| General information | |
| ACovPid: | ACoVP100117 |
| Trivial Name: | HR2-38 |
| Amino Acids Sequence: | GDISGINASVVNIQKEIDRLNEVAKNLNESLIDLQELG |
| Length: | 38 |
| C-Terminal Modification: | None |
| N-Terminal Modification: | None |
| Chemical Modification: | None |
| Peptide Source: | Middle East respiratory syndrome-related coronavirus (isolate United Kingdom/H123990006/2012) (MERS-CoV) (Betacoronavirus England 1) : 1263720 |
| Source Description: | |
| Against Virus: | |
| Inhibition Value Type: | IC50 |
| Inhibitory Effect: | |
| Inhibitory Unit: | |
| Target Domain Name: | |
| Assay: | Cytopathic effect assay |
| Assay Description: | For the inhibition experiments, Vero E6 cell cultures growing in 96-well microplates were infected with 100X TCID50/well (TCID50 was virus titers causing 50% of CPE on Vero E6 cell monolayer and the TCID50 used in this experiment was 1.263 X e6/ml). The serial 10-fold dilutions of polypeptides (8 repeats for each dilution) were added at the same time as virus adsorption for 1 h at 37℃. Then the mixtures of virus and the polypeptides were replaced by DMEM containing 2% FBS and continued to cultivate for 96 h until calculating the well numbers of CPE and inhibition of CPE. The IC50 was calculated according to Reed–Muench method. |
| Anti-CoV activity in vivo: | |
| Reference: | 15158473 |
| Comment: | The HR2, either as a synthetic peptide or as a GST-fusion polypeptide, is a potent inhibitor of virus entry. The results do show that SARS-CoV follows the general fusion mechanism of class I viruses and this lays the ground for identification of virus fusion/entry inhibitors for this devastating emerging virus. |
| 3D structure: | |
| Structure Experiment Verified: | NO |
| Similar Peptides: | ACoVP100125 ACoVP100119 ACoVP100120 ACoVP100118 ACoVP100389 |