Reactive Oxygen Species (ROS) Activator

Traumatic Acid is a wound healing agent and a cytokinin (phytohormone). Traumatic Acid enhances the biosynthesis of collagen in cultured human skin fibroblasts. Traumatic Acid inhibits MCF-7 breast cancer cells viability and enhances apoptosis and oxidative stress. Traumatic Acid can be used in studies of cancer, circulatory disorders (including arterial hypertension), and skin diseases associated with oxidative stress and impaired collagen biosynthesis.

20-5,14-HEDGE is a 20-HETE analog. 20-5,14-HEDGE induces cell death in organotypic hippocampal slice cultures (OHSCs). 20-5,14-HEDGE enhances ROS production and reduces hypoxia-reoxygenation (HR)-induced apoptosis in ex vivo rat lung slices. 20-5,14-HEDGE protects against lung ischemic reperfusion injury in rats. 20-5,14-HEDGE can be used for the study of pulmonary vascular signaling and lung injury-related research.

Ethyl 3,4-dihydroxybenzoate (Protocatechuic acid ethyl ester) is an orally effective, blood-brain barrier-permeable, competitive prolyl hydroxylase (PHD) inhibitor that inhibits the hydroxylation modification of hypoxia-inducible factor (HIF) by PHD. Ethyl 3,4-dihydroxybenzoate stabilizes HIF-1α by inhibiting PHD, activates downstream pathways to induce autophagy and apoptosis of tumor cells, and regulates inflammatory responses, inhibits the NF-κB pathway, improves vascular permeability, and promotes osteoblast differentiation. Ethyl 3,4-dihydroxybenzoate has anti-tumor, anti-hypoxic injury, and bone metabolism regulation effects. It can also be used in the research of cardiovascular protection (such as reducing myocardial ischemic damage), bone tissue engineering (promoting osteogenesis/inhibiting osteoclast differentiation), and prevention and treatment of high-altitude cerebral edema.

Propiconazole is an orally active N-substituted triazole used as a fungicide. Propiconazole is a mouse liver hepatotoxicant and a hepatocarcinogen that has adverse reproductive and developmental toxicities in experimental animals.

Diuron is an orally active phenylurea herbicide. Diuron inhibits photosynthesis in plants by blocking the formation of ATP and NADH. Diuron increases the production of ROS. Diuron increases expression of p53 in certain cell lines. Diuron has herbicidal activity against annual and perennial broadleaf weeds and grass weeds. Diuron promotes DMBA/BBN-induced bladder cancer. Diuron can be used in breast cancer research.

Verrucarin A (Muconomycin A), a Type D macrocyclic mycotoxin derived from the pathogen fungus Myrothecium verrucaria, is an inhibitor of protein synthesis. Verrucarin A inhibits growth of leukemia cell lines and activates caspases and apoptosis and inflammatory signaling in macrophages. Verrucarin A effectively increased the phosphorylation of p38 MAPK and diminished the phosphorylation of ERK/Akt. Verrucarin A caused cell cycle deregulation through the induction of p21 and p53.

ε-Poly-L-lysine (Epsilon-polylysine; ε-Polylysine) hydrochloride (MV 2000-5000) is a polycationic antibacterial agent with broad-spectrum activity against Gram-positive bacteria, Gram-negative bacteria, fungi, yeasts and specific bacteriophages. ε-Poly-L-lysine hydrochloride (MV 2000-5000) exerts bactericidal effects through mechanisms such as disrupting microbial membranes, inducing ROS production, inhibiting metabolism and spore germination. ε-Poly-L-lysine hydrochloride (MV 2000-5000) also regulates the expression of multiple key genes including sodA, oxyR and recA. ε-Poly-L-lysine hydrochloride (MV 2000-5000) exhibits properties such as low eukaryotic cytotoxicity, thermal stability and pH stability, and supports tissue regeneration and anti-tumor applications. ε-Poly-L-lysine hydrochloride (MV 2000-5000) can be applied in research fields including bacterial and fungal infections, diabetic ulcers, and methicillin-resistant Staphylococcus aureus infections.

Mito-LND (Mito-Lonidamine) is an orally active and mitochondria-targeted inhibitor of oxidative phosphorylation (OXPHOS). Mito-LND inhibits mitochondrial bioenergetics, stimulates the formation of reactive oxygen species, and induces autophagic cell death in lung cancer cells.

Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.

KY386 is a DHX33 helicase inhibitor with an IC₅₀ of 0.019 μM. KY386 inhibits the cell viability of various cancer cells. KY386 induces ferroptosis in cancer cells, and induces apoptosis in some cancer cell lines. KY386 increases the intracellular levels of ROS, LPO and Fe²⁺, and decreases the level of GSH in cancer cells. KY386 inhibits the growth of gastric cancer and colon cancer xenografts in nude mice. KY386 is applicable to the related research on liver cancer, lung cancer, pancreatic cancer, colorectal cancer, gastric cancer, breast cancer, leukemia, renal cancer, prostate cancer, esophageal cancer, cervical cancer, brain cancer (glioblastoma) and melanoma.

