Actinonin ((-)-Actinonin) is a naturally occurring antibacterial agent produced by Actinomyces and a potent reversible peptide deformylase (PDF) inhibitor with a Ki of 0.28 nM, it also is an apoptosis inducer. Actinonin inhibits aminopeptidase M, aminopeptidase N and leucine aminopeptidase, it also inhibits MMP-1, MMP-3, MMP-8, MMP-9, and hmeprin α with Ki values of 300 nM, 1,700 nM, 190 nM, 330 nM, and 20 nM, respectively. Actinonin has antiproliferative and antitumor activities[1][2][3][4][5].
Aminopeptidase N (AP-N) inhibitor is a reversible inhibitor of AP-N CD13 (IC50 = 25 μM). It is selective for AP-N CD13 over matrix metalloproteinase-9 (MMP-9), angiotensin converting enzyme (ACE), neutral endopeptidase (NEP), γ-glutamyl transpeptidase, and the serine proteases dipeptidyl peptidase 4 (DPP-4) and cathepsin G at a concentration of 1 mM. AP-N inhibitor is non-cytotoxic to U937 cells at a concentration of 100 μM.
RB 101 suppresses enkephalinase and aminopeptidases; biologically cleaved at disulfide to produce inhibitors of both aminopeptidase N and neutral endopeptidase.
APN AKT-IN-1 is a potent dual inhibitor of aminopeptidase N (APN) and protein kinase B (AKT), exhibiting IC50 values of 0.21 μM and 0.27 μM for APN and AKT inhibition, respectively. This compound effectively suppresses the phosphorylation of glycogen synthase kinase 3 beta (GSK3β), which serves as an intracellular substrate of AKT [1].
NGR peptide Trifluoroacetate containing the asparagine-glycine-arginine (NGR) motif is recognized by CD13/aminopeptidase N (APN) receptor isoforms that are selectively overexpressed in tumor neovasculature.