Calpain Inhibitor I, ALLN

• CAT Number: I000413
• CAS Number: 110044-82-1
• Molecular Formula: C₂₀H₃₇N₃O₄
• Molecular Weight: 383.54
• Purity: ≥95%
• Target: Calpains
• Solubility: 10 mM in DMSO
• Storage: Store at -20°C
• IC50: 150 nM (Ki)
• InChI: InChI=1S/C20H37N3O4/c1-7-8-9-16(12-24)22-19(26)18(11-14(4)5)23-20(27)17(10-13(2)3)21-15(6)25/h12-14,16-18H,7-11H2,1-6H3,(H,21,25)(H,22,26)(H,23,27)/t16-,17-,18-/m0/s1
• InChIKey: FMYKJLXRRQTBOR-BZSNNMDCSA-N
• SMILES: CCCCC(C=O)NC(=O)C(CC(C)C)NC(=O)C(CC(C)C)NC(=O)C

Calpain Inhibitor I, also known as ALLN (CAT: I000413), is a synthetic compound that acts as an irreversible inhibitor of calpain enzymes. Calpains are calcium-dependent proteases involved in various cellular processes. ALLN binds to the active site of calpain enzymes, preventing the degradation of target proteins. It has been extensively used in research to study calpain biology, protein turnover, and its potential role in disease. ALLN provides valuable insights into calpain-mediated processes and has implications in areas such as neurodegenerative diseases and muscle disorders.

Reference

1. Biochem Biophys Res Commun. 2013 Jul 26;437(2):325-30. doi:
10.1016/j.bbrc.2013.06.088. Epub 2013 Jul 2.

ALLN hinders HCT116 tumor growth through Bax-dependent apoptosis.

Li SZ(1), Zhang HH, Zhang JN, Zhang ZY, Zhang XF, Zhang XD, Du RL.

Author information:
(1)College of Life Sciences, Wuhan University, Wuhan, Hubei 430072, China.

Continual high expression of cysteine proteases calpain I and II have been
implicated in tumorigenicity; conversely, N-acetyl-leu-leunorleucinal (ALLN),
which inhibits calpain I and II, should also influence tumor growth and
carcinogenesis. To explore the role of ALLN against colon cancer and in promoting
apoptosis, we used colon cancer HCT116 cell lines, p53 or Bax-deficient HCT116
cell lines. Cell viability and tumor growth decreased in a
concentration-dependent manner when treated with 0-26μM ALLN. Treatment with ALLN
induced apoptosis in HCT116 cell; however, flow cytometry showed that apoptosis
significantly decreased in Bax-deficient HCT116 cell lines, but not in
p53-deficient HCT116 cell lines. In addition, the ALLN-induced apoptosis response
was through Bax translocation from cytosol to mitochondria. In this study we
showed intraperitoneally injected ALLN to inhibit colon tumor formation in nude
mice, and found ALLN to inhibit tumor growth in colon cancer cells, mainly
through apoptosis that depends on translocation of Bax to a mitochondrial
endogenous pathway; this implies a molecular mechanism for ALLN against human
colon cancer. These results suggest that ALLN could become a novel agent for
prevention of colon cancer.