stress-mediated

YUM70 is a potent and selective inhibitor of glucose-regulated protein 78 (GRP78), with an IC50 of 1.5 μM for inhibiting GRP78 ATPase activity of the full-length protein. It induces endoplasmic reticulum (ER) stress-mediated apoptosis in pancreatic cancer.

Elesclomol (STA-4783) is an oxidative stress inducer and a highly lipophilic copper ion carrier. Elesclomol induces apoptosis in tumor cells and is used in copper death related studies. Elesclomol also inhibits FDX1-mediated Fe-S cluster biosynthesis.

Zingerone (Vanillylacetone) is a nontoxic methoxyphenol isolated from Zingiber officinale, with potent anti-inflammatory, antidiabetic, antidiarrhoeic, antilipolytic, antispasmodic, and anti-tumor properties. Zingerone (Gingerone) alleviates oxidative stress and inflammation, down-regulates NF-κB mediated signaling pathways, acts as an anti-mitotic agent, and inhibits the growth of neuroblastoma cells.

6-Dehydrogingerdione sensitizes human hepatoblastoma Hep G2 cells to TRAIL-induced apoptosis via a reactive oxygen species-mediated mechanism that enhances DR5 expression, up-regulates Ser-15 phosphorylation, and triggers nuclear translocation of p53. Abrogation of p53 using small interfering RNA markedly reduces 6-Dehydrogingerdione-induced DR5 and diminishes TRAIL responsiveness. ROS generation accompanies DR5 activation, and pretreatment with N-acetyl-L-cysteine significantly attenuates these apoptotic responses, confirming 6-Dehydrogingerdione acts through p53-dependent and oxidative stress-mediated apoptotic pathways.

Calhex 231 hydrochloride is the salt form of Calhex 231, a potent calcium-sensing receptor (CaSR) negative-conversion modulator that blocks the increase in [3H]inositol phosphate, inhibits oxidative stress and mir-208a-mediated mitochondrial fission for vasculoprotection and treatment of traumatic hemorrhagic shock.

ABTL-0812 induces endoplasmic reticulum (ER) stress-mediated autophagy, and with anti-cancer activity.

CORM-401 is an oxidant-sensitive CO-releasing molecule used in the research of oxidative stress-mediated pathologies and inflammation [inflammatory].

PKR-IN-C16 is a specific protein kinase (PKR) inhibitor. PKR-IN-C16 is able to inhibit the autophosphorylation of PKR and unlock the translation blockade induced by PKR in primary neuronal cultures.PKR-IN-C16 binds the ATP-binding site of PKR and blocks autophosphorylation with an IC50 value of 186-210 nM. PKR-IN-C16 protects human neuroblastoma cells against cell damage triggered by tunicamycin-mediated endoplasmic reticulum stress.

Rotigaptide is a novel and specific modulator of Cx43 and is a potent AAP. Rotigaptide prevents the uncoupling of Cx43-mediated gap junction communication and normalizes cell-to-cell communication during acute metabolic stress.

Rotigaptide TFA(355151-12-1 free base) is a novel and specific modulator of Cx43 and is a potent AAP. Rotigaptide TFA(355151-12-1 free base) prevents the uncoupling of Cx43-mediated gap junction communication and normalizes cell-to-cell communication during acute metabolic stress.

Tauroursodeoxycholate (TUDCA ,Taurolite) dihydrate is a water-soluble bile acid with endoplasmic reticulum stress inhibitory, mitochondrial stabilizing, and anti-apoptotic effects, which significantly reduces the expression of apoptotic molecules, such as Caspase-3 and Caspase-12, and inhibits ERK, reducing endoplasmic reticulum stress mediated cell death.

ERK-MYD88 Interaction Inhibitor 1, an agent that disrupts the interaction between ERK and MYD88, has demonstrated the ability to trigger an HRI-mediated integrated stress response (ISR) that specifically promotes immunogenic cell apoptosis (apoptosis) in cancer cells. Additionally, in models using Lewis lung cancer mice, this compound has been shown to stimulate anti-tumor T cell responses, thereby exhibiting significant anti-tumor activity.

PSP205 is an effective anticancer agent with cytotoxic properties. It induces apoptosis and triggers autophagy mediated by ER stress. Furthermore, PSP205 enhances the expression of LC3BII protein and increases the expression of CHOP and spliced XBP1 at both mRNA and protein levels.

DIM-C-pPhtBu is an orally active endoplasmic reticulum stress activator. It induces mitochondrial and lysosomal dysfunction, excessive mitosis, ROS production, and cell death mediated by the unfolded protein response in cervical cancer cells. DIM-C-pPhtBu exhibits antitumor activity.

