TrxR Inhibitor

Aurothiomalate sodium acts as an inhibitor of PKCI and TrxR1. Aurothiomalate sodium disrupts the PKCI-Par6-Rac1 signaling pathway, and also inhibits TrxR1 activity, TNFα-induced NF-κB activation, and the expression of pro-inflammatory genes. Aurothiomalate sodium blocks Kras-mediated BASC expansion and lung tumor growth, inhibits anchorage-independent growth and tumorigenicity of lung cancer cells, and suppresses neutrophil chemotaxis, phagocytosis, and leukocyte extravasation. Aurothiomalate sodium can be used in research related to rheumatoid arthritis and non-small cell lung cancer.

ROS-generating agent 1 is a selective ROS-generating agent. ROS-generating agent 1 inhibits TrxR activity and expression in cancer cells. ROS-generating agent 1 induces ROS-dependent apoptosis and ferroptosis in cancer cells. ROS-generating agent 1 selectively kills lung cancer cells and inhibits the growth of cancer cell xenograft tumors in nude mice. ROS-generating agent 1 can be used for the research of non-small cell lung cancer.

Necroptosis inducer 1 is a necroptosis inducer. Necroptosis inducer 1 inhibits the activity of thioredoxin reductase (TrxR), elevates intracellular ROS levels, triggers ROS-mediated necroptosis, and induces necroptosis-dependent immunogenic cell death. Necroptosis inducer 1 inhibits tumor growth, remodels the tumor immune microenvironment, and exerts a synergistic effect with anti-PD-1 in animal models. Necroptosis inducer 1 is applicable to the research of colon cancer.

Fa-Au is a TrxR inhibitor. Fa-Au downregulates GPX4, induces oxidative stress, mitochondria-associated ferroptosis (ferroptosis) and immunogenic cell death. Fa-Au induces ROS production in hepatoma cells. Fa-Au remodels the tumor immune microenvironment via M1 macrophage polarization, dendritic cell maturation, CD8+ T cell activation and reduction of regulatory T cells. Fa-Au induces an anti-tumor immune feedback loop through the IFNγ/STAT1/SLC7A11 axis. Fa-Au inhibits tumor growth. Fa-Au is applicable to hepatocellular carcinoma-related research.

TrxR-IN-9 is a thioredoxin reductase (TrxR) inhibitor with an IC₅₀ of 0.26 μM. TrxR-IN-9 disrupts cellular redox balance. TrxR-IN-9 induces S-phase cell cycle arrest, promotes apoptosis and exhibits antiproliferative activity across cancer cells. TrxR-IN-9 exerts effects via synergistic nitric oxide (NO) and reactive oxygen species (ROS) action. TrxR-IN-9 can be used for the research of breast cancer, gastric cancer, colorectal cancer, liver cancer.

Aurothiomalate tetramer sodium is the tetrameric form of Aurothiomalate sodium (HY-106381). Aurothiomalate sodium acts as an inhibitor of PKCI and TrxR1. Aurothiomalate sodium disrupts the PKCI-Par6-Rac1 signaling pathway, and also inhibits TrxR1 activity, TNFα-induced NF-κB activation, and the expression of pro-inflammatory genes. Aurothiomalate sodium blocks Kras-mediated BASC expansion and lung tumor growth, inhibits anchorage-independent growth and tumorigenicity of lung cancer cells, and suppresses neutrophil chemotaxis, phagocytosis, and leukocyte extravasation. Aurothiomalate sodium can be used in research related to rheumatoid arthritis and non-small cell lung cancer.

Evernic Acid is an orally active thioredoxin reductase 1 (TrxR1) inhibitor and antiproliferative agent. Evernic Acid inhibits the proliferation and migration of human breast cancer cells. Evernic Acid blocks the NF-κB pathway by inhibiting p65 nuclear translocation and IκBα phosphorylation, thereby suppressing downstream inflammatory mediators. Evernic Acid acts as an antioxidant, anti-inflammatory agent and neuroprotective agent, protects neurons from cell death, mitochondrial dysfunction and oxidative stress damage, reduces astrocyte activation, and ameliorates dopaminergic neuron loss and neuroinflammation. Evernic Acid inhibits enoyl reductases FabI and FabZ of Plasmodium falciparum. Evernic Acid downregulates the expression of lasB and rhlA genes in Pseudomonas aeruginosa, inhibits quorum sensing and biofilm formation, and exerts antibacterial activity against Gram-positive bacteria, Gram-negative bacteria and fungi. Evernic Acid is applicable to research related to breast cancer, Parkinson's disease, bacterial infections and fungal infections.

Nitrovin hydrochloride is an antibacterial growth promoter. Nitrovin hydrochloride induces ROS-mediated non-apoptotic and apoptotic-like cell death by targeting TrxR1. Nitrovin hydrochloride has anticancer activity, with IC₅₀ values of 1.31-6.60 μM for tumor and normal cells.

