mitochondria stress

Chloramphenicol (Chloromycetin) is a broad-spectrum antibiotic that inhibits the biosynthesis of bacterial proteins. Chloramphenicol acts primarily on the 50S subunit of the bacterial 70S ribosome and is active against peptidyltransferases, inhibiting the formation of peptide bonds.

Nur77 modulator 1 is an effective Nur77 binder (KD = 3.58 μM) that up-regulates Nur77 expression, mediates its sub-cellular localization, induces Nur77-dependent ER stress and autophagy, and leads to cell apoptosis, demonstrating anti-hepatoma activity.

4-Hydroxynonenal (4-HNE) (4-HNE) is an oxidative/nitrosative stress biomarker. It is a substrate and an inhibitor of acetaldehyde dehydrogenase 2 (ALDH2).

SP11 is a mitochondrial reactive oxygen species (ROS) inhibitor. It activates Fis1 with an IC50 of 9.4 µM by binding to Cys41 and enhances the translocation of Drp1 to mitochondria. SP11 is utilized for research into oxidative stress damage.

NLRP3-IN-85 (compound 5d) is a potent inhibitor of NLRP3 that operates independently of mitochondrial membrane potential (ΔΨm). It protects mitochondria from oxidative stress and inflammatory damage while inhibiting key inflammatory factors (NO, TNF-α, IL-6). NLRP3-IN-85 alleviates acute lung injury in mice and reduces paw edema in rats, making it useful for acute lung injury (ALI) research.

DdBIC is a pyroptosis inducer that associates with Nur77, facilitating its translocation to the mitochondria. This interaction activates the depletion of SDHA succinyl-CoA, disrupts hemeostasis, causes electron leakage, and stimulates mitochondrial ROS generation. Mitochondrial ROS, induced by DdBIC, oxidatively activates OMA1, leading to OPA1 cleavage and release into the cytoplasm, triggering the PERK-activated integrated stress response, ultimately activating granzyme B (granzyme B) to cleave GSDMC. DdBIC is applicable in melanoma research.

Mitoquinol is a mitochondria-targeted antioxidant used in the study of cardiovascular disease by modulating the mitochondrial antioxidant defense system to reduce DEN-induced oxidative stress.

QD325 is a potent redox modulator for the Treatment of Pancreatic Ductal Adenocarcinoma. Nascent RNA sequencing following treatments with QD325 revealed induction of stress responses in the nucleus, endoplasmic reticulum, and mitochondria of pancreatic ca

MitoEbselen-2 chloride is a mitochondria-targeted antioxidant combining TPP and Ebselen. It enriches in mitochondria to scavenge ROS/RNS, protecting mitochondrial function and mitigating oxidative stress-induced neurotoxicity.

MitoPQ (MitoParaquat) is a mitochondria-targeted small molecule compound that selectively enhances mitochondrial superoxide and hydrogen peroxide levels and inhibits insulin-stimulated glucose uptake and translocation of glucose transport protein 4 (GLUT4) to the plasma membrane in adipocytes and myotubes.MitoPQ can be used to MitoPQ can be used to study mitochondrial oxidative stress and regulated GLUT4 transporter.

Vatiquinone, also known as EPI 743, is an orally bioavailable para-benzoquinone being developed for inherited mitochondrial diseases. The mechanism of action of EPI-743 involves augmenting the synthesis of glutathione, optimizing metabolic control, enhanc

PGBx is a mixture of oligomers of PGB1 with a molecular weight of 1,000-1,500. It has antioxidant and free radical trapping activity that was first studied in isolated mitochondria.1 PGBx has anti-inflammatory and cytoprotective activity which may be attributed to inhibition of the 14 kDa sPLA2.2,3 At a dose of 1 mg/kg, PGBx significantly reduces the incidence of ulcers in rats.2References1. Polis, B.D., Polis, E., and Kwong, S. Protection and reactivation of oxidative phosphorylation in mitochondria by a stable free-radical prostaglandin polymer (PGBΧ). Proceedings of the National Academy of Sciences of the United States of America 76, 1598-1602 (1979).2. Kumashiro, R., Devlin, T.M., Kholoussy, A.M., et al. Prostaglandin BΧ in the prevention of stress ulcers in rats. International Surgery 70, 247-250 (1985).3. Franson, R.C., Rosenthal, M.D., and Regelson, W. Mechanism(s) of cytoprotective and anti-inflammatory activity of PGB1 oligomers: PGBx has potent anti-phospholipase A2 and anti-oxidant activity. Prostaglandins, Leukotrienes and Essential Fatty Acids 43, 63-70 (1991). PGBx is a mixture of oligomers of PGB1 with a molecular weight of 1,000-1,500. It has antioxidant and free radical trapping activity that was first studied in isolated mitochondria.1 PGBx has anti-inflammatory and cytoprotective activity which may be attributed to inhibition of the 14 kDa sPLA2.2,3 At a dose of 1 mg/kg, PGBx significantly reduces the incidence of ulcers in rats.2 References1. Polis, B.D., Polis, E., and Kwong, S. Protection and reactivation of oxidative phosphorylation in mitochondria by a stable free-radical prostaglandin polymer (PGBΧ). Proceedings of the National Academy of Sciences of the United States of America 76, 1598-1602 (1979).2. Kumashiro, R., Devlin, T.M., Kholoussy, A.M., et al. Prostaglandin BΧ in the prevention of stress ulcers in rats. International Surgery 70, 247-250 (1985).3. Franson, R.C., Rosenthal, M.D., and Regelson, W. Mechanism(s) of cytoprotective and anti-inflammatory activity of PGB1 oligomers: PGBx has potent anti-phospholipase A2 and anti-oxidant activity. Prostaglandins, Leukotrienes and Essential Fatty Acids 43, 63-70 (1991).

