Peptide name : Lactoferricin B

Source/Organism : Temporins family

Linear/Cyclic : Linear

Chirality : L

Peptide length: 15

C-terminal modification: Linear

N-terminal modification : Amidation

Non-natural peptide information: None

Assay type : MTT/MTS assay

Assay time : 48h

Activity : IC50 : 15.5 µM

Cell line : Kelly

Cancer type : Brain tumor

Other activity : Not found

Amino acid composition bar chart :

Molecular mass : 1994.4378 Dalton

Aliphatic index : 0.326

Instability index : 64.3667

Hydrophobicity (GRAVY) : -1.206

Isoelectric point : 11.735

Charge (pH 7) : 5.7472

Aromaticity : 0.2

Molar extinction coefficient (cysteine, cystine): (11000, 11000)

Hydrophobic/hydrophilic ratio : 1.14285714

hydrophobic moment : -0.680

Missing amino acid : H,T,P,I,E,S,D,Y,N,V

Most occurring amino acid : K

Most occurring amino acid frequency : 3

Least occurring amino acid : F

Least occurring amino acid frequency : 1

Secondary structure fraction (Helix, Turn, Sheet): (0.4, 0.0, 0.2)

SMILES Notation: CSCC[C@H](NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](Cc1c[nH]c2ccccc12)NC(=O)[C@H](CCC(N)=O)NC(=O)[C@H](Cc1c[nH]c2ccccc12)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](CS)NC(=O)[C@H](CCCCN)NC(=O)[C@@H](N)Cc1ccccc1)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CC(C)C)C(=O)NCC(=O)N[C@@H](C)C(=O)O

1 : Eliassen LT, et al. The antimicrobial peptide, lactoferricin B, is cytotoxic to neuroblastoma cells in vitro and inhibits xenograft growth in vivo. Int J Cancer. 2006; 119:493-500. doi: 10.1002/ijc.21886

Paper title : The antimicrobial peptide, lactoferricin B, is cytotoxic to neuroblastoma cells in vitro and inhibits xenograft growth in vivo.

Doi : https://doi.org/10.1002/ijc.21886

Abstract : Antimicrobial peptides have been shown to exert cytotoxic activity towards cancer cells through their ability to interact with negatively charged cell membranes. In this study the cytotoxic effect of the antimicrobial peptide, LfcinB was tested in a panel of human neuroblastoma cell lines. LfcinB displayed a selective cytotoxic activity against both MYCN-amplified and non-MYCN-amplified cell lines. Non-transformed fibroblasts were not substantially affected by LfcinB. Treatment of neuroblastoma cells with LfcinB induced rapid destabilization of the cytoplasmic membrane and formation of membrane blebs. Depolarization of the mitochondria membranes and irreversible changes in the mitochondria morphology was also evident. Immuno- and fluorescence-labeled LfcinB revealed that the peptide co-localized with mitochondria. Furthermore, treatment of neuroblastoma cells with LfcinB induced cleavage of caspase-6, -7 and -9 followed by cell death. However, neither addition of the pan-caspase inhibitor, zVAD-fmk, or specific caspase inhibitors could reverse the cytotoxic effect induced by LfcinB. Treatment of established SH-SY-5Y neuroblastoma xenografts with repeated injections of LfcinB resulted in significant tumor growth inhibition. These results revealed a selective destabilizing effect of LfcinB on two important targets in the neuroblastoma cells, the cytoplasmic- and the mitochondria membrane.