overload

CP-060 is a potent Ca2+ antagonist and inhibits Ca2+ overload with antioxidant and cardioprotective activities.

HBED (CHELII) is an iron chelator and can be used in research on the treatment of chronic iron overload and acute iron poisoning.

Deferasirox (CGP-72670) is an oral iron chelating agent used to treat chronic iron overload.

Ammonium iron(III) citrate (Ferric ammonium citrate) is a physiological form of non-ferritin-bound iron that causes intracellular iron overload leading to cellular ferroptosis and enhances protein production.

Aniline-d5 is a deuterated isotope marker of Aniline, which can be used for isotope tracing.Aniline induces toxicity to the spleen through iron overload and oxidative stress via heme oxygenase 1 up-regulation and is able to lead to a significant increase in p-IKKα and p-IKKβ, which in turn increases NF-κB and AP-1 binding activity.

Deferasirox (Fe3+ chelate) is an orally available iron chelator with potential anticancer activity, inhibits the anti-apoptotic activity of MCL-1, and can be used to study iron overload.

Deferitrin (GT-56-252) is an iron chelator. It potentially for the treatment of thalassemia and iron overload.

O-Desmethylcarvedilol (Desmethylcarvedilol) is an active metabolite of Carvedilol, a non-selective β-adrenergic receptor (β-AR) antagonist. This compound inhibits store overload-induced calcium release in HEK293 cells expressing the RyR2 R4496C mutation (IC50= 7.62 µM). Additionally, O-Desmethylcarvedilol slows the increase in heart rate and prevents diastolic pressure reduction induced by Isoproterenol in conscious rabbits (ED50s = 32 and 5 µg kg).

Deferitazole magnesium is a potential chelator for iron overload treatment.

Secoisolariciresinol diglucoside (LGM2605) was cytoprotective in an in vitro model of iron overload-induced redox-inflammatory damage. Secoisolariciresinol diglucoside (25 mg kg b.w.) exerts the antihyperglycemic effect by preventing the liver from peroxidation damage through inhibition of ROS level mediated increased level of enzymatic and non-enzymatic antioxidants.

4-(3-Methyl-5-oxo-2-pyrazolin-1-yl)benzoic acid demonstrates hypoglycemic activity by acting through a mechanism reliant on the response to oral glucose overload.

CYP11B1-IN-2 (compound 7aa) is a selective, orally active inhibitor of CYP11B1 with an IC50 of 9 nM for human CYP11B1 and 25 nM for rat CYP11B1. It can be used to study diseases caused by cortisol overload.

NP-04634 is a calcium antagonist and protective agent against calcium overload and mitochondrial disruption.

Ferulic acid 4-O-sulfate (Ferulic acid 4-sulfate) is a metabolite of Ferulic acid.Ferulic acid 4-O-sulfate relaxes arteries, lowers blood pressure, and resists oxidative stress under conditions of iron overload in mice and HepG2 cells.Ferulic acid 4-O-sulfate is a metabolite of Ferulic acid.

Folic acid disodium, an orally active disodium salt form of Folic acid, showcases an intrinsic dissolution rate (IDR) of 4.96·10^5 g s [1]. It acts as a cofactor in single-carbon transfer reactions and has protective roles against neural tube defects, ischemic events, and cancer. However, an overload of Folic acid disodium can impair brain development during embryogenesis and encourage the growth of precancerous cells, whereas its deficiency results in megaloblastic anemia [2].

CN128, an orally bioavailable iron chelator, features a side chain hydroxy group serving as an alternate sacrificial glucuronidation site to mitigate metabolic inactivation at the 3-hydroxy group. When administered at doses of 150 and 450 µmol/kg, CN128 enhances iron mobilization by 24.8% in a 59Fe-ferritin-loaded rat model of iron overload.

Homo-VK-II-36 (Homo-V-II-36) is a carvedilol analogue that acts by inhibiting store- overload-induced calcium release through the RyR2 channel.

Dehydrotrametenolic acid (Dehydroeburicoic acid) induces necrotic cell death that involves Ca(2+) overload, mitochondrial dysfunction, and calpain activation in human glioblastomas.

Pinostrobin, a potent flavonoid inducer, exerts a neuroprotective effect against Aα²(25-35)-induced neurotoxicity in PC12 cells, at least in part, via inhibiting oxidative damage and calcium overload, as well as suppressing the mitochondrial pathway of ce

Strophanthidin (Strophanthidine) can induce calcium overload in vivo.