2-Acetonaphthone is a synthetic fragrance material. 2-Acetonaphthone increases ROS under UVA/sunlight, leading to endoplasmic reticulum stress and decreased mitochondrial membrane potential. 2-Acetonaphthone can be used as an adulterant in a variety of cosmetics. 2-Acetonaphthone can be used for the study of skin keratinization

Alisol B 23-acetate is an orally active prototerpane-type triterpenoid. Alisol B 23-acetate can be isolated from Alisma orientalis. Alisol B 23-acetate induces Apoptosis, promotes ROS generation, downregulates CDK4/6, MMP-2/9, upregulates cleaved PARP, activates FXR and inhibits Syk. Alisol B 23-acetate has anti-inflammatory and hepatoprotective activities. Alisol B 23-acetate protects the kidney from ischemia-reperfusion injury. Alisol B 23-acetate has anticancer activity against ovarian cancer, colon cancer, lung cancer, and gastric cancer. Alisol B 23-acetate can be used in the study of atherosclerosis and allergic asthma.

Ziyuglycoside II is a triterpenoid saponin compound extracted from Sanguisorba officinalis L.. Ziyuglycoside II induces reactive oxygen species (ROS) production and apoptosis. Anti-inflammation and anti-cancer effect.

Emamectin Benzoate (MK-244) is an orally active nervoussystem toxicant by binding g-aminobutyric (GABA) receptor in insects. Emamectin Benzoate is one of semi-synthetic derivative of Avermectin (HY-15311) with a broadspectrum of insecticidal and acaricidal activity. Emamectin Benzoate induces ROS-mediated DNA damage and cell apoptosis. Emamectin Benzoate, a mixture of the natural Emamectin B1a benzoate and Emamectin B1b benzoate, has the main component of Emamectin B1a benzoate.

Sodium metavanadate, 99% (Sodium vanadate (V), 99%) is an orally active phosphate structural analog and protein tyrosine phosphatase (PTPases) inhibitor. Sodium metavanadate, 99% mimics phosphate to interfere with phosphoprotein reactions, inhibits GAPDH, Na⁺/K⁺-ATPase and microbial membrane ATPase, and acts as a terminal electron acceptor for anaerobic respiration. Sodium metavanadate, 99% induces ROS production, G2/M phase arrest, mitochondrial membrane potential loss and apoptosis in breast cancer cells, and reduces tumor volume in tumor-bearing mice. Sodium metavanadate, 99% also exhibits oral insulin-sensitizing and metabolic regulatory activities, and reduces plasmodium parasitemia levels. Sodium metavanadate, 99% can be used in studies related to cadmium exposure-induced metabolic syndrome, plasmodium infection, breast cancer and type 1 diabetes.

Mollugin is an orally active and potent NF-κB inhibitor. Mollugin induces S-phase arrest of HepG2 cells, and increased intracellular reactive oxygen species (ROS) levels. Mollugin induces DNA damage in HepG2 cells, as well as an increase in the expression of p-H2AX. Mollugin shows anti-cancer effect by inhibiting TNF-α-induced NF-κB activation. Mollugin enhances the osteogenic action of BMP-2 (bone morphogenetic protein 2) via the p38-Smad signaling pathway.

Camalexin is a phytoalexin isolated from Camelina sativa (Cruciferae) with antibacterial, antifungal, antiproliferative and anticancer activities. Camalexin can induce reactive oxygen species (ROS) production.

Lexibulin (CYT-997) is a potent and orally active tubulin polymerisation inhibitor with IC50s of 10-100 nM in cancer cell lines; with potent cytotoxic and vascular disrupting activity in vitro and in vivo. Lexibulin induces cell apoptosis and induces mitochondrial ROS generation in GC cells.

PK11007 is a mild thiol alkylator with anticancer activity. PK11007 stabilizes p53 via selective alkylation of two surface-exposed cysteines without compromising its DNA binding activity. PK11007 induces mutant p53 cancer cell death by increasing reactive oxygen species (ROS) levels.

Moracin N is a benzofuran compound. At low concentrations, Moracin N activates the Keap1/Nrf2 pathway, downregulates the expression of FTH1 and ACSL4, enhances glutathione synthesis, and inhibits neuronal ferroptosis. At high concentrations, Moracin N induces ROS accumulation, activates mitochondrial apoptosis, and triggers autophagy-mediated cell death by inhibiting the AKT/mTOR pathway. Moracin N can be used in research related to non-small cell lung cancer, hepatocellular carcinoma and ischemic brain injury.