Atg4

RNF5 inhibitor inh-02 is a selective inhibitor of the E3 ubiquitin ligase RNF5/RMA1, demonstrating significant biological activity by restoring F508del-CFTR function in F508del-CFTR-expressing immortalized cell lines (CFBE41o⁻, EC50 = 2.6 μM; FRT, EC50 = 2.2 μM). This compound promotes autophagy through increased LC3IIB expression and enhanced autophagic vacuole formation by reducing ATG4B ubiquitylation. RNF5 inhibitor inh-02 is valuable for research into cystic fibrosis and related cellular mechanisms.

S130 is a high affinity, selective inhibitor of ATG4B (a major cysteine protease) with an IC50 of 3.24 ?M. S130 suppresses autophagy flux.

MJO445 is a selective inhibitor of ATG4B, a key regulator in the autophagy pathway. Its inhibition of ATG4B disrupts the autophagic process in glioblastoma cells, thereby enhancing the efficacy of therapeutic strategies against this aggressive cancer. MJO445 is particularly relevant for research focused on cancer biology, autophagy modulation, and the development of novel cancer treatments.

LV-320 is a potent uncompetitive inhibitor of cathepsin ATG4B, exhibiting an IC50 of 24.5 μM and a Kd of 16 μM. This compound effectively inhibits the enzymatic activity of ATG4B, thereby obstructing autophagic flux in cellular environments. Due to its stability and low toxicity, LV-320 is suitable for in vivo applications, making it a valuable tool for research on autophagy-related pathways.

Atg4B-IN-2 is a selective inhibitor of Atg4B with a competitive mechanism, exhibiting a Ki value of 3.1 μM. In addition, it displays moderate inhibitory activity against phospholipase A2, with IC50 values of 11 μM and 3.5 μM for Atg4B and PLA2, respectively. This compound effectively enhances the anticancer efficacy of agents targeting castration-resistant prostate cancer through the inhibition of autophagy, making it a valuable tool for cancer research.