ALLN (110044-82-1) is a cell-permeable, peptide aldehyde inhibitor of calpain I (Ki=190 nM), calpain II (Ki=150 nM), cathepsin L (Ki=0.5 nM) and other neutral cysteine proteases.1Inhibits cell cycle progression at G1/Sand metaphase/anaphase in CHO cells by inhibiting cyclin B degradation.2Inhibits proteolytic degradation of IκBα and IκBβ in RAW macrophages induced with LPS.3Blocks AIF-mediated necroptosis.4Cell permeable.
white to off-white powder
Calpain inhibitor I inhibits calpain, which activates myosin light chain kinase and protein kinase C by partial proteolysis. The inhibitor should be membrane permeable due to low molecular weight and lack of charged residues.
Calpain Inhibitor I is used for western blotting methods.
Calpain inhibitor I reversibly blocks the calcium-dependent neutral cysteine protease calpain I. Calpains have been implicated in various cellular processes, including cell proliferation, apoptosis, and cell differentiation.
It inhibits apoptosis in thymocytes and metamyelocytes. It also inhibits cell cycle progression at the G1/S border and metaphase/anaphase in CHO cells by inhibiting cyclin B degradation. ALLN inhibits the proteolysis of IκBα and IκBβ by the ubiquitin-proteasome complex. ALLN also prevents nitric oxide production by activated macrophages by interfering with transcription of the inducible nitric oxide synthase gene.
ChEBI: A tripeptide composed of N-acetylleucyl, leucyl and norleucinal residues joined in sequence.
Calpain Inhibitor I is a strong, competitive inhibitor of the Ca2+-dependent neutral cysteine proteases calpain I and calpain II.
Calpain inhibitor (IC 50 = 0.09 μ M) that activates p53-dependent apoptosis in tumor cell lines. Increases activated p53, p21 and caspase levels and promotes cell cycle arrest through inhibition of cyclin D degradation in vitro . Also attenuates ischemia/reperfusion injury in cardiomyocytes, hepatocytes and renal tubular cells through downregulation of iNOS and COX-2 expression.
Calpain Inhibitor I inhibits tumor necrosis factor-induced (TNF-induced) cleavage of Poly (ADP-ribose) polymerase (PARP) and calpastatin in apoptosis. It also inhibits oxygen/glucose deprivation (OGD) induced cleavage of caspase-12 and Bcl-xL..
[1] T SASAKI. Inhibitory effect of di- and tripeptidyl aldehydes on calpains and cathepsins.[J]. Journal of enzyme inhibition, 1990, 3 3: 195-201. DOI:
10.3109/14756369009035837[2] S W SHERWOOD. In vivo inhibition of cyclin B degradation and induction of cell-cycle arrest in mammalian cells by the neutral cysteine protease inhibitor N-acetylleucylleucylnorleucinal.[J]. Proceedings of the National Academy of Sciences of the United States of America, 1993, 90 8: 3353-3357. DOI:
10.1073/pnas.90.8.3353[3] N-acetyl-leucinyl-leucinyl-norleucinal inhibits lipopolysaccharide-induced NF-kappaB activation and prevents TNF and IL-6 synthesis in vivo
[4] LEI SHANG. Calpain: a molecule to induce AIF-mediated necroptosis in RGC-5 following elevated hydrostatic pressure.[J]. BMC Neuroscience, 2014, 15: 63. DOI:
10.1186/1471-2202-15-63
