 1.8 µM[1].
TrxR-IN-3 (0.01-10 μM; 24 h) increases ROS levels in MDA-MB-231 cells[1].
TrxR-IN-3 (0.6-1.8 µM; 24 h) dose-dependently induces the accumulation of autophagosomes and autolysosomes in MDA-MB-231 cells[1].
TrxR-IN-3 (72 h) regulates autophagy-related proteins in MDA-MB-231 cells[1].
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:MDA-MB-231 cells
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Concentration:0.2, 0.6, 1.8 µM
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Incubation Time:72 h
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Result:Diminished TrxR1 protein expression dose-dependently.\n
Reduced Bcl-2 and Bcl-xL expression dose-dependently and caused cleavage of caspase-3.
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Cell Line:MDA-MB-231 cells
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Concentration:0.2, 0.6, 1.8 µM
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Incubation Time:72 h
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Result:Induced apoptosis with apoptotic rates of 20.7%, 45.6%, and 56.8% at 0.2, 0.6, and 1.8 µM, respectively.
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Cell Line:MDA-MB-231 cells
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Concentration:0.6, 1.8 µM
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Incubation Time:24 h
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Result:Increased red and yellow fluorescence spots dose-dependently, representing autophagosomes and autolysosomes.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude (female, 5-6 weeks old)[1]
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Dosage:10 mg/kg; 25 mg/kg
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Administration:i.p.; 21 days
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Result:Reduced tumor mass by 63.3% (0.57 g vs 1.56 g) at 25 mg/kg.
Chemical Information
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CAS No. 2445565-58-0
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Molecular Weight 268.23
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Formula C14H11F3O2
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SMILES
O=C1C=CCC/C1=C\C2=CC=C(OC(F)(F)F)C=C2
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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.
Protocols
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Western Blot
Western blotting (WB) is a commonly used experimental method in molecular biology, biochemistry, and immunogenetics for identifying and quantifying target proteins. It combines gel electrophoresis with immunoassay, enabling researchers to analyze protein expression, post-translational modifications, and molecular weight.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
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Protocol For Protein Expression And Purification
Recombinant protein expression in Escherichia coli followed by purification of a His-tagged soluble protein by immobilized metal affinity chromatography (IMAC), with optional MBP fusion and TEV tag removal when the construct includes these elements. The biological readout is production of the encoded target protein, detected as an inducible band at the expected molecular mass by SDS-PAGE and quantified by total protein assay or chromatographic absorbance; the purification readout is enrichment of the target protein in elution fractions after selective binding of polyhistidine residues to immobilized Ni2+/metal-chelate resin and elution by imidazole-containing buffer. Expression is driven by an inducible bacterial expression system, commonly T7/lac-based, in which IPTG or lactose/auto-induction activates transcription and translation of the cloned gene; lower induction temperature, lower inducer concentration, induction timing, and solubility-enhancing fusion tags can influence the frac
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Autophagy
Autophagy is a process in which eukaryotic cells use lysosomes to degrade their own cytoplasmic proteins and damaged organelles under the regulation of autophagy related gene (Atg). Microtubule-associated proteins light chain 3 (LC3) is recognized as autophagy marker, which transfers from cytoplasmic LC3 (LC3-I) to membrane type (LC3-II). LC3-II/I ratio could be detected by Western Blot and fluorescence microscopy.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Lysosome and acidic-vesicle live-cell staining
Lysosome and acidic-vesicle live-cell staining detects acidic intracellular compartments by using membrane-permeant acidotropic probes that accumulate in low-pH vesicles, including lysosomes, late endosomes, autolysosomes, and acidic phagosomes. LysoTracker staining is commonly used as an intensity-based readout of acidic lysosomal compartment abundance or enlargement, while acridine orange produces green fluorescence in less concentrated compartments and red fluorescence after concentration-dependent accumulation in acidic vesicular organelles. Loss or reduction of acridine-orange red signal can be used as a readout of lysosomal membrane permeabilization or reduced acidic-vesicle integrity. This protocol is designed for live cultured cells and can be adapted for fluorescence microscopy, high-content imaging, plate-reader readout, or flow cytometry when the selected literature supports the readout. Because these dyes report acidotropic accumulation rather than lysosome identity alone,
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Macroautophagy Solutions
Macroautophagy is a conserved lysosome-dependent degradation pathway in which cytoplasmic material is sequestered into double-membrane autophagosomes and delivered to lysosomes for degradation and recycling. The pathway supports cellular homeostasis during nutrient limitation, organelle stress, protein-aggregate accumulation, infection, differentiation, and tissue remodeling by coupling cargo sequestration, autophagosome maturation, lysosomal fusion, and degradation of cargo-derived macromolecules. The core molecular sequence includes initiation by nutrient- and stress-regulated autophagy machinery, autophagosome nucleation, LC3/ATG8-family conjugation to autophagosomal membranes, cargo selection through receptors such as SQSTM1/p62, autophagosome-lysosome fusion, and lysosomal degradation. LC3 was identified as a mammalian homolog of yeast Atg8 that localizes to autophagosomal membranes after processing, and p62/SQSTM1 was shown to connect ubiquitinated cargo with autophagic degradati
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)