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Ferroptosis is a non-apoptotic form of regulated cell death. It is distinct from other regulated cell death phenotypes, such as apoptosis and necroptosis. Ferroptosis is characterized by extensive lipid peroxidation, which can be suppressed by iron chelators or lipophilic antioxidants. Mechanistically, Ferroptosis inducers are divided into two classes: (1) inhibitors of cystine import via system xc− (e.g., Erastin), which subsequently causes depletion of glutathione (GSH), and (2) covalent inhibitors (e.g., (1S, 3R)-RSL3) of glutathione peroxidase 4 (GPX4). Since GPX4 reduces lipid hydroperoxides using GSH as a co-substrate, both compound classes ultimately result in loss of GPX4 activity, followed by elevated levels of lipid reactive oxygen species (ROS) and consequent cell death.
Ferroptosis is an iron- and ROS-dependent form of regulated cell death (RCD). Misregulated Ferroptosis has been implicated in multiple physiological and pathological processes, including cancer cell death, neurotoxicity, neurodegenerative diseases, acute renal failure, drug-induced hepatotoxicity, hepatic and heart ischemia/reperfusion injury, and T-cell immunity.
3-Hydroxyindole is a member of the class of hydroxyindoles with antioxidant activity. It showes inhibitory effects against DPPH and crocin. 3-hydroxyindole is also used as a inhibitor of ferroptosis.
trans-3-Indoleacrylic acid (Standard) is the analytical standard of trans-3-Indoleacrylic acid. This product is intended for research and analytical applications. Trans-3-Indoleacrylic acid is a tryptophan metabolite, which promotes tumor development through inhibition of RSL3 (HY-100218A) induced ferroptosis via AHR-ALDH1A3-FSP1-CoQ10 axis, and facilitates colorectal carcinogenesis[1]
Sulfasalazine (Standard) is the analytical standard of Sulfasalazine. This product is intended for research and analytical applications. Sulfasalazine (NSC 667219) is an anti-rheumatic agent for the research of rheumatoid arthritis and ulcerative colitis. Sulfasalazine can suppress NF-κB activity. Sulfasalazine is a type 1 ferroptosis inducer.
Auriculasin is an anticancer agent that inhibits VEGFR2, PI3K/AKT/mTOR, MAPK. Auriculasin can inhibit cell proliferation, induce cell apoptosis, and inhibit angiogenesis, and promotes mitochondrial oxidative stress and ferroptosis. Auriculasin is also active at the cannabinoid receptorCB1 with an IC50 of 8.92 μM. Auriculasin can be used in cancer research, especially related diseases such as prostate cancer and non-small cell lung cancer, as well as research on the development of anti-angiogenic drugs.
GPX4-IN-6 (Compound C25) is a GPX4 covalent inhibitor with an IC50 value of 0.13 μM. GPX4-IN-6 (Compound C25) can induce ferroptosis for the research of triple-negative breast cancer (TNBC) .
Theasaponin E1 is an orally effective tea saponin. Theasaponin E1 inhibits the proliferation of cancer cells by activating apoptosis. Theasaponin E1 inhibits angiogenesis in ovarian cancer cells and HUVECs by reducing the expression of VEGF. Theasaponin E1 upregulates the phosphorylation level of ATM protein and the expression level of PTEN protein in cancer cells, decreases the phosphorylation levels of Akt, mTOR, p70S6K and 4E-BP1 proteins, downregulates the expression of HIF-1α and NF-κB, and reduces the protein expression of Notch ligands Dll4 and Jagged1. Theasaponin E1 exerts neuroprotective effects by inhibiting the activity of acetylcholinesterase, activating α-secretase and neprilysin, reducing the concentration of Aβ, and inhibiting the activities of β-secretase and γ-secretase. Theasaponin E1 exhibits toxic effects on cancer cells and quinone reductase-inducing activity, and inhibits tumor growth in vivo. Theasaponin E1 induces ferroptosis in Pomacea canaliculata by synergistically disrupting cholesterol homeostasis and sphingolipid metabolism. Theasaponin E1 possesses anti-biofilm activity against Candida albicans. Theasaponin E1 can be used in the research of ovarian cancer, obesity, Alzheimer's disease and fungal infections.
JKE-1716 is a potent and selective nitrolic acid-containing GPX4 inhibitor. JKE-1716 is able of inducing ferroptosis selectively through covalent GPX4 inhibition.
Ferroptosis-IN-21 is a ferroptosis inhibitor that protects against renal I/R injury by suppressing ferroptosis and directly scavenging peroxyl radicals. Ferroptosis-IN-21 displays broad-spectrum anti-ferroptotic efficacy across multiple inducers in renal tubular epithelial cells, with nanomolar potency and robust suppression of lipid Reactive Oxygen Species (ROS). Ferroptosis-IN-21 significantly ameliorates renal I/R injury in mice, reducing histological damage, functional impairment, and inflammatory cytokine expression, while decreasing lipid peroxidation biomarkers such as 4-hydroxynonenal. Ferroptosis-IN-12 can be used for research in the field of ferroptosis-targeted drug development.
L-Glutamic acid-13C5,15N,d5 is the deuterium, 13C-, and 15-labeled L-Glutamic acid. L-Glutamic acid acts as an excitatory transmitter and an agonist at all subtypes of glutamate receptors (metabotropic, kainate, NMDA, and AMPA). L-Glutamic acid shows a direct activating effect on the release of DA from dopaminergic terminals.
