PERK Activator

Gy-CATH is an anionic antimicrobial peptide. Gy-CATH activates MAPK and NF-κB signaling pathways (elevated levels of phospho-ERK, -p38, -JNK, -p65, and -IκBα). Gy-CATH upregulates the expression levels of three physiological anticoagulant pathways. Gy-CATH inhibits ADP-, Collagen-, and PMA-induced platelet aggregation. Gy-CATH has no direct antimicrobial activity, but shows significant preventive abilities against mice infected with Staphylococcus aureus, Escherichia coli, and Methicillin (HY-121544)-resistant Staphylococcus aureus. Gy-CATH exhibits potent immunomodulatory activity, enhancing macrophage-and neutrophil-mediated bactericidal functions. Gy-CATH significantly reduces the extent of pulmonary fibrin deposition and prevents thrombosis in mice.

Chalcomoracin is an orally active anticancer agent. Chalcomoracin exhibits anticancer, antibacterial, and α-glucosidase inhibitory activities, with an IC₅₀ of 14.23 µM against yeast α-glucosidase and an IC₅₀ of 5.5 μM against FabI of Staphylococcus aureus. Chalcomoracin reduces the phosphorylation levels of ERK, JNK, and P38; enhances the phosphorylation level of ERK1/2; regulates the MAPK, mTOR, AKT, and p53 signaling pathways; upregulates the expression of Chop, Bip, PINK1, GRP78, and GADD153; and downregulates the expression of Alix. Chalcomoracin induces apoptosis (apoptosis), endoplasmic reticulum stress (endoplasmic reticulum stress), paraptosis (paraptosis), ROS production, mitophagy (mitophagy), and autophagy (autophagy); it inhibits cancer cell viability, colony-forming ability, migration, invasion, proliferation, tumorigenesis, fatty acid synthesis, S. aureus growth, vitreous-stimulated retinal cell activity, and cell cycle progression at the G0/G1 phase. Chalcomoracin can be used in research related to hepatocellular carcinoma, non-small cell lung cancer, triple-negative breast cancer, prostate cancer, proliferative vitreoretinopathy, pancreatic cancer, diabetes, and bacterial infections.

CDC25A/NF-κB-IN-1 is an effective dual-target inhibitor of CDC25A and NF-κB, and is a prodrug of Pt(IV). CDC25A/NF-κB-IN-1 has anticancer activity and low cytotoxicity to normal cells. CDC25A/NF-κB-IN-1 can trigger a variety of anticancer mechanisms, including S phase cell cycle arrest, mitochondrial endogenous apoptosis, endoplasmic reticulum stress, autophagy-dependent ferroptosis. CDC25A/NF-κB-IN-1 has good safety and can be used for ovarian cancer research.

L-Azetidine-2-carboxylic acid is a proline analog. L-Azetidine-2-carboxylic acid upregulates the lipid autophagy marker LC3-II via activation of the PERK pathway. L-Azetidine-2-carboxylic acid increases pro-apoptotic BAX protein. L-Azetidine-2-carboxylic acid induces ATF6 cleavage and upregulates phosphorylated eIF2α levels. L-Azetidine-2-carboxylic acid induces ER stress, inducing protein misfolding and aggregation. L-Azetidine-2-carboxylic acid shows teratogenic, pro-inflammatory and pro-apoptotic effects.

DGAT-1 inhibitor 2 (Standard) is the analytical standard of DGAT-1 inhibitor 2 (HY-50670). This product is intended for research and analytical applications. DGAT-1 inhibitor 2 is an orally active DGAT-1 inhibitor with IC₅₀ values of 15 nM and 9 nM for human DGAT-1 and rat DGAT-1, respectively. DGAT-1 inhibitor 2 increases ROS concentration, GRP78, and PERK protein abundance. DGAT-1 inhibitor 2 increases SREBF1, CPT1A, and MTTP mRNA in fatty acid-treated cells. DGAT-1 inhibitor 2 improves obesity.

