erastin

Erastin is an iron death activator that acts on the mitochondrial VDAC in a ROS- and iron-dependent manner. Erastin has anti-tumor activity and acts selectively on tumor cells with RAS-carcinogenic mutations.

Piperazine erastin, an analog of erastin, induces ferroptosis, an iron-dependent form of non-apoptotic cell death.

Erastin2 is a ferroptosis inducer and inhibitor of the system xc- cystine/glutamate transporter.[1][2] It inhibits glutamate release in CCF-STTG1 cells (IC50 = 0.0035 µM) and induces cell death in HAP1 cells at 5 µM, an effect blocked by ferrostatin-1 or deferoxamine.[1][2] Erastin2 also induces ferroptotic cell death in HT-1080 cells (EC50 = 0.15 µM), an effect blocked by β-mercaptoethanol (EC50 > 20 µM).[3] Additionally, it increases lipid peroxidation in HT-1080 cells at 1 µM.

Imidazole ketone erastin (IKE) is an ferroptosis inducer with inhibitory effects on system Xc-cystine/glutamate transporter proteins. Imidazole ketone erastin has antitumor activity and induces glutathione depletion and lipid peroxidation.

Levobupivacaine is an amino-amide local anaesthetic drug belonging to the family of n-alkylsubstituted pipecoloxylidide. It is the S-enantiomer of bupivacaine. Levobupivacaine hydrochloride is commonly marketed by AstraZeneca under the trade name Chirocaine. Compared to bupivacaine, levobupivacaine is associated with less vasodilation and has a longer duration of action. It is approximately 13 per cent less potent (by molarity) than racemic bupivacaine.Levobupivacaine is indicated for local anaesthesia including infiltration, nerve block, ophthalmic, epidural and intrathecal anaesthesia in adults; and infiltration analgesia in children. Adverse drug reactions (ADRs) are rare when it is administered correctly. Most ADRs relate to administration technique (resulting in systemic exposure) or pharmacological effects of anesthesia, however allergic reactions can rarely occur.

Levobupivacaine hydrochloride ((S)-(-)-Bupivacaine monohydrochloride) is a reversible neuronal sodium channel inhibitor and the pure S(-)-enantiomer of bupivacaine, used as a long-acting local anesthetic.

Noberastine (R 64947) is a novel histamine H1 antagonist with potent and specific peripheral antihistamine activity.

Cloperastine hydrochloride (HT-11 hydrochloride) is a type of flavonoid.

Cloperastine fendizoate (Hustazol) inhibits the hERG K+ currents in a concentration-dependent manner (IC50: 27 nM).

Perastine is a biochemical.

Esterastin is an Inhibitor of esterases.

Noberastine citrate, a histamine H1 antagonist, has potent and specific peripheral antihistaminic activity. Noberastine, a furan derivative of nor-astemizole (an astemizole metabolite), has been shown to have a more rapid onset, and shorter duration of action than astemizole with peak antihistaminic activity at 4h following ingestion. Noberastine is rapidly absorbed and the peak plasma levels are obtained within 2 h of oral dosing. In preclinical studies Noberastine has been shown to lack central nervous system effects. After subacute (steady-state) administration of noberastine, there was increasing inhibition of weal and flare formation with higher doses of the drug. The 30 mg daily dose showed maximum antihistaminic effects.

Noberastine maleate, a histamine H1 antagonist, has potent and specific peripheral antihistaminic activity. Noberastine, a furan derivative of nor-astemizole (an astemizole metabolite), has been shown to have a more rapid onset, and shorter duration of action than astemizole with peak antihistaminic activity at 4h following ingestion. Noberastine is rapidly absorbed and the peak plasma levels are obtained within 2 h of oral dosing. In preclinical studies Noberastine has been shown to lack central nervous system effects. After subacute (steady-state) administration of noberastine, there was increasing inhibition of weal and flare formation with higher doses of the drug. The 30 mg daily dose showed maximum antihistaminic effects.

