Peptide name : LfcinB-P13

Source/Organism : Synthetic analog of LFcinB

Linear/Cyclic : Linear

Chirality : L

Peptide length: 13

C-terminal modification: Linear

N-terminal modification : Free

Non-natural peptide information:

Assay type : MTT assay

Assay time : 24-h

Activity : IC50 = 41.8 µg/ml

Cell line : SMMC-7721

Cancer type : Liver Cancer

Other activity : Anticancer

Amino acid composition bar chart :

Molecular mass : 1703.1769 Dalton

Aliphatic index : 0.6

Instability index : 118.861

Hydrophobicity (GRAVY) : -1.415

Isoelectric point : 11.745

Charge (pH 7) : 6.7462

Aromaticity : 7.692

Molar extinction coefficient (cysteine, cystine): (1, 0)

Hydrophobic/hydrophilic ratio : 0.8571

hydrophobic moment : -0.070

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

Most occurring amino acid : K

Most occurring amino acid frequency : 4

Least occurring amino acid : C

Least occurring amino acid frequency : 1

Secondary structure fraction (Helix, Turn, Sheet): (53., 7.6, 23.)

SMILES Notation: CSCC[C@H](NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](CCCCN)NC(=O)[C@H](CC(C)C)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](N)CCCCN)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CC(C)C)C(=O)NCC(=O)O

1 : Meng L, et al. Bovine lactoferricin P13 triggers ROS-mediated caspase-dependent apoptosis in SMMC7721 cells. Oncol Lett. 2017; 13:511-517. doi: 10.3892/ol.2016.5415

Paper title : Bovine lactoferricin P13 triggers ROS-mediated caspase-dependent apoptosis in SMMC7721 cells.

Doi : https://doi.org/10.3892/ol.2016.5415

Abstract : Bovine lactoferricin P13 (LfcinB-P13) is a peptide derived from LfcinB. In the present study, the effect of LfcinB-P13 on the human liver cancer cell line SMMC7721 was investigated in vitro and in vivo. The results of the present study indicate that LfcinB-P13 significantly decreased SMMC7721 cell viability in vitro (P=0.032 vs. untreated cells), while exhibiting low cytotoxicity in the wild-type liver cell line L02. In addition, the rate of apoptosis in SMMC7721 cells was significantly increased following treatment with 40 and 60 µg/ml LfcinB-P13 (P=0.0053 vs. the control group), which was associated with an increase in the level of reactive oxygen species (ROS) and the activation of caspase-3 and -9. Furthermore, ROS chelation led to the suppression of LfcinB-P13-mediated caspase-3 and -9 activation in SMMC7721 cells. LfcinB-P13 was demonstrated to markedly inhibit tumor growth in an SMMC7721-xenograft nude mouse model. The results of the present study indicate that LfcinB-P13 is a novel candidate therapeutic agent for the treatment of liver cancer.