Atg4

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

NSC 185058 is an inhibitor of ATG4B, a cysteine protease that activates LC3B during the initiation of autophagy.

ATG4 Autophagy Related 4 Homolog B Human Recombinant

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.

STK683963 is an activator of the autophagy-related protein ATG4B, which plays a critical role in the regulation of autophagy and cellular homeostasis. This compound enhances ATG4B activity, contributing to the redox-regulation mechanisms within cells. STK683963 is valuable for research applications focused on cancer biology, particularly in studies investigating the modulation of autophagy 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.

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.

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.

RNF5 Agonist 1 is a potent activator of RNF5, enhancing its biological function. This compound significantly increases the ubiquitylation of ATG4B in F508del-CFTR-expressing CFBE41o- cells, indicating its potential utility in studies of protein degradation pathways and cystic fibrosis research. RNF5 Agonist 1 serves as a valuable tool for investigating the role of RNF5 in cellular processes and therapeutic interventions.