Fosamprenavir-13C6
Fosamprenavir-13C6 is the 13C-labeled Fosamprenavir (HY-78726). Fosamprenavir is an orally active inhibitor targeting HIV-1 protease and is a prodrug of Amprenavir (HY-17430). Fosamprenavir is hydrolyzed into Amprenavir (VX-478) by cell phosphatases in the intestinal epithelium. Amprenavir binds to the active site of HIV-1 protease, preventing the processing of viral gag and gag-pol polyprotein precursors, thereby inhibiting the formation of mature infectious virus particles and exerting anti-HIV-1 infection activity. Fosamprenavir can be used for the study of human immunodeficiency virus (HIV-1) infection.
For research use only. We do not sell to patients.
- Formula: C1913C6H32N3O9PS
- Molecular Weight:587.53
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
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HIV-1 |
In Vitro
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Application
1. This compound can be used as a tracer
2. This compound can be used as an internal standard for quantitative analysis by NMR, GC-MS, or LC-MS.
Chemical Information
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Unlabeled CAS 226700-79-4
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Molecular Weight 587.53
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Formula C1913C6H32N3O9PS
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SMILES
O=C(O[C@@H]1COCC1)N[C@@H](CC2=CC=CC=C2)[C@H](OP(O)(O)=O)CN(S(=O)([13C]3=[13C][13C]=[13C](N)[13C]=[13C]3)=O)CC(C)C
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Synonyms
Amprenavir phosphate-13C6; GW 433908-13C6
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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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.
Purity & Documentation
References
[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216. [Content Brief]
[2]. Hester EK, et al. Fosamprenavir: drug development for adherence. Ann Pharmacother. 2006 Jul-Aug;40(7-8):1301-10. [Content Brief]
[3]. Johnston N, et al. Oral and Inhaled Fosamprenavir Reverses Pepsin-Induced Damage in a Laryngopharyngeal Reflux Mouse Model. Laryngoscope. 2023 Jan;133 Suppl 1(Suppl 1):S1-S11. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)