ML291 (Standard) is the analytical standard of ML291 (HY-101991). This product is intended for research and analytical applications. ML291 is a UPR (unfolded protein response)-inducing sulfonamidebenzamide. ML291 overwhelms the adaptive capacity of the UPR and induces apoptosis in a variety of solid cancer models. ML291 can activate the PERK/eIF2a/CHOP (apoptotic) arm of the UPR and reduce leukemic cell burden.

Lard oil is an orally active biochemical reagent. Lard oil upregulates PERK, eIF2a, CHOP, OPN, TLR2, TLR4, TNF-α, and downregulates GRP78 and IRE1a. Lard oil induces responses such as body fat accumulation, elevated serum insulin levels, increased HOMA-IR, hepatic ectopic lipid deposition, hepatic endoplasmic reticulum stress, and hepatic inflammation. Lard oil can be used in studies related to diet-induced obesity, insulin resistance, and non-alcoholic fatty liver disease.

Bromuconazole is a triazole fungicide with oral efficacy and blood-brain barrier permeability. Bromuconazole protects crops from various fungal contaminations. Bromuconazole exhibits cytotoxicity against a variety of cancer cells, induces G0/G1 cell cycle arrest and inhibits DNA synthesis in cancer cells, and triggers cytoskeletal structural disorder, genotoxic damage, apoptotic (apoptosis) cell death, and mitochondrial membrane depolarization. Bromuconazole activates caspase-3, induces excessive production of ROS, p53 and Bax, lipid peroxidation, increased activities of SOD and CAT, and downregulates Bcl-2. By upregulating p-ERK1/2 and p-JNK, Bromuconazole disrupts the MAPK signaling pathway, impairs the cellular stress response of human trophoblast cells and endometrial cells, and damages the implantation process. Bromuconazole is applicable to research related to glioma, colon cancer, reproductive injury (implantation dysfunction), and cardiac dysfunction.

Osteoprotegerin (OPG) belongs to the tumor necrosis factor receptor (TNFR) superfamily. Osteoprotegerin blocks the RANKL-RANK interaction as well as the binding of TRAIL to its receptor. Osteoprotegerin activates NF-κB to induce the expression of ICAM-1, VCAM-1 and E-selectin, and activates the phosphorylation of ERK1/2. Osteoprotegerin regulates osteoclast activity, inhibits osteoclast maturation and formation, bone lysis and bone resorption, and increases bone mass. Osteoprotegerin regulates vascular endothelial cell function. Osteoprotegerin can be used in the research of cardio-cerebrovascular and bone-related diseases.

p-MPPF dihydrochloride is a selective 5-HT antagonist that dose-dependently antagonizes the reduction of phosphorylated Erk1/2 levels in the hippocampus induced by 8-OH-DPAT (HY-112061) in rats. p-MPPF dihydrochloride can be used for neurological disease research.

1,2,4-Trihydroxybenzene (Hydroxyhydroquinone) (Standard) is the analytical standard of 1,2,4-Trihydroxybenzene (HY-W010451). This product is intended for research and analytical applications. 1,2,4-Trihydroxybenzene (Hydroxyhydroquinone) is an ER stress inducer that targets proteins such as PKR-like ER kinase PERK to induce cytotoxicity. 1,2,4-Trihydroxybenzene selectively activates eIF2α phosphorylation, activates the PERK-eIF2α signaling pathway and induces stress granule formation. 1,2,4-Trihydroxybenzene subsequently exacerbates oxidative stress and causes DNA double-strand breaks, destroying organelles such as mitochondria and ER, and inducing cell death. 1,2,4-Trihydroxybenzene also has the potential to exhibit anti-tumor effect, increase blood pressure, and relieve spasm.

p-MPPF is a selective 5-HT antagonist that dose-dependently antagonizes the reduction of phosphorylated Erk1/2 levels in the hippocampus induced by 8-OH-DPAT (HY-112061) in rats. p-MPPF can be used for neurological disease research.