Mitophagy Inducer

HK2-IN-3 is a selective HK2 inhibitor with a human IC₅₀ of 0.0564 μM (56.4 nM). HK2-IN-3 induces mitophagy in oral squamous cell carcinoma cells. HK2-IN-3 exerts anti-cancer activity in oral squamous cell carcinoma cells. HK2-IN-3 can be used for the research of oral squamous cell carcinoma.

Dexpramipexole ((R)-Pramipexole) dihydrochloride (Standard) is the analytical standard of Dexpramipexole (dihydrochloride). This product is intended for research and analytical applications. Dexpramipexole dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Na_v1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.

NSCLC-IN-1 (Compound A10-2) induces mitophagy and ferroptosis through targeting transmembrane BAX inhibitor motif containing 6 (TMBIM6). NSCLC-IN-1 induces mitochondrial Ca²⁺ imbalance, leading to mitochondrial damage. NSCLC-IN-1 reduces intracellular glutathione (GSH), increases the accumulation of lipid peroxides (LPO) and malondialdehyde (MDA) content. NSCLC-IN-1 is a potent anti-NSCLC agent.

ADSS2-IN-1 is a ADSS2 inhibitor. ADSS2-IN-1 inhibits de novo AMP biosynthesis by targeting ADSS2, downregulates AMPK activity and promotes mitophagy in drug-resistant cells. ADSS2-IN-1 alone induces mild apoptosis in acute myeloid leukemia cells, and acts synergistically with BH3 mimetics to enhance the apoptotic effect. ADSS2-IN-1 restores the sensitivity of drug-resistant acute myeloid leukemia cells and reduces disease burden in immunocompetent mouse models. ADSS2 antagonist-1 can be used for the research of acute myeloid leukemia.

Antiproliferative agent-70 (compound 23) is a potent antiproliferative agent. Antiproliferative agent-70 shows antiproliferative activities and induces MMP depolarization. Antiproliferative agent-70 induces mitochondrial dysfunction. Antiproliferative agent-70 induces mitophagy and ferroptosis. Antiproliferative agent-70 increases the protein expression of PINK1, p-Parkin, p53 and p21. Antiproliferative agent-70 increases intracellular ROS levels. Antiproliferative agent-70 shows anticancer activity.

USP30-IN-2, a fused pyrroline, is an USP30 inhibitor with an IC₅₀ <0.1 μM. USP30-IN-2 is expected to promote mitophagy and restore mitochondrial health. USP30-IN-2 can be used for research on Parkinson's disease.

Solenopsin ((-)-Solenopsin A) is an ATP-competitive and selective Akt-1 inhibitor with an IC₅₀ of 5-10 μM, and also acts as an RSK1 inhibitor. Solenopsin inhibits the activities of PDK1 in lipid rafts, downregulates PI3K, blocks PI3K-dependent generation of 3-phosphoinositides, and suppresses the phosphorylation of FOXO1a. Solenopsin induces Mitophagy and ROS production, reduces mitochondrial oxygen consumption, and exhibits antiproliferative and antiangiogenic activities. Solenopsin can be used in research related to hyperproliferative skin diseases and malignant diseases.

ATB1071 is a brain-penetrant and orally active p62/SQSTM1 activator. ATB1071 binds to the p62-ZZ domain, promotes PB1-dependent p62 self-polymerization, and activates p62-mediated mitophagy. ATB1071 can be used for the research of Leigh syndrome, cerebral ischemia-reperfusion injury^[1].

Anticancer agent 227 (compound YNU-1c) is a potent anticancer agent. Anticancer agent 227 shows antiproliferative activity. Anticancer agent 227 induces apoptosis and mitophagy.

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.

NZ-66 is a ULK1-Recruiting Chimera (ULKREC) and heterobifunctional chimeric molecule composed of a BL-918-derived ULK1 agonist linked to a mitochondrial outer membrane-targeting TSPO ligand via a six-carbon hexane linker. NZ-66 is a mitophagy inducer recruits ULK1 to mitochondria to induce ULK1-dependent mitophagy, enhanced by mitochondrial insult, independently of the PRKN/PINK axis. NZ-66 can be used for the research of parkinson’s disease.

SHS206 (compound 6n) is an orally active mitochondrial uncoupler that reduces hepatic triglyceride levels. SHS206 exhibits in vivo efficacy in the GAN mouse model and shows inhibitory effects on metabolic dysfunction-associated steatohepatitis (MASH).

LCL768 is a ceramide analog. LCL768 attenuates PARKIN succination to promote PARKIN activation and mitophagy. LCL768 induces CerS1-mediated endogenous C18-ceramide accumulation in mitochondria to mediate mitophagy, which is dependent on DRP1 activation via nitrosylation at C644. LCL768 alters mitochondrial metabolism, resulting in fumarate depletion and leading to tumor suppression. LCL768 improves sensorimotor defects in neurodegenerative diseases like ALS.

Dexpramipexole-d₃ ((R)-Pramipexole-d₃) dihydrochloride is the deuterium labeled Dexpramipexole. Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Na_v1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.

DS96432529 (Standard) is the analytical standard of DS96432529 (HY-145121). This product is intended for research and analytical applications. DS96432529 is an orally active CDK8 inhibitor with an IC₅₀ of 33 nM. DS96432529 enhances ALPase activity, with an EC₂₀₀ of 63 nM. DS96432529 inhibits TNF-α-induced activation of the RLR signaling pathway, activates mitophagy, accelerates mineralized nodule formation, and suppresses the proliferation of periodontal ligament stem cells. DS96432529 promotes bone formation, alleviates ligation-induced alveolar bone loss, and increases bone mineral density in ovariectomized animal models. DS96432529 can be used in studies related to periodontitis and osteoporosis.

Diquat (dibromide hydrate) (Standard) is the analytical standard of Diquat (dibromide hydrate). This product is intended for research and analytical applications. Diquat dibromide hydrate is a comprehensive herbicide. Diquat dibromide hydrate increases the production of ROS and triggers mitophagy. Diquat dibromide hydrate generates free radicals such as superoxide anions through redox cycles, which induce oxidative stress. Diquat dibromide hydrate is cytotoxic, reproductive, and neurotoxic. Diquat dibromide hydrate is used in cotton, soybean, and other crops to combat noxious weeds.