(R)-MC2571
(R)-MC2571 is a non-nucleoside HIV-1 reverse transcriptase inhibitor with an ID50 of 2 nM against wild-type HIV-1 reverse transcriptase. (R)-MC2571 also inhibits the K103N mutant reverse transcriptase with an ID50 of 14 nM. (R)-MC2571 exhibits anti-HIV-1 activity, inhibiting wild-type HIV-1 and multidrug-resistant clinical isolates at subnanomolar concentrations in cells. (R)-MC2571 can be used for research related to HIV-1 infection.
For research use only. We do not sell to patients.
- Formula: C15H16ClFN2OS2
- Molecular Weight:358.88
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
HIV-1 NL4-3 0.3 nM (EC50) |
HIV-1 (Y181C) 15 nM (EC50) |
HIV-1 (Y188L) 55 nM (EC50) |
HIV-1 (K103N) 4 nM (EC50) |
HIV-1 (K103N+Y181C) 7 nM (EC50) |
In Vitro
(R)-MC2571 (Compound (R)-17d) (5 days) inhibited wild-type HIV-1 NL4-3 in MT-4 cells with an EC50 of 0.3 nM, inhibited IRLL98 with an EC50 of 0.9 nM; and maintained low nanomolar activity against K103N and K103N + Y181C mutant strains[1].
(R)-MC2571 (20 min) inhibits wild-type HIV-1 reverse transcriptase with an ID50 of 2 nM, and against K103N RT, the ID50 is 14 nM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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Molecular Weight 358.88
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Formula C15H16ClFN2OS2
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SMILES
ClC1=CC=CC(F)=C1[C@@H](C)C2=C(C)C(NC(SCSC)=N2)=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)
Keywords
- (R)-MC2571
- Reverse Transcriptase
- HIV
- HIV-1 infection
- HIV-1 reverse transcriptase
- K103N mutant reverse transcriptase
- L100I mutant reverse transcriptase
- MT-4 cells
- RNA-dependent DNA polymerase
- Y181I mutant reverse transcriptase
- anti-HIV-1 activity
- non-nucleoside reverse transcriptase inhibitor
- wild-type HIV-1
- Inhibitor
- inhibitor
- inhibit