MitoTEMPO hydrate is a mitochondria-targeted antioxidant and superoxide scavenger. It mimics SOD activity to protect against mitochondrial oxidative stress in hypertension and neurodegeneration research.

Demethyleneberberine, which is composed of a potential antioxidant structure, could penetrate the membrane of mitochondria and accumulate in mitochondria either in vitro or in vivo.Demethyleneberberine suppresses CYP2E1, hypoxia inducible factor α, and inducible nitric oxide synthase, which contributes to oxidative stress and restored sirtuin 1/AMP-activated protein kinase/peroxisome proliferator-activated receptor-γ coactivator-1α pathway-associated fatty acid oxidation in chronic ethanol-fed mice.

BI-6C9 is an inhibitor of tBid (Kd = 20 µM).BI-6c9 prevented MOMP and mitochondrial fission, and protected the cells from cell death.

FABPs ligand 6 (MF6) is a selective inhibitor of FABP5 and FABP7 that reduces levels of oxidative stress in the mouse spinal cord as well as lipopolysaccharide-stimulated interleukin-1β and tumor necrosis factor α accumulation in primary astrocyte cultures.FABPs ligand 6 has a potent protective function in oligodendrocytes of EAE mice through FABP5 inhibition. mitochondria with a strong protective function.

NecroIr1, an iridium(III) complex, acts as a necroptosis inducer in Cisplatin-resistant lung cancer cells (A549R). It selectively targets mitochondria, causing oxidative stress and reducing mitochondrial membrane potential (MMP). By activating receptor-interacting serine-threonine kinase 3 (RIPK3) and Mixed Lineage Kinase (MLKL), and modulating CDK4 expression, NecroIr1 facilitates cell death mechanisms [1].

NecroIr2, an iridium(III) complex, functions as a necroptosis inducer in cisplatin-resistant lung cancer cells (A549R). It preferentially accumulates in mitochondria, causing oxidative stress and a reduction in mitochondrial membrane potential (MMP). Moreover, NecroIr2 initiates the activation of receptor-interacting serine/threonine kinase 3 (RIPK3) and mixed lineage kinase domain-like pseudokinase (MLKL), while also regulating CDK4 expression [1].

RPS6-IN-1 (Compound 22o) inhibits cell migration and induces apoptosis (increasing the expression of Bax, p53, cleaved-caspase 3, and cleaved-PARP). It reduces mitochondrial membrane potential and activates autophagy (Autophagy) through the PI3K-Akt-mTOR signaling pathway, damaging mitochondria and lysosomes within the cell and causing endoplasmic reticulum stress. RPS6-IN-1 also inhibits the phosphorylation of RPS6. Notably, RPS6-IN-1 is a low systemic toxicity anticancer agent.

Ginkgo Biloba Extract (Standard) is the standard reference of Ginkgo Biloba Extract, suitable for quantitative analysis, quality control and biochemical research. Ginkgo Biloba Extract is a natural active ingredient extracted from ginkgo leaves. It maintains the structural and functional homeostasis of mitochondria, regulates the expression of Bcl-2 family proteins, blocks caspase cascade activation, and thereby alleviates neuronal apoptosis mediated by oxidative stress. Meanwhile, it upregulates SKP2 expression, inhibits non-Beclin1-dependent autophagy pathways, and ameliorates testicular tissue injury. In animal experimental models, it exerts protective effects on multiple types of neuronal damage and alleviates behavioral sensitization in rats. Against β-amyloid (Aβ)-mediated neurotoxicity, Ginkgo Biloba Extract produces multiple antagonistic effects: inhibiting Aβ-induced abnormal glucose uptake, ROS accumulation, AKT signaling disorder and mitochondrial dysfunction, regulating JNK and ER1/2 signaling pathways, blocking neuronal apoptosis, and suppressing the aggregation and formation of Aβ oligomers. Current research confirms that Ginkgo Biloba Extract has potential research value and application prospects in various neurological and tissue injury diseases including cerebral insufficiency, testicular injury, Alzheimer's disease, Parkinson's disease, multi-infarct dementia, stroke, traumatic brain injury and amyotrophic lateral sclerosis.