autophagosome

Indophagolin is a potent, indoline-containing autophagy inhibitor with an IC50 of 140 nM, and it antagonizes the purinergic receptor P2X4 as well as P2X1 and P2X3 with IC50s of 2.71, 2.40, and 3.49 μM, respectively.

MHY1485 is an mTOR activator that is cell-permeable. MHY1485 inhibits autophagosome and lysosome fusion, leading to accumulation of LC3II proteins and increased autophagosomes, thereby inhibiting cellular autophagy.

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.

ML-9 suppresses MLCK, PKA, and PKC activity with Ki values of 4, 32, and 54 μM, respectively. ML-9 is a selective and effective inhibitor of Akt kinase, inhibits myosin light-chain kinase (MLCK), and stromal interaction molecule 1 (STIM1) activity. ML-9 causes autophagy by stimulating autophagosome formation and inhibiting their degradation.

ML-9 (free base) suppresses MLCK, PKA, and PKC activity (Ki: 4, 32, and 54 μM, respectively). ML-9 (free base) is a selective and effective inhibitor of Akt kinase, inhibits myosin light-chain kinase (MLCK), and stromal interaction molecule 1 (STIM1) acti

TrxR EGFR-IN-1 (Compound L1Au2) is a TrxR EGFR inhibitor with activity against both gefitinib-sensitive and -resistant lung cancer, effectively suppressing tumor proliferation and promoting apoptosis. It enhances GPX4 degradation through autophagosome-lysosome and proteasome pathways, leading to ferroptosis. Additionally, it induces endoplasmic reticulum stress and triggers immunogenic cell death, making it applicable for studies on gefitinib-resistant lung cancer.

Autophagyagonist-1 (compound 22) is an autophagy agonist. It exhibits significant anticancer activity against HepG2 cells and normal cells, with IC50 values of 8.8 μM and > 50 μM, respectively. The compound induces G1 S phase cell cycle arrest, suppresses the expression of CDK4 and CyclinD1, and upregulates P21. Additionally, Autophagyagonist-1 enhances autophagosome, LC3, and PINK1 accumulation, thereby promoting autophagy and mitophagy in HepG2 cells.

Crisdesalazine (AAD 2004) is an inhibitor of microsomal prostaglandin E2 synthase-1 (mPGES-1). Crisdesalazine reduces autophagosome formation, axonopathy, and motor neuron degeneration, improving motor function and increasing life span.

Tubastatin inhibits TGF-β1-induced phosphorylation of S6K, HIF-1α expression and VEG F expression.Tubastatin inhibits TGF-β1-induced inhibition of LC3B-II, a marker of autophagosome formation.

C18 dihydro Ceramide is a bioactive sphingolipid and precursor in the de novo synthesis of C18 ceramide that lacks the 4,5-trans double bond. [1] Increased C18 dihydroceramide lipid levels lead to increased triacylglycerol storage and autophagosome accumulation as well as upregulation of the fibrosis markers α-SMA and FGF2 in Chang and LX-2 liver cells. C18 dihydro Ceramide is elevated in the plasma of pre-diabetics up to 9 years prior to the onset of type 2 diabetes. [2] It is also elevated in the skin of patients with lesional atopic dermatitis.[3]

LY-294002 hydrochloride (NSC 697286) is a synthetic molecule inhibitor of PI3Kα δ β (IC50: 0.5 0.57 0.97 μM, in cell-free assays); more stable than Wortmannin in solution, and also is a blocker of autophagosome formation.

Liensinine Diperchlorate is an isoquinoline alkaloid extracted from the embryonic seeds of the sacred lotus. It inhibits late autophagy by blocking autophagosome-lysosome fusion and exhibits biological activities such as anti-arrhythmic, anti-hypertensive, anti-pulmonary fibrosis, and vascular smooth muscle relaxation.

LC3-mHTT-IN-AN2 (5,7-Dihydroxy-4-phenylcoumarin) is found in the plant Passiflora serratodigitata with the antibacterial activity.

CA-5f is a potent late-stage macroautophagy autophagy inhibitor that works by inhibiting autophagosome-lysosome fusion.

TrxR-IN-3 (Compound 2c) is an effective TrxR inhibitor that exhibits strong antiproliferative activities against five human cancer cell lines, particularly breast tumor cells. It increases ROS levels, induces apoptosis by regulating apoptosis-related protein expression in breast cancer cells, and promotes autophagosome and autolysosome formation by enhancing LC3-II and Beclin-1 expression and reducing LC3-I and p62 protein expression [1].

Coibamide A, an N-methyl-stabilized cytotoxic depsipeptide, exhibits potent antiproliferative activity, induces autophagosome accumulation via an mTOR-independent mechanism, and triggers apoptosis. Furthermore, it inhibits VEGFA VEGFR2 expression, effectively suppressing tumor growth in glioblastoma xenografts [1] [2].

LC3-mHTT-IN-AN1 is a mHTT-LC3 linker compound that interacts with both mutant huntingtin protein (mHTT) and LC3B. LC3-mHTT-IN-AN1 targeted mHTT to autophagosomes reduces the levels of mHTT in an allele-selective manner in cultured Huntington disease (HD) mouse neurons.

XIE62-1004 is a chemical compound that induces the interaction between p62 and LC3 by binding to the ZZ domain of p62. This interaction promotes p62 self-aggregation and its subsequent interaction with LC3 on autophagosome membranes, thereby facilitating the delivery of cargo proteins to the autophagosome for degradation. XIE62-1004 is effective both in vitro and in vivo, displaying specificity for the wild type of p62 and exhibiting its actions in a concentration- and time-dependent manner. Additionally, it induces the degradation of mutant huntingtin in vitro and can be employed in AUTAC protein degradation systems to trigger autophagy via p62 self-aggregation and LC3 interaction.