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    Autophagy is a conserved cellular degradation and recycling process in the lysosome. In mammalian cells, there are three primary types of autophagy: microautophagy, macroautophagy, and chaperone-mediated autophagy (CMA). Microphagy captures cargoes by means of invaginations or protrusions of the lysosomal membrane directly, CMA uses chaperones to identify cargo proteins and then unfolds and transfers them into the lysosomal, while macroautophagy sequesters cargo by autophagosomes-de novo synthesized of double-membrane vesicles-and subsequently transport it to the lysosome.

    Macroautophagy is the best studied and it occurs at a low level constitutively and can also be further induced under stress conditions, such as nutrient or energy starvation with a salient feature of autophagy protein degradation. Stress-induced macrophagy plays an important role in protein catabolism with another key protein degradation pathway, the ubiquitin–proteasome system (UPS).

    As the study progressed, autophagy gains its importance under basal, nutrient-rich conditions, and is now recognized as a critical housekeeping pathway in catabolism of diverse cellular constituents, such as protein aggregates (aggrephagy), lipid droplets (lipophagy), iron complex (Ferritinophagy) and carbohydrate. Except for macromolecules, autophagy can also target several organelles and structures, such as mitochondria (mitophagy), peroxisome (pexophagy), endoplasmic reticulum (reticulophagy or ER-phagy), ribosome (ribophagy), spermatozoon-inherited organelles following fertilization (allophagy), secretory granules within pancreatic cells (zymophagy) and intracellular pathogens (xenophagy).Autophagy and its dysfunction are associated with a variety of human pathologies, including ageing, cancer, neurodegenerative disease, heart disease and metabolic diseases, such as diabetes. Plenty of drugs and natural products are involved in autophagy modulation through multiple signaling pathways. Small molecules that can regulate autophagy seem to have great potential to intervene such diseases in animal models or clinical courses.

Cat. No. Product Name CAS No. Information



ROC-325 (ROC 325, ROC325) is a novel, orally available inhibitor of lysosomal-mediated autophagy; exhibits superior in vitro anticancer effects compared with the existing autophagy inhibitor hydroxychloroquine (HCQ) in different cancer cell lines, including accumulation of autophagosomes with undegraded cargo, lysosomal deacidification, p62 stabilization, and disruption of autophagic flux; antagonizes RCC growth and survival in an ATG5/7-dependent manner, induces apoptosis and exhibited favorable selectivity; significantly more effective at inhibiting tumor progression than HCQ, and inhibited autophagy in vivo.




Lys01 is a 10-fold more potent lysosomal autophagy inhibitor than hydroxychloroquine (HCQ).




AUTEN-67 is a small molecule autophagy enhancer that specificly inhibits myotubularin-related phosphatase MTMR14; at concentrations of 2, 10, and 100 uM, AUTEN-67 inhibits MTMR14 by nearly 3%, 25%, and 70%, respectively; shows no activity for CDC25B , other phosphatase, PTPN1; significantly increases autophagic flux in cell lines and in vivo models, promotes longevity and protects neurons from undergoing stress-induced cell death; also restores nesting behavior in a murine model of Alzheimer disease, without apparent side effects.




IITZ-01 (Autophagy inhibitor IITZ-01) is a novel potent lysosomotropic autophagy inhibitor, exhibits >10-fold potent autophagy inhibition along with 12- to 20-fold better cytotoxic action than Chloroquine; enhances autophagosome accumulation but inhibit autophagosomal degradation by impairing lysosomal function, finally resulting in the inhibition of autophagy, also abolishes mitochondrial membrane potential and triggers apoptosis through the mitochondria-mediated pathway (TNBC cells IC50=1.54 uM, 48 h); displays potent antitumor action in vivo through autophagy inhibition and apoptosis induction in MDA-MB-231 breast cancer xenograft model.




PHY34 is a potent autophagy inhibitor with cytotoxic effects by inhibiting autophagy at a late stage (MDA-MB-435 IC50=23 nM, MDA-MB-231 IC50=5.2 nM); disrupts lysosomal function, significantly inhibits the growth of cancer cell lines in hollow fibers, as well as reduces ovarian tumor burden in a xenograft model.




STF-62247 is a small molecule Autophagy inducer that induces autophagy and selectively induces lethality in VHL-deficient RCC cells; induces cytotoxicity and reduces tumor growth in VHL-deficient cells in a HIF-independent manner, PI3K and Golgi trafficking are required as initial signals in STF-62247-induced autophagy.




A small-molecule enhancer/inducer of Autophagy; decreases the levels of Aβ peptide (EC50=10 uM) and APP-CTF (EC50 of 20 uM) in a γ-secretase-independent manner in primary neuronal cultures, Atg5, Beclin1 and Ulk1 are shown to be involved in the degradation of Aβ and APP-CTF; enhances erythropoiesis in a range of in vitro and in vivo models of DBA, and protects against neurodegeneration in Drosophila model of Huntington’s disease.




A small molecule autophagy enhancer that induces autophagy independently of rapamycin in mammalian cells and enhances the clearance of autophagy substrates such as mutant huntingtin and A53T alpha-synuclein; reduces toxicity in Huntington's disease models.




Auten-99 is a small molecule autophagy enhancer that inhibit the myotubularin-related phosphatase MTMR14/Jumpy; induces autophagic flux and promotes cell survival in mammalian cell cultures; increases the number of autophagic structures in mice and Drosophila, and effectively penetrates through a blood-brain barrier model; impedes the progression of neurodegenerative symptoms in Drosophila models of Parkinson's and Huntington's diseases.




Lys05 (Lys01 trihydrochloride, PS-1001) is the water-soluble salt of Lys01, is a 10-fold more potent lysosomal autophagy inhibitor than hydroxychloroquine (HCQ); shows IC50 values of 3.6, 3.8, 6 and 7.9 uM for 1205Lu, c8161, LN229 and HT-29 cell line in the MTT assay; more potently accumulates within and deacidifies the lysosome, resulting in impaired autophagy and tumor growth; enhances sunitinib-mediated suppression of clear cell ovarian carcinoma (CCOC) cell viability.

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