L-Glutamine-13C5,15N2,d5 is the deuterium, 13C-, and 15N-labeled L-Glutamine (HY-N0390). L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na+-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity.
L-Glutamic acid-13C is the 13C-labeled L-Glutamic acid. L-Glutamic acid acts as an excitatory transmitter and an agonist at all subtypes of glutamate receptors (metabotropic, kainate, NMDA, and AMPA). L-Glutamic acid shows a direct activating effect on the release of DA from dopaminergic terminals.
HDAC11-IN-3 (Compound A9) is a selective HDAC11 inhibitor (IC50: 4.1 nM). HDAC11-IN-3 has inhibitory effects on U937 and OCI-AML2 acute myeloid leukemia (AML) cell lines (IC50: 10 μM). HDAC11-IN-3 has significant anti-AML activity, inducing apoptosis, cell cycle arrest, and differentiation. HDAC11-IN-3 upregulates the iron transporters transferrin (TF) and transferrin receptor (TFRC), and activates the p62-Keap1-Nrf2-HMOX1 pathway, which together lead to increased intracellular iron levels and induce ferroptosis in AML cells. HDAC11-IN-3 can be used alone or in combination with Cytarabine (HY-13605) for AML research.
2-Acetamidophenol-d3 (Orthocetamol-d3) is the deuterium labeled 2-Acetamidophenol (HY-W015600). 2-Acetamidophenol (Orthocetamol) is a regulator that targets ferroptosis and glutathione metabolic pathways, is the ortho-regioisomer of Paracetamol (HY-66005). 2-Acetamidophenol has anti-atherosclerotic activity, and inhibiting total cholesterol (TC) and triglyceride (TG) in a zebrafish hyperlipidemia model with IC50s for 30 μM and 40 μM, respectively. 2-Acetamidophenol upregulates the expression of glutathione synthesis-related genes (such as GCLC, GCLM, GSS) and iron ion transport genes (such as FPN1, FTH), reduces the accumulation of intracellular reactive oxygen species (ROS) and ferrous ions (Fe2+), and enhances the activity of glutathione peroxidase GPX4, thereby inhibiting macrophage phagocytosis of oxidized low-density lipoprotein (ox-LDL) and foam cell formation.
GPX4-IN-9 (Compound A16) is a glutathione peroxidase 4 (GPX4) inhibitor that specifically targets GPX4 under both in vitro and in vivo conditions, inducing ferroptosis. GPX4-IN-9 exhibits cytotoxicity against pancreatic cancer cells and can be used in cancer research.
Sorafenib-13C,d3 is the 13C- and deuterium labeled Sorafenib. Sorafenib (Bay 43-9006) is a potent and orally active Raf inhibitor with IC50s of 6 nM and 20 nM for Raf-1 and B-Raf, respectively. Sorafenib is a multikinase inhibitor with IC50s of 90 nM, 15 nM, 20 nM, 57 nM and 58 nM for VEGFR2, VEGFR3, PDGFRβ, FLT3 and c-Kit, respectively. Sorafenib induces autophagy and apoptosis. Sorafenib has anti-tumor activity. Sorafenib is a ferroptosis activator.
Ferroptosis-IN-19 (compound C18) is a strong cellular ferroptosis inhibitor with an IC50 value of 0.097 μM. Ferroptosis-IN-19 shows high metabolic stability and favorable BBB permeability prediction. Ferroptosis-IN-19 has in vivo neuroprotection against ischemic brain injury in mice.
DB0614 is a PROTAC based on Cereblon ligand, which is a selective and potent targeted protein degrader of NEK9 inhibitor. DB0614 can degrade ABL1, ABL2, BLK, CDK11B, CDK4, CSK, EPHA3, FER, GAK, LIMK1, MAP3K20, MAP4K1, MAP4K2, MAP4K3, MAP4K5, MAPK14, MAPK7, MAPK8, MAPK9, MAPKAPK2, MAPKAPK3, NLK, PDIK1L, PTK2B, RIPK1, RPS6KA1, RPS6KA3, SIK2, SIK3, STK35, TNK2 and ULK1. DB0614 can be used for research of disease or disorder mediated by aberrant kinase activity.(Blue: Thalidomide-4-OH (HY-103596), Black: linker, Pink: FLT3-IN-17 (HY-148070))
W1131 TFA is a potent STAT3 inhibitor that induces ferroptosis. W1131 inhibits cancer progression in subcutaneous xenograft, organoid, and PDX models of gastric cancer. W1131 effectively alleviates cancer cell chemoresistance to 5-FU (HY-90006). W1131 regulates the cell cycle, DNA damage response, and oxidative phosphorylation, including the IL6-JAK-STAT3 pathway and the ferroptosis pathway.
JST‑TfR09 (PPMX‑T003) is a human monoclonal antibody (mAb) targeting transferrin receptor 1 (TfR1/CD71). JST‑TfR09 blocks the binding of transferrin to TfR1, inhibits TfR1 internalization, and suppresses cellular iron uptake. JST‑TfR09 triggers ferritin degradation via activating the autolysosomal system, promotes ROS production and lipid peroxidation, and ultimately induces ferroptosis. JST‑TfR09 exhibits cytotoxicity toward human erythroblasts differentiated from hematopoietic stem cells. JST-TfR09 can be used in leukemia research. Recommended isotype control: Human IgG1 lambda, Isotype Control (HY-P99992).
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