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MG-101 CAS: 110044-82-1

Category: Inhibitors
Product Name: MG-101
Cat No: I000413
CAS No: 110044-82-1
Synonyms: 2-acetamido-4-methyl-N-[4-methyl-1-oxo-1-(1-oxohexan-2-ylamino)pentan-2-yl]pentanamide
Molecular Formula: C20H37N3O4
Molecular Weight: 383.5
InChI: None
Solubility: 10 mM in DMSO
Target: Calpains
IC50: 150 nM (Ki)
Storage: Store at -20°C
CAS 110044-82-1,MG-101
  • Description

MG-101(CAS 110044-82-1), also known as Calpain Inhibitor I and ALLN,  is a potent inhibitor of cysteine proteases including calpain I (Ki = 190 nM), calpain II (Ki = 220 nM), cathepsin B (Ki = 150 nM), and cathepsin L (Ki = 500 pM). Activities of MG-101 includes: (1) reduce colon injury caused by dinitrobenzene sulphonic acid; (2) overcome acquired resistance to TRAIL; (3) protect against atractyloside-induced toxicity. (4). reduce colon injury caused by dinitrobenzene sulphonic acid.

  • Spec

Appearance:white solid powder
Purity: > 98%

  • References

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.

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