IDOi-Pt(IV) prodrug-1 (Compound 10) is an IDOi-Pt(IV) prodrug that suppresses IDO expression. It induces apoptosis, reduces mitochondrial membrane potential, and inhibits tumor cell migration and invasion. Additionally, IDOi-Pt(IV) prodrug-1 triggers reactive oxygen species-mediated endoplasmic reticulum stress and the secretion of damage-associated molecular patterns (DAMPs), leading to immunogenic cell death (ICD). Compared to cisplatin, IDOi-Pt(IV) prodrug-1 exhibits relatively high efficiency and low toxicity in its antitumor activity.

Nur77 modulator 4 (Compound 15h) is a Nur77 inducer with a KD of 0.477 μM. It significantly promotes Nur77 expression and apoptosis, exhibiting excellent growth inhibitory effects on HepG2 and MCF-7 cells, with an IC50 of less than 5 μM. Nur77 modulator 4 activates Nur77-mediated ER stress through the PERK-ATF4 and IRE1 signaling pathways, leading to apoptosis. This compound is applicable in cancer research.

PT-129 is a PROTAC degrader targeting the NTF2 domain of G3BP1/2, capable of inhibiting and degrading stress granules in stressed cells, disrupting ATF4 trafficking, and suppressing fibroblast-mediated cancer cell proliferation.

Me4Phen (compound 3) is an oxorhenium (V) complex that disrupts mitochondrial membrane potential and increases intracellular reactive oxygen species (ROS), leading to endoplasmic reticulum stress-mediated cancer cell necrosis (necrosis). With high lipophilicity, Me4Phen effectively overcomes Cisplatin resistance in various cancer cells.

7,4'-Dimethoxy-3-hydroxyflavone is an orally active PAR4 antagonist. This compound inhibits PAR4-mediated human platelet aggregation with an IC50 of 1.4 μM. It disrupts PAR4-mediated aggregation and related signaling pathways, including NF-κB, Ca2+/protein kinase C (PKC), Akt, ERK, and p38. In a streptozotocin (STZ)-induced diabetic mouse model, 7,4'-Dimethoxy-3-hydroxyflavone inhibits vascular PAR4 expression, improves endothelial dysfunction, and reduces oxidative stress. Additionally, it prevents thrombosis in mice without affecting bleeding time.

PROTACPI3K/110β degrader-2 is a selective PI3K/p110β PROTAC degrader. It effectively degrades the 110β protein and inhibits the expression of P-glycoprotein. Additionally, it increases reactive oxygen species (ROS) levels. PROTACPI3K/110β degrader-2 exerts antitumor effects by activating the endoplasmic reticulum stress (ERS) mediated mitochondrial apoptosis pathway and inhibiting the AKT/Bcl-2 signaling pathway. This compound is applicable in cancer research.

Keap1-IN-2 (Compound 164) is an inhibitor of KEAP1 with an IC50 of 2 nM. It indirectly activates Nrf2 by blocking KEAP1, thereby enhancing cellular antioxidant capacity. By preventing KEAP1-mediated degradation of Nrf2, Keap1-IN-2 promotes the accumulation and nuclear translocation of Nrf2. This compound is used in research on diseases related to oxidative stress, such as inflammatory bowel disease, Crohn's disease, and ulcerative colitis, which are immune-related conditions.

Tubulin polymerization-IN-82 is a tubulin inhibitor that effectively hinders cell migration and invasion. It induces apoptosis (cellular self-destruction) through pathways mediated by mitochondrial and endoplasmic reticulum stress. Tubulin polymerization-IN-82 exhibits antitumor activity against drug-resistant cancer cells and suppresses tumor growth, making it suitable for liver cancer research.

8-iso Prostaglandin F2α ethanolamide (iPF2α-III ethanolamide; 8-Isoprostane ethanolamide; 8-iso PGF2α ethanolamide) is a derivative of isoprostane ethanolamide produced through the non-enzymatic free radical oxidation of arachidonoyl ethanolamide (AEA). It is commonly used as a biomarker for oxidative stress, helping to distinguish non-enzymatic breakdown products from enzyme-mediated prostamides generated via pathways such as COX-2.

Narasin (sodium salt) (HainanMycin) induces tumor necrosis factor-related apoptosis-induced ligand (TRAIL)-mediated apoptosis by ER stress in glioma cells and inhibits NF-κB signaling by suppressing the phosphorylation of IκBα.