az2

AZ2 is a highly selective, active PI3Kγ inhibitor (pIC50=9.3) for use in inflammatory and immune disorders.

USP25/28-IN-AZ2 is a novel potent, selective, dual usp25/28 inhibitor

BAZ2-ICR is an epigenetic chemical probe and it also is a potent, selective, cell active and orally active BAZ2A/B bromodomains inhibitor with IC50s of 130 nM and 180 nM, and Kds of 109 nM and 170 nM, respectively. BAZ2-ICR shows 10-15-fold selectivity for binding BAZ2A/B over CECR2 and >100-fold selectivity over all other bromodomains.

AZ20 is an effective and specific inhibitor of ATR kinase (IC50: 5 nM, in a cell-free assay), 8-fold selectivity over mTOR.

BAZ2A/B ligand 1 (compound 1) serves as a ligand for target proteins in PROTAC applications. It can be utilized in the synthesis of dBAZ2.

dBAZ2 is a pioneering PROTAC degrader targeting BAZ2A and BAZ2B, with DC50 values of 180 nM for BAZ2A and 250 nM for BAZ2B.

dBAZ2B is a BAZ2B PROTAC degrader with a DC50 value of 19 nM. (Pink: BAZ2A/B ligand; Black: linker; Blue: CRBN Ligand)

NAZ2329 is the first cell-permeable inhibitor of the R5 subfamily of receptor-type protein tyrosine phosphatases (RPTPs), which is a variant and preferentially inhibits PTPRZ (IC50=7.5 μM for hPTPRZ1) and PTPRG (IC50=4.8 μM for hPTPRG) compared to other PTPs. NAZ2329 inhibited the tumor growth of glioblastoma cells and exhibited stem cell-like properties compared to the whole (D1 + D2) fragment of PTPRZ.

AZ-2 is an inducer of ABCA1 and apoE. It enhances ABCA1 activity and decreases P2X7 receptor activity. AZ-2 activates endogenous LXR signaling but shows no direct LXRα or LXRβ agonist activity.

Cyclo(L-Pro-L-Val), a 2,5-diketopiperazine extracted from the fruits of Mycobacterium chiliolyticum AZ2 and Mycobacterium leprae, possesses anti-inflammatory activity and virulence activity against phytopathogenic microorganisms (e.g., R. fascians LMG 3605) and inhibits Gram-positive plant pathogens.Cyclo(L-Pro-L-Val) significantly inhibited IKKα phosphorylation and IκBα and NF-κB activation as well as iNOS and COX-2 activation in a concentration Cyclo(L-Pro-L-Val) significantly inhibited the phosphorylation of IKKα, IKKβ, IκBα, and NF-κB, as well as the activation of iNOS and COX-2 in a concentration-dependent manner, and is a potential therapeutic agent for the treatment of inflammation-related diseases.