autophagic flux

EACC, a reversible autophagy inhibitor, selectively impedes Stx17, an autophagosome-specific SNARE, from translocating, hence obstructing the fusion between autophagosomes and lysosomes. This compound effectively halts autophagic flux.

Clarithromycin (A-56268) is a Macrolide Antimicrobial. The mechanism of action of clarithromycin is as a Cytochrome P450 3A4 Inhibitor, and Cytochrome P450 3A Inhibitor, and P-Glycoprotein Inhibitor. The chemical classification of clarithromycin is Macrolides.

LV-320 is a potent, uncompetitive ATG4B inhibitor with an IC50 of 24.5 μM and a Kd of 16 μM. LV-320 inhibits ATG4B enzymatic activity, blocks autophagic flux in cells, and is stable, non-toxic, and active in vivo. These findings suggest that LV-320 will serve as a relevant chemical tool to study the various roles of ATG4B in cancer and other contexts [1].

PBA-1105 TFA is an autophagy-targeting chimera (AUTOTAC) that induces p62 self-oligomerization. This compound selectively binds to the exposed hydrophobic regions of misfolded proteins, promoting their degradation through the autophagy (autophagy) pathway. Additionally, PBA-1105 TFA enhances the autophagic flux of Ub-bound aggregates.

N6-Isopentenyladenosine, an end product of the mevalonate pathway, is an autophagy inhibitor with anti-melanoma activity. N6-Isopentenyladenosine, an RNA modification found in cytokinins, regulates plant growth differentiation and improves the efficiency

ML-SA5 is a MCOLN1 agonist that blocks autophagic flux by disrupting fusion between autophagosomes and lysosomes.

Autophagy-IN-2 (Compound 7h) is an autophagic flux inhibitor that induces cancer cell apoptosis, making it a valuable agent for triple-negative breast cancer research [1].

Autophagy-IN-1 is a potent inhibitor of autophagy mitophagy that blocks autophagosomal-lysosomal fusion in cancer cells while selectively increasing autophagic flux. It significantly inhibits tumor growth in the HCT116 mouse xenograft tumour model with low toxicity and can be used to study colorectal cancer.

Indomethacin farnesil (Infree) is a prodrug of indomethacin. It acts as a nonsteroidal anti-inflammatory drug (NSAID) and disease-modifying anti-rheumatic drug (DMARD).

DCAP, a broad-spectrum antibiotic, disrupts the membranes of both Gram-positive and Gram-negative bacteria. Additionally, it inhibits late-stage autophagy by blocking autophagolysosome maturation and interrupting autophagic flux [1].

NEO214, an autophagy inhibitor and a covalent conjugate of the PDE4 inhibitor Rolipram and perillyl alcohol, exhibits anti-cancer activity and blood-brain barrier (BBB) permeability. It prevents autophagy-lysosome fusion, blocking autophagic flux and triggering glioma cell death via mTOR activation and TFEB (Transcription Factor EB) aggregation. NEO214 inhibition of Macroautophagy autophagy in glioblastoma cells may overcome chemotherapy resistance in glioblastoma [1].

Nur77 modulator 3 (9e) binds to Nur77 and inhibits TGF-β1-induced α-SMA and COLA1 expression in a Nur77-dependent manner. It induces Nur77 expression and enhances autophagic flux by inhibiting the mTORC1 signaling pathway in vitro and in vivo. Nur77 modulator 3 blocks the progression of hepatic fibrosis [1].

PBA-1105, an autophagy-targeting chimeric molecule (AUTOTAC), facilitates the self-oligomerization of p62. Additionally, PBA-1105 enhances the autophagic flux of Ub-conjugated aggregates.

PBA-1105b, a longer PEGylated derivative of PBA-1105, is an autophagy-targeting chimeric compound (AUTOTAC) that can induce self-oligomerization of p62. It enhances the autophagic flux of Ub-bound aggregates.

PHTPP-1304, a chimeric autophagy-targeting compound (AUTOTAC) based on PHTPP, induces p62 self-oligomerization and degrades estrogen receptor ERβ (DC50: ~2 nM, HEK293T). Additionally, PHTPP-1304 facilitates the formation of p62+ERβ+ puncta in a dose-dependent manner, influencing autophagic flux.

GW406108X (GW108X) is a Kif15 inhibitor with an IC50 of 0.82 uM in ATPase assays. GW406108X is also an ULK1 kinase inhibitor with pIC50 values of 6.37 (427 nM) and block autophagic flux.

CTB (Cholera Toxin B subunit) is an activator of p300 histone acetyltransferase and induces apoptosis in MCF-7 cells.

Gypenoside L inhibits autophagic flux and induces cell death in human esophageal cancer cells through endoplasm reticulum stress-mediated Ca2+ release. It also inhibit non-small cell lung carcinoma A549 cell inhibitory activity.

Lup-20(29)-en-28-oic acid exhibits anticancer activities in various cancer types by inhibiting autophagic flux and synergistically enhancing the effectiveness of chemotherapeutic agents against HeLa cells. Pulsatilla saponin D demonstrates strong haemolytic activity.