Fosalvudine tidoxil
Fosalvudine tidoxil is an orally active nucleoside reverse transcriptase inhibitor (NRTI). Fosalvudine tidoxil is a prodrug derived from Alovudine (HY-B1516). Fosalvudine tidoxil is less toxic than Alovudine and can be used for the research of HIV-1 infection.
For research use only. We do not sell to patients.
- CAS No.: 763903-67-9
- Formula: C35H64FN2O8PS
- Molecular Weight:722.93
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
Nucleoside reverse transcriptase[1]
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley rats[1]
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Dosage:15, 40, or 100 mg/kg/day
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Administration:Oral gavage, 8 weeks
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Result:Induced significant mtDNA depletion. At doses of 15, 40, and 100 mg/kg, the mean hepatic mtDNA values were 62, 64, and 47% of control values, respectively.
Chemical Information
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CAS No. 763903-67-9
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Molecular Weight 722.93
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Formula C35H64FN2O8PS
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SMILES
O=P(OC[C@H]1O[C@@H](N(C(N2)=O)C=C(C)C2=O)C[C@@H]1F)(OCC(OCCCCCCCCCC)CSCCCCCCCCCCCC)O
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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
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)