Levocloperastine-d4 ((S)-Cloperastine-d4) is the deuterium-labeled version of Levocloperastine.

Levocloperastine-d10 ((S)-Cloperastine-d10) is the deuterium-labeled form of Levocloperastine.

Liproxstatin-1 is a potent and selective inhibitor of ferroptosis (IC50=22 nM). Liproxstatin-1 protects cells from ferroptosis induced by ferroptosis inducers (e.g., Erastin, RSL3).

Ferrostatin-1 (Fer-1) is a potent and selective inhibitor of iron death. Ferrostatin-1 potently inhibits Erastin-induced iron death in HT-1080 cells with an EC50 of 60 nM. Ferrostatin-1 also exhibits antioxidant and antifungal activities.

PRLX-93936 HCL is an analog of erastin and demonstrated synergistic effects against non-small cell lung cancer (NSCLC) cells with cisplatin.

SLC7A11-IN-2 (Compound 1) is an inhibitor of SLC7A11/xCT. It disrupts the oxidative balance in HeLa cells by decreasing intracellular glutathione levels and increasing oxidative stress, thereby inducing cell death with an IC50 of 10.23 μM. Molecular dynamics simulations have demonstrated that SLC7A11-IN-2 exhibits a stronger binding affinity to SLC7A11 compared to Erastin. This compound is useful for research in the field of cervical cancer.

Ferroptosis-IN-12 (Cpd-A1) is an inhibitor of ferroptosis. It effectively suppresses ferroptosis in mouse renal tubular epithelial cells (mTECs) treated with Erastin and improves renal function in dose-dependent manners in mouse models of acute kidney injury (AKI) induced by ischemia/reperfusion (I/R) or cecal ligation and puncture (CLP). This compound also reduces renal tubular damage and eliminates inflammation. Exhibiting good plasma stability and high distribution in renal tissues during pharmacokinetic studies in mice, Ferroptosis-IN-12 shows promising potential for research in the field of AKI.

Ferroptosis-IN-22 is a selective inhibitor of ferroptosis, which functions by targeting NCOA4 and disrupting its interaction with ferritin, exhibiting an EC50 of 520 nM and a Kd value of 0.78 μM. It effectively inhibits ferroptosis induced by various agents (RSL3, Erastin, ML210, FIN56) but does not inhibit cell necrosis induced by H2O2 or apoptosis induced by STS. Additionally, Ferroptosis-IN-22 significantly ameliorates Concanavalin A-induced acute liver injury and can be used in the study of ferroptosis-related diseases.

SV119 hydrochloride is a sigma-2 ligand with a Ki value of 5.2 nM. It enhances the efficient transport of drugs across cancer cell membranes. Combining dm-Erastin with SV119 hydrochloride successfully overcomes internalization barriers observed in pancreatic cancer while retaining the inherent antitumor activity of Erastin. Additionally, SV119 hydrochloride exhibits cytotoxic effects on triple-negative breast cancer (TNBC) cells and induces apoptosis (apoptosis).

1(R)-(Trifluoromethyl)oleyl alcohol is an analog of oleic acid .1It inhibits ferroptosis induced by erastin in primary fibroblasts isolated from patients with Friedreich ataxia, a neuro- and cardiodegenerative disorder characterized by loss or impaired activity of frataxin (FXN), when used at concentrations of 5, 10, or 20 μM. 1(R)-(Trifluoromethyl)oleyl alcohol (5 μM) reduces lipid peroxidation induced byFXNsiRNA knockdown in NBT human myoblasts. 1.Cotticelli, M.G., Forestieri, R., Xia, S., et al.Identification of a novel oleic acid analog with protective effects in multiple cellular models of Friedreich ataxiaACS Chem. Neurosci.11(17)2535-2542(2020)

PRLX-93936 is a selective Ras pathway protein inhibitor that modulates RAS/JNK pathway-associated protein phosphorylation, induces caspase-dependent apoptosis and cell cycle arrest, and exhibits anticancer activity.