Ammonium iron(III) citrate (Ammonium ferric citrate), a physiological form of nonetransferrin-bound iron, induces intracellular iron overload to cause ferroptosis[1]. Ammonium iron(III) citrate can enhance protein production[2].
viFSP1 is a species-independent inhibitor of FSP1 that induces ferroptosis in FSP1-dependent cells. viFSP1 targets the highly conserved NAD(P)H binding pocket of FSP1 and directly inhibits FSP1. viFSP1 induces lipid peroxidation and has anticancer activity[1].
Roxadustat-d5 is deuterium labeled Roxadustat. Roxadustat is an oral hypoxia-inducible factor prolyl-hydroxylase inhibitor (HIF-PHI) that promotes erythropoiesis through increasing endogenous erythropoietin, improving iron regulation, and reducing hepcidin[1].
CP-24879 (hydrochloride) is a potent, selective and combined delta5D/delta6D inhibitor. CP-24879 (hydrochloride) can significantly reduce intracellular lipid accumulation and inflammatory injury in hepatocytes. CP-24879 (hydrochloride) exhibits superior antisteatotic and anti-inflammatory actions in fat-1 and ω-3-treated hepatocytes, and can be used for non-alcoholic steatohepatitis research[1][2].
Cycloheximide (Naramycin A) is an eukaryote protein synthesis inhibitor, with IC50s of 532.5 nM and 2880 nM for protein synthesis and RNA synthesis in vivo, respectively.
FINO2 is a potent ferroptosis inducer. FINO2 inhibits GPX4 activity. FINO2 is a stable oxidant that oxidizes ferrous iron and stable at varying pH levels. FINO2 causes widespread lipid peroxidation[1].
L-Glutamic acid-5-13C 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.
L-Cystine-d4 is the deuterium labeled L-Cystine. L-Cystine is an amino acid and intracellular thiol, which plays a critical role in the regulation of cellular processes.
Simvastatin-d3 is the deuterium labeled Simvastatin[1]. Simvastatin (MK 733) is a competitive inhibitor of HMG-CoA reductase with a Ki of 0.2 nM[2].
Liproxstatin-1 is a potent ferroptosis inhibitor, with IC50 of approximately 38 nM.
Imidazole ketone erastin (IKE) s a potent, selective, and metabolically stable inhibitor of the cystine-glutamate antiporter, system Xc- and an activator of ferroptosis.
Erastin2 is a ferroptosis inducer and a potent, selective inhibitor of the system xc(-) cystine/glutamate transporter[1][2].
Vildagliptin-d7 is deuterium labeled Vildagliptin. Vildagliptin (LAF237) is a potent, stable, selective dipeptidyl peptidase IV (DPP-IV) inhibitor with an IC50 of 3.5 nM in human Caco-2 cells. Vildagliptin possesses excellent oral bioavailability and potent antihyperglycemic activity[1].
Fluorescein-diisobutyrate-6-amide is a potent ferroptosis inducer. Fluorescein-diisobutyrate-6-amide has the potential for the research of cancer[1].
L-Glutamic acid-d3 is the deuterium 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.
Acetylcysteine-d3 (N-Acetylcysteine-d3) is the deuterium labeled Acetylcysteine. Acetylcysteine (N-Acetylcysteine) is a mucolytic agent which reduces the thickness of the mucus. Acetylcysteine is a ROS inhibitor[1]. Acetylcysteine is a cysteine precursor, prevents hemin-induced ferroptosis by neutralizing toxic lipids generated by arachidonate-dependent activity of 5-lipoxygenases[5]. Acetylcysteine induces cell apoptosis[2][3]. Acetylcysteine also has anti-influenza virus activities[7].
L-Glutamic acid-d5 is the deuterium 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-5-13C (L-Glutamic acid 5-amide-5-13C) is the 13C-labeled L-Glutamine. L-Glutamine (L-Glutamic acid 5-amide) is a non-essential amino acid present abundantly throughout the body and involved in many metabolic processes. L-Glutamine provides a source of carbons for oxidation in some cells[1][2].
Troglitazone-d4 is deuterium labeled Troglitazone. Troglitazone is a PPARγ agonist, with EC50s of 550 nM and 780 nM for human and murine PPARγ receptor, respectively.
Ferroptosis inducer-1 (compound BX-3a) is a Ferroptosis inducer with antitumor potential[1].
icFSP1 is a potent ferroptosis suppressor protein-1 (FSP1) inhibitor. icFSP1 does not competitively inhibit FSP1 enzyme activity, but instead triggers subcellular relocalization of FSP1 from the membrane and FSP1 condensation before ferroptosis induction, in synergism with GPX4 inhibition[1].
FIN56 is a specific inducer of ferroptosis.
Pioglitazone-d4 (alkyl) (U 72107-d4 (alkyl)) is the deuterium labeled Pioglitazone. Pioglitazone (U 72107) is a potent and selective PPARγ agonist with high affinity binding to the PPARγ ligand-binding domain with EC50 of 0.93 and 0.99 μM for human and mouse PPARγ, respectively[1][2].
Gallic acid (3,4,5-Trihydroxybenzoic acid) hydrate is a natural polyhydroxyphenolic compound and an free radical scavenger to inhibit cyclooxygenase-2 (COX-2)[1]. Gallic acid hydrate has various activities, such as antimicrobial, antioxidant, antimicrobial, anti-inflammatory, and anticance activities[2].
SRS16-86 is a potent inhibitor of ferroptosis[1]. SRS16-86 is more stable than more stable to metabolism and plasma than Ferrostatin-1 in vivo. SRS16-86 can be used for renal ischemia-reperfusion injury (IRI) and spinal cord injury (SCI) research[2][3].
Pioglitazone (U 72107) potassium is an orally active and selective PPARγ (peroxisome proliferator-activated receptor) agonist with high affinity binding to the PPARγ ligand-binding domain with EC50 of 0.93 μM and 0.99 μM for human and mouse PPARγ, respectively. Pioglitazone potassium can be used in diabetes research[2][3][4].
Vildagliptin-d3 (LAF237-d3) is the deuterium labeled Vildagliptin. Vildagliptin (LAF237) is a potent, stable, selective dipeptidyl peptidase IV (DPP-IV) inhibitor with an IC50 of 3.5 nM in human Caco-2 cells. Vildagliptin possesses excellent oral bioavailability and potent antihyperglycemic activity[1][2].
L-Glutamic acid-13C2 is the 13C labeled L-Glutamic acid[1]. 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[2].
L-Glutamic acid-13C5,15N is the 13C- and 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.
Pravastatin sodium is an HMG-CoA reductase inhibitor against sterol synthesis with IC50 of 5.6 μM.Target: HMG-CoA reductasePravastatin (marketed as Pravachol or Selektine) is a member of the drug class of statins, used in combination with diet, exercise, and weight-loss for lowering cholesterol and preventing cardiovascular disease.Pravastatin is primarily used for the treatment of dyslipidemia and the prevention of cardiovascular disease. It is recommended to be used only after other measures such as diet, exercise, and weight reduction have not improved cholesterol levels.The evidence for the use of pravastatin is generally weaker than for other statins. The antihypertensive and lipid-lowering treatment to prevent heart attack trial (ALLHAT), failed to demonstrate a difference in all-cause mortality or nonfatal myocardial infarction/fatal coronary heart disease rates between patients receiving pravastatin 40mg daily (a common starting dose) and those receiving usual care.