dbacp03720
General Description
Peptide name : LCP-3
Source/Organism : Plant sources
Linear/Cyclic : Cyclic
Chirality : L
Sequence Information
Sequence : WLHV
Peptide length: 4
C-terminal modification: Cyclic
N-terminal modification : Not found
Non-natural peptide information: None
Activity Information
Assay type : Not specified
Assay time : Not found
Activity : Not found
Cell line : Caco-2
Cancer type : Not specified
Other activity : Not found
Physicochemical Properties
Amino acid composition bar chart :
Molecular mass : 553.6531 Dalton
Aliphatic index : 1.7
Instability index : 38.35
Hydrophobicity (GRAVY) : 0.975
Isoelectric point : 6.7411
Charge (pH 7) : -0.1527
Aromaticity : 0.25
Molar extinction coefficient (cysteine, cystine): (5500, 5500)
Hydrophobic/hydrophilic ratio : 3
hydrophobic moment : 0.8868
Missing amino acid : T,P,I,M,E,K,F,D,N,G,C,R,Q,S,Y,A
Most occurring amino acid : W
Most occurring amino acid frequency : 1
Least occurring amino acid : W
Least occurring amino acid frequency : 1
Structural Information
3D structure :
Secondary structure fraction (Helix, Turn, Sheet): (0.2, 0, 0.7)
SMILES Notation: CC(C)C[C@H](NC(=O)[C@@H](N)Cc1c[nH]c2ccccc12)C(=O)N[C@@H](Cc1c[nH]cn1)C(=O)N[C@H](C(=O)O)C(C)C
Secondary Structure :
| Method | Prediction |
|---|---|
| GOR | EEEE |
| Chou-Fasman (CF) | CCCC |
| Neural Network (NN) | HEHH |
| Joint/Consensus | CCCC |
Molecular Descriptors and ADMET Properties
Molecular Descriptors: Click here to download
ADMET Properties: Click here to download
Cross Referencing databases
CancerPPD : Not available
ApIAPDB : Not available
CancerPPD2 ID : Not available
Reference
1 : Preetham HD, et al. Identification of β-aminopyrrolidine containing peptides as β-amyloid aggregation inhibitors for Alzheimer's disease. J Pept Sci. 2022; 28:e3386. doi: 10.1002/psc.3386
Literature
Paper title : Identification of β-aminopyrrolidine containing peptides as β-amyloid aggregation inhibitors for Alzheimer's disease.
Doi : https://doi.org/10.1002/psc.3386
Abstract : Alzheimer's disease (AD) is caused by a series of events initiated by the production and aggregation of the amyloid β-protein (Aβ). In the early stages of the disease, Aβ is released in a soluble form then progressively forms oligomeric, multimeric, and fibrillar aggregates, triggering neurodegeneration. Thus, development of inhibitors that initiate reverse Aβ aggregation is thought to be a logical approach in treating AD. In this context, we developed β-aminopyrrolidine containing 12 mer peptide 3 which is very potent in inhibiting the Aβ aggregation and also reducing Aβ(42)-induced cytotoxicity.