ADI-14359
ADI-14359 is an antibody that binds to RSV postF, with a KD value of 387 nM, and exhibits non-neutralizing activity. ADI-14359 binds to antigenic site I on RSV postF through interactions of its conserved CDR H3 motif, germline-encoded IGKV1-39 light chain residues and heavy chain residues, where the light chain mediates preferential binding to postF by conflicting with the rearranged preF region. ADI-14359 can be used in studies related to respiratory syncytial virus (RSV) infection.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Biologische Aktivität
Beschreibung
Isotype
Human IgG1 kappa
Recommend Isotype Controls
Species Reactivity
Human
In Vitro
ADI-14359 binds to epitope I of RSV postF via convergent CDR H3 motifs and germline-encoded features of its IGKV1-39 light chain and IGHV2-70 heavy chain, with key interactions mediated by specific hydrogen bonds and electrostatic contacts[1].
ADI-14359 (6.25 nM-1600 nM) binds to RSV postF with a KD value of 387 nM; the heavy chain Arg50 residue and postF Lys390 residue are critical for this interaction, as disruption of these residues significantly reduces or even completely abolishes binding[1].
ADI-14359 recognizes antigenic epitope I on RSV F, preferentially binds to the post-fusion conformation, and does not neutralize RSV[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Accession
A0A0X8XRK2
Target
RSV-F
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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Product Image
Anwendung
ELISA, FACS, Functional assay
Chemical Information
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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