autophagy-in-c-1

Autophagy-IN-C1 is a cinchona alkaloid derivative containing urea. Autophagy-IN-C1 not only induces apoptosis but also blocks autophagy in hepatocellular carcinoma (HCC) cells.

HT-2 toxin-13C22is intended for use as an internal standard for the quantification of HT-2 toxin by GC- or LC-MS. HT-2 toxin is a type A trichothecene mycotoxin and an active, deacetylated metabolite of the trichothecene mycotoxin T-2 toxin .1,2Like T-2 toxin, HT-2 toxin inhibits protein synthesis and cell proliferation in plants.2HT-2 toxin also reduces viability of HepG2, A549, HEp-2, Caco-2, A-204, U937, Jurkat, and RPMI-8226 cancer cells with IC50values ranging from 3.1 to 23 ng/ml and human umbilical vein endothelial cells with an IC50value of 56.4 ng/ml.1It induces oxidative stress, DNA damage, and autophagy in, as well as halts the development of, cultured mouse embryos when used at a concentration of 10 nM.3HT-2 toxin has been found in cereal grains and food products.4,5 1.Nielsen, C., Casteel, M., Didier, A., et al.Trichothecene-induced cytotoxicity on human cell linesMycotoxin Res.25(2)77-84(2009) 2.Nathanail, A.V., Varga, E., Meng-Reiterer, J., et al.Metabolism of the fusarium mycotoxins T-2 toxin and HT-2 toxin in wheatJ. Agric. Food Chem.63(35)7862-7872(2015) 3.Zhang, L., Li, L., Xu, J., et al.HT-2 toxin exposure induces mitochondria dysfunction and DNA damage during mouse early embryo developmentReprod. Toxicol.85104-109(2019) 4.Langseth, W., and Rundberget, T.The occurrence of HT-2 toxin and other trichothecenes in Norwegian cerealsMycopathologia147(3)157-165(1999) 5.Al-Taher, F., Cappozzo, J., Zweigenbaum, J., et al.Detection and quantitation of mycotoxins in infant cereals in the U.S. market by LC-MS/MS using a stable isotope dilution assayFood Control72(Part A)27-35(2017)

Telaglenastat (CB-839) hydrochloride is a first-in-class, reversible, and orally active inhibitor of glutaminase 1 (GLS1), selectively inhibiting the splice variants KGA (kidney-type glutaminase) and GAC (glutaminase C), as opposed to GLS2. Telaglenastat hydrochloride has an IC50 of 23 nM for endogenous glutaminase in mouse kidney and 28 nM in the brain, inducing autophagy and exhibiting antitumor activity.

ABO acts as an annexin A7 modulator, specifically binding to Thr286 to inhibit its phosphorylation on threonine (not on serine or tyrosine) residues within human umbilical vein endothelial cells (HUVECs). This compound furthers the annexin A7 interaction with the EF-hand protein GCA, leading to reduced GCA phosphorylation, lowered intracellular calcium levels, and enhanced autophagy in COS-7 cells. Moreover, ABO lessens phosphorylation of the microtubule-associated protein 1 light chain (LC3) in HUVECs and impedes the upregulation of phosphatidylcholine-specific phospholipase C (PC-PLC) due to oxidized low-density lipoprotein in vascular endothelial cells (VECs). In animal models, specifically apoE-/- mice on a Western diet, administration of ABO (50 or 100 mg/kg per day) has been shown to decrease PC-PLC expression, promote autophagy, and reduce apoptosis, lipid accumulation, and the extent of atherosclerotic plaques in the aortic endothelium.

D-CopA3 is an inhibitor of MDM2 and an activator of the p53 signaling pathway. It exhibits cytotoxicity in colorectal cancer cells HCT-116, LoVo, and RKO with IC50 values of 15-18 μM and induces JNK Beclin-1 mediated autophagy. D-CopA3 downregulates the expression of the cell cycle inhibitor protein p21Cip1 Waf1, enhances mucosal barrier function, and reduces infiltration of inflammatory mediators. It shows anti-inflammatory properties in mouse models of acute enteritis induced by C. difficile toxin A and chronic colitis induced by DSS. Additionally, D-CopA3 demonstrates antitumor activity in a mouse HCT-116 xenograft model.