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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.
L-Glutamic acid-15N is the 15N-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.
Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosisapoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway. Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes.
TfR-1-IN-1 is a transferrin receptor-1 (TfR-1) inhibitor with tumor cell-specific activity. TfR-1-IN-1 reduces TfR-1 expression, impairs mitochondrial function, induces cell apoptosis, necroptosis and ferroptosis, and increases intracellular iron (II) levels. TfR-1-IN-1 decreases the metabolic activity of cancer cells. TfR-1-IN-1 can be used for the research of ovarian cancer, breast cancer and acute myeloid leukemia.
Dopamine-d5 (hydrochloride) is the deuterium labeled Dopamine (hydrochloride). Dopamine hydrochloride (ASL279) is a catecholamine neurotransmitter that is produced in the substantia nigra, ventral tegmental area, and hypothalamus of the brain. Dopamine hydrochloride (ASL279) plays several important roles in the brain and body. Dopamine hydrochloride (ASL279) acts through D2 dopamine receptors to induce endocytosis of VEGFR2, which is critical for promoting angiogenesis.
Angelic acid is a ferroptosis inducer, targeting NRF2 degradation. Angelic acid binds to NRF2 protein and promotes NRF2 degradation via ubiquitination-proteasome pathway, relieves the inhibitory effect of NRF2 on oxidative stress and lipid peroxidation. Then, Angelic acid induces ferroptosis in tumor cells. Angelic acid can enhance the accumulation of intracellular reactive oxygen species (ROS), upregulate ferroptosis-related markers CHAC1 and PTGS2, and synergize with ferroptosis inducers to enhance anti-tumor effects. Angelic acid also has the activity of scavenging UVA-induced ROS in vitro, inhibiting skin fibroblast senescence and extracellular matrix degradation. Angelic Acid helps wound healing with sedative activity.
Moracin N is a ferroptosis inhibitor that can be isolated from mulberry leaf. Moracin N exerts neuroprotective activity through preventing from oxidative stress.
L-Glutamic acid monosodium hydrate is an excitatory amino acid neurotransmitter that acts as an agonist for all subtypes of glutamate receptors (metabolic rhodophylline, NMDA, and AMPA). L-Glutamic acid monosodium hydrate has an agonist effect on the release of DA from dopaminergic nerve endings. L-Glutamic acid monosodium hydrate can be used in the study of neurological diseases. L-Glutamic acid monosodium hydrate acts at ionotropic and?metabotropic glutamate receptors.
Gallic acid (Standard) is the analytical standard of Gallic acid. This product is intended for research and analytical applications. Gallic acid (3,4,5-Trihydroxybenzoic acid) is a natural polyhydroxyphenolic compound and an free radical scavenger to inhibit cyclooxygenase-2 (COX-2). Gallic acid has various activities, such as antimicrobial, antioxidant, antimicrobial, anti-inflammatory, and anticance activities.
Sipeimine (Imperialine) is an inhibitor targeting the PI3K/AKT/NF-κB pathway and NLRP3 inflammasome, which can competitively bind to PI3K and p65. Sipeimine inhibits PI3K/AKT phosphorylation, blocks NF-κB nuclear translocation and NLRP3 inflammasome activation. Sipeimine exerts anti-inflammatory activities, inhibits pyroptosis and ferroptosis, and protects the extracellular matrix. Sipeimine can reduce cartilage degradation and synovial inflammation in osteoarthritis and improve PM2.5-induced lung injury. Sipeimine is mainly used in the study of anti-inflammatory and degenerative diseases.
Spexin (Neuropeptide Q) is a selective agonist of galanin receptors GAL2 and GAL3, and is a conserved peptide that functions as a neurotransmitter/neuromodulator and endocrine factor. Spexin can function through both central and peripheral actions. Spexin upregulates Beclin 1 to inhibit ferroptosis induced by excessive autophagy, reduces the uptake of long-chain fatty acids by adipocytes, and regulates energy metabolism by increasing lipid oxidation (e.g., reducing the respiratory exchange ratio in rodents). Spexin improves cardiac function in the Doxorubicin hydrochloride (HY-15142)-induced cardiotoxicity model, protects mitochondrial membrane potential, and reduces iron accumulation and lipid peroxidation. Spexin can be used to study obesity and its related metabolic disorders, cardiovascular diseases (e.g., cardioprotection), and side effects of tumor chemotherapy.
NADPH tetracyclohexanamine functions as an important cofactor in a variety of metabolic and biosynthetic pathways. NADPH tetracyclohexanamine is an endogenous inhibitor of ferroptosis. NADPH tetracyclohexanamine plays a vital role in the biosynthesis of agents, chiral alcohols, fatty acids and biopolymers, while also being required for lipid biosynthesis, biomass formation, and cell replication.
DL-alpha-Tocopherol (Standard) is the analytical standard of DL-alpha-Tocopherol. This product is intended for research and analytical applications. DL-alpha-Tocopherol is a synthetic vitamin E, with antioxidation effect. DL-alpha-Tocopherol protects human skin fibroblasts against the cytotoxic effect of UVB.
Rosolutamide (ASC-JM17) is an orally active Nrf1/Nrf2 activator. Rosolutamide activates Hsf1 pathways, upregulates proteasome subunits and antioxidant enzymes, induces proteasome complex structural rearrangement, and enhances ubiquitin-proteasome system-mediated degradation. Rosolutamide reduces mutant androgen receptor and ataxin-3 aggregates, restores mitochondrial function, attenuates reactive oxygen species (ROS) levels, induces apoptosis and ferroptosis, and inhibits cancer cell growth. Rosolutamide can be used for the research of spinal and bulbar muscular atrophy, Huntington’s disease, and temozolomide-resistant glioblastoma.
Coenzyme Q10 (Standard) is the analytical standard of Coenzyme Q10. This product is intended for research and analytical applications. Coenzyme Q10 is an essential cofactor of the electron transport chain and a potent antioxidant agent.
Sorafenib (Standard) is the analytical standard of Sorafenib. This product is intended for research and analytical applications. 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.
Seratrodast (AA 2414), an orally active antiasthmatic agent, is a thromboxane A2 receptor (TP) antagonist and ferroptosis inhibitor. Seratrodast reduces lipid ROS production, modulates the systemic xc-/GSH/GPX4 axis, and inhibits JNK phosphorylation and p53 expression. Seratrodast exhibits anti-asthmatic and anti-epileptic activity.
5-O-Methylvisammioside (4'-O-β-D-Glucosyl-5-O-methylvisamminol) is an orally active natural chromone glycoside and multiple biological activities. 5-O-Methylvisammioside inhibits ferroptosis by activating the Nrf2/HO-1 signaling axis. 5-O-Methylvisammioside alleviates intestinal barrier damage by inhibiting the ROS/NF-κB/NLRP3 pathway. 5-O-Methylvisammioside exerts a protective effect against acute liver injury by reducing ALT/AST, decreasing inflammatory infiltration, and inhibiting IκB-α phosphorylation and NF-κB nuclear translocation. 5-O-Methylvisammioside blocks the HMGB1/RAGE/MEK/ERK signaling axis to exert anti-tumor and anti-angiogenic effects. 5-O-Methylvisammioside improves depression-like behaviors by inhibiting Src kinase and the NF-κB pathway.
WJ460 is a potent inhibitor of myoferlin (MYOF) that interacts directly with MYOF. WJ460 inhibits the migration and growth, induces cell cycle arrest, mitochondrial autophagy, lipid peroxidation and ferroptosis in tumor cells. WJ460 has anti-tumor activity.
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