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Figure 1.

The flowchart of dual-target H1N1 experimental procedures.

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Figure 2.

Structures of the top three de novo derivatives and their corresponding native TCM compounds.

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Table 1.

Docking results of top ten de novo derivatives.

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Figure 3.

Docking pose of TCM candidates and Tamiflu® in N1.

(A) Xylopine_2, (B) Rosmaricine_14, (C) Rosmaricine_15 and (D) Tamiflu®.

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Figure 4.

Correlation between observed and predicted activities (pIC50) of 27 neuraminidase inhibitors using different prediction models.

(A) MLR and (B) SVM.

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Table 2.

N1 activity prediction (pIC50) of top three de novo derivatives by MLR and SVM models.

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Figure 5.

RMSD and total energy profiles of top three de novo derivatives and Tamiflu® in N1 complexes during 20 ns MD simulation.

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Figure 6.

Important locations for ligand-N1 stability (left) and relative spatial arrangements (right) within the N1 protein binding site.

(A) Xylopine_2, (B) Rosmaricine_14, (C) Rosmaricine_15, and (D) Tamiflu®. Ligands are presented in cyan, amino acids in yellow, and hydrogen bond formations in white dashed lines.

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Figure 7.

H-bond distance profile between N1 and TCM candidates or Tamiflu®.

(A) Xylopine_2, (B) Rosmaricine_14, (C) Rosmaricine_15, and (D) Tamiflu®.

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Table 3.

H-bond analysis of top three de novo derivatives and Tamiflu® in N1 during MD simulation.

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Figure 8.

Torsion angles of TCM candidates and Tamiflu in H1 and N1.

(A) Xylopine_2, (B) Rosmaricine_14, (C) Rosmaricine_15 and (D) Tamiflu®. Lower case letters specify the bonds on which the torsion angle were monitored.

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Figure 9.

Protein-ligand interactions of TCM candidates and Tamiflu® in H1.

H1-ligand interactions following MD are illustrated for (A) Xylopine_2, (B) Rosmaricine_14, (C) Rosmaricine_15, and (D) Tamiflu®. Hydrogen bonds are indicated by green dashed lines between the atoms involved. Amino acids forming H-bonds with the ligand are shown in red. Hydrophobic contacts are represented by arcs with spokes radiating towards the ligand atoms they contact. The contacted atoms are shown with spokes radiating back.

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Figure 10.

Protein-ligand interactions of TCM candidates and Tamiflu® in N1.

H1-ligand interactions following MD are illustrated for (A) Xylopine_2, (B) Rosmaricine_14, (C) Rosmaricine_15, and (D) Tamiflu®. Hydrogen bonds are indicated by green dashed lines between the atoms involved. Amino acids forming H-bonds with the ligand are shown in red. Hydrophobic contacts are represented by arcs with spokes radiating towards the ligand atoms they contact. The contacted atoms are shown with spokes radiating back.

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Table 4.

CoMFA and CoMSIA analysis for N1 using PLS.

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Table 5.

Observed and predicted activities of 27 neuraminidase inhibitors by CoMFA and CoMSIA models.

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Figure 11.

CoMFA (left) and CoMSIA (right) models of the N1 conformation with TCM candidates and Tamiflu® at 20 ns simulation time.

Respective CoMFA and CoMSIA models of Xylopine_2 (A, B), Rosmaricine_14 (C, D), Rosmaricine_15 (E, F) and Tamiflu (G, H) are given. Contours in CoMFA represent the following features: favors bulky substituent (green), disfavors bulky substituent (yellow), favors electropositive groups (blue), and disfavors electropositive groups (red). Features in CoMSIA model include: hydrophobic (cyan), hydrophilic (yellow), favorable H-bond acceptor (magenta), unfavorable H-bond acceptor (green), H-bond donor (orange), disfavor H-bond donors (purple).

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Figure 12.

CoMFA (left) and CoMSIA (right) models of the latest N1 conformation with TCM candidates and Tamiflu® at 20 ns simulation time within the H1 protein binding site.

Respective CoMFA and CoMSIA models of Xylopine_2 (A, B), Rosmaricine_14 (C, D), and Rosmaricine_15 (E, F). Contours in CoMFA represent the following features: favors bulky substituent (green), disfavors bulky substituent (yellow), favors electropositive groups (blue), and disfavors electropositive groups (red). Features in CoMSIA model include: hydrophobic (cyan), hydrophilic (yellow), favorable H-bond acceptor (magenta), unfavorable H-bond acceptor (green), H-bond donor (orange), disfavor H-bond donors (purple).

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Figure 13.

Key features of TCM candidates for stable binding in H1 and N1.

(A) Xylopine_2 in H1, (B) Rosmaricine_14 in H1, (C) Rosmaricine_15 in H1, (D) Xylopine_2 in N1, (E) Rosmaricine_14 in N1, and (F) Rosmaricine_15 in N1.

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Table 6.

HA mutation points between the 1918 H1N1 and H1N1/09 viruses.

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Table 7.

NA mutation points between 1918 H1N1 and H1N1/09 viruses.

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