TrxR-IN-2 is a thioredoxin reductase (TrxR) inhibitor. TrxR-IN-2 increases reactive oxidative species (ROS) levels and decreases mitochondrial transmembrane potential levels. TrxR-IN-2 triggers DNA damage via H2AX regulation, and induces autophagy via LC3, beclin-1, and p62 regulation. TrxR-IN-2 can be used for the research of drug-resistant hepatocellular carcinoma^[1].

8α-Tigloyloxyhirsutinolide 13-O-acetate (8αTGH) is a potent and orally active STAT3 inhibitor. 8α-Tigloyloxyhirsutinolide 13-O-acetate induces early oxidative stress and pyroptosis, and late DNA damage, cell cycle arrest, apoptosis in the TNBC cells. 8α-Tigloyloxyhirsutinolide 13-O-acetate suppresses tumor cell growth in vitro and tumor growth in vivo.

Nitrovin (Difurazon) is a thioredoxin reductase 1 (TrxR1) inhibitor with both antibacterial and anticancer activities. Nitrovin interacts with TrxR1 to generate reactive oxygen species (ROS), which in turn induces cytoplasmic vacuolization, activates MAPK and inhibits Alix. Nitrovin induces paraptosis-like non-apoptotic cell death, thereby exerting significant cytotoxicity against cancer cells. Nitrovin can be used in the research of heart disease and glioblastoma multiforme.

TrxR1 prodrug-1 (compound 5u) is a potent inhibitor of TrxR1. TrxR1 prodrug-1 exhibits significant antitumor efficiency in nude mice and NSCLC organoids.

BGC4 is a biphenyl-based gold(III) complex. BGC4 inhibits human recombinant thioredoxin reductase (TrxR) with an IC₅₀ of 10.7 μM, exhibits cytotoxicity (IC₅₀ for MDA-MB-231 is 5.4 μM), and induces apoptosis. BGC4 exhibits antitumor efficacy in mouse models.

As-CA11 is a Thioredoxin reductase (TrxR) inhibitor with an IC₅₀ of 18.7 nM. As-CA11 can induce cancer cells apoptosis and ROS production. As-CA11 can reduce the level of reduced Trx and increase the level of oxidized Trx. As-CA11 demonstrates anti-tumor activity in the 4T1 tumor-bearing mouse model.

TrxR1-IN-3 is a selective TrxR1 inhibitor with an IC₅₀ of 1.19 μM. TrxR1-IN-3 increases intracellular reactive oxygen species (ROS) levels, induces endoplasmic reticulum (ER) stress, and activates Caspase-dependent Apoptosis. TrxR1-IN-3 exhibits anticancer activity against multiple breast cancer subtypes, including triple-negative breast cancer (TNBC). TrxR1-IN-3 can be used in breast cancer-related research.

TrxR1-IN-1 (Compound 5j) is a TrxR1 inhibitor (IC₅₀: 8.8 μM). TrxR1-IN-1 has anticancer activity, with IC₅₀s of MCF-7 (1.5 μM), HeLa (1.7 μM), BGC-823 (2.4 μM), SW-480 (2.8 μM), A549 (2.1 μM). TrxR1-IN-1 has antioxidant activity, and scavenges DPPH radical.

CS47 is a Thioredoxin Reductase 1 (TRXR1) inhibitor and ferroptosis inducer. CS47 binds non-covalently to sites between the FAD and NADPH pockets of TRXR1. CS47 drives glutathione depletion, lipid reactive oxygen species accumulation, HMOX1-dependent iron overload, and selective cytotoxicity in lung cancer cells. CS47 can be used for the research of lung cancer.

Aurothiomalate disodium acts as an inhibitor of PKCI and TrxR1. Aurothiomalate disodium disrupts the PKCI-Par6-Rac1 signaling pathway, and also inhibits TrxR1 activity, TNFα-induced NF-κB activation, and the expression of pro-inflammatory genes. Aurothiomalate disodium blocks Kras-mediated BASC expansion and lung tumor growth, inhibits anchorage-independent growth and tumorigenicity of lung cancer cells, and suppresses neutrophil chemotaxis, phagocytosis, and leukocyte extravasation. Aurothiomalate disodium can be used in research related to rheumatoid arthritis and non-small cell lung cancer.

TrxR-IN-6 is a thioredoxin reductase (TrxR) inhibitor. TrxR-IN-6 induces reactive oxygen species (ROS) accumulation and cell apoptosis. TrxR-IN-6 induces mitochondrial dysfunction, endoplasmic reticulum stress and DNA damage. TrxR-IN-6 can be used for the research of breast cancer, leukemia.

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.