Drug Information

Drug (ID: DG01412) and It's Reported Resistant Information

• Name: Palivizumab
• Indication:
  In total 1 Indication(s)
  Respiratory syncytial virus infection [ICD-11: 1C80]; Approved; [1]
• Drug Resistance Disease(s):
  Disease(s) with Resistance Information Validated by in-vivo Model for This Drug (1 diseases)
  Respiratory trac infection [ICD-11: CA45]; [1]
• Target: Respiratory syncytial virus protein F (RSV F); FUS_HRSVA; [1]
• TTD Drug ID: D0A1AS

Type(s) of Resistant Mechanism of This Drug

  ADTT: Aberration of the Drug's Therapeutic Target

Drug Resistance Data Categorized by Their Corresponding Diseases

ICD-12: Respiratory system diseases

Respiratory trac infection [ICD-11: CA45]

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Aberration of the Drug's Therapeutic Target (ADTT)

Key Molecule: Fusion glycoprotein F0 (F) [1]

• Molecule Alteration: Missense mutation; p.N262D
• Resistant Disease: Respiratory trac infection [ICD-11: CA45.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• In Vitro Model: Schistosoma haematobium strain; 6185
• Mechanism Description: Clinical isolates N262D, K272E/M/Q, and S275F/L were reported as possessing mutations in the F protein region palivizumab-binding site (amino acids 258-275) and exhibiting resistance to palivizumab neutralization, while laboratory induced isolates N268I, and K272N/T/M/Q have also been reported.

Key Molecule: Fusion glycoprotein F0 (F) [1]

• Molecule Alteration: Missense mutation; p.N268I
• Resistant Disease: Respiratory trac infection [ICD-11: CA45.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• In Vitro Model: Schistosoma haematobium strain; 6185
• Mechanism Description: Clinical isolates N262D, K272E/M/Q, and S275F/L were reported as possessing mutations in the F protein region palivizumab-binding site (amino acids 258-275) and exhibiting resistance to palivizumab neutralization, while laboratory induced isolates N268I, and K272N/T/M/Q have also been reported.

Key Molecule: Fusion glycoprotein F0 (F) [1]

• Molecule Alteration: Missense mutation; p.K272E
• Resistant Disease: Respiratory trac infection [ICD-11: CA45.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• In Vitro Model: Schistosoma haematobium strain; 6185
• Mechanism Description: Clinical isolates N262D, K272E/M/Q, and S275F/L were reported as possessing mutations in the F protein region palivizumab-binding site (amino acids 258-275) and exhibiting resistance to palivizumab neutralization, while laboratory induced isolates N268I, and K272N/T/M/Q have also been reported.

Key Molecule: Fusion glycoprotein F0 (F) [1]

• Molecule Alteration: Missense mutation; p.K272M
• Resistant Disease: Respiratory trac infection [ICD-11: CA45.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• In Vitro Model: Schistosoma haematobium strain; 6185
• Mechanism Description: Clinical isolates N262D, K272E/M/Q, and S275F/L were reported as possessing mutations in the F protein region palivizumab-binding site (amino acids 258-275) and exhibiting resistance to palivizumab neutralization, while laboratory induced isolates N268I, and K272N/T/M/Q have also been reported.

Key Molecule: Fusion glycoprotein F0 (F) [1]

• Molecule Alteration: Missense mutation; p.K272Q
• Resistant Disease: Respiratory trac infection [ICD-11: CA45.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• In Vitro Model: Schistosoma haematobium strain; 6185
• Mechanism Description: Clinical isolates N262D, K272E/M/Q, and S275F/L were reported as possessing mutations in the F protein region palivizumab-binding site (amino acids 258-275) and exhibiting resistance to palivizumab neutralization, while laboratory induced isolates N268I, and K272N/T/M/Q have also been reported.

Key Molecule: Fusion glycoprotein F0 (F) [1]

• Molecule Alteration: Missense mutation; p.S275F
• Resistant Disease: Respiratory trac infection [ICD-11: CA45.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• In Vitro Model: Schistosoma haematobium strain; 6185
• Mechanism Description: Clinical isolates N262D, K272E/M/Q, and S275F/L were reported as possessing mutations in the F protein region palivizumab-binding site (amino acids 258-275) and exhibiting resistance to palivizumab neutralization, while laboratory induced isolates N268I, and K272N/T/M/Q have also been reported.

Key Molecule: Fusion glycoprotein F0 (F) [1]

• Molecule Alteration: Missense mutation; p.S275L
• Resistant Disease: Respiratory trac infection [ICD-11: CA45.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• In Vitro Model: Schistosoma haematobium strain; 6185
• Mechanism Description: Clinical isolates N262D, K272E/M/Q, and S275F/L were reported as possessing mutations in the F protein region palivizumab-binding site (amino acids 258-275) and exhibiting resistance to palivizumab neutralization, while laboratory induced isolates N268I, and K272N/T/M/Q have also been reported.

Key Molecule: Fusion glycoprotein F0 (F) [1]

• Molecule Alteration: Missense mutation; p.K272N
• Resistant Disease: Respiratory trac infection [ICD-11: CA45.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• In Vitro Model: Schistosoma haematobium strain; 6185
• Mechanism Description: Clinical isolates N262D, K272E/M/Q, and S275F/L were reported as possessing mutations in the F protein region palivizumab-binding site (amino acids 258-275) and exhibiting resistance to palivizumab neutralization, while laboratory induced isolates N268I, and K272N/T/M/Q have also been reported.

Key Molecule: Fusion glycoprotein F0 (F) [1]

• Molecule Alteration: Missense mutation; p.K272T
• Resistant Disease: Respiratory trac infection [ICD-11: CA45.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• In Vitro Model: Schistosoma haematobium strain; 6185
• Mechanism Description: Clinical isolates N262D, K272E/M/Q, and S275F/L were reported as possessing mutations in the F protein region palivizumab-binding site (amino acids 258-275) and exhibiting resistance to palivizumab neutralization, while laboratory induced isolates N268I, and K272N/T/M/Q have also been reported.

Key Molecule: Fusion glycoprotein F0 (F) [1]

• Molecule Alteration: Missense mutation; p.K272M
• Resistant Disease: Respiratory trac infection [ICD-11: CA45.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• In Vitro Model: Schistosoma haematobium strain; 6185
• Mechanism Description: Clinical isolates N262D, K272E/M/Q, and S275F/L were reported as possessing mutations in the F protein region palivizumab-binding site (amino acids 258-275) and exhibiting resistance to palivizumab neutralization, while laboratory induced isolates N268I, and K272N/T/M/Q have also been reported.

Key Molecule: Fusion glycoprotein F0 (F) [1]

• Molecule Alteration: Missense mutation; p.K272Q
• Resistant Disease: Respiratory trac infection [ICD-11: CA45.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• In Vitro Model: Schistosoma haematobium strain; 6185
• Mechanism Description: Clinical isolates N262D, K272E/M/Q, and S275F/L were reported as possessing mutations in the F protein region palivizumab-binding site (amino acids 258-275) and exhibiting resistance to palivizumab neutralization, while laboratory induced isolates N268I, and K272N/T/M/Q have also been reported.

References

• Ref 1: Neutralizing epitopes of RSV and palivizumab resistance in Japan .Fukushima J Med Sci. 2017 Dec 19;63(3):127-134. doi: 10.5387/fms.2017-09. Epub 2017 Sep 1. 10.5387/fms.2017-09