U 95133
U 95133 is a non-nucleoside reverse transcriptase inhibitor. U 95133 exhibits activity against both wild-type and mutant HIV-1 reverse transcriptase. U 95133 can be used in studies related to HIV infection.
Nos produits utilisent uniquement pour la recherche. Nous ne vendons pas aux patients.
- CAS No.: 177577-59-2
- Formule: C25H34N6O3S
- Masse moléculaire:498.64
-
Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
In Vitro
U 95133 (compound 16) (0-100 μM) potently inhibits wild-type HIV-1 reverse transcriptase, with an IC50 of 2.2 μM and an inhibition rate of 98% at a concentration of 100 μM[1].
U 95133 potently inhibits HIV-1 replication in human peripheral blood mononuclear cells, with an ED50 of <0.0001 μM[1].
U 95133 (10 minutes) exhibits an IC50 of 0.50 μM against wild-type HIV-1 reverse transcriptase, an IC50 of 1.5 μM against HIV-1 reverse transcriptase P236L, and an IC50 of 1.1 μM against HIV-1 reverse transcriptase Y181C[1].
U 95133 (4 days) potently inhibits the replication of wild-type HIV-1IIIB in MT4 cells with an IC90 of 0.02 μM, and exhibits submicromolar activity against a variety of NNRTI-resistant HIV-1 variants[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
-
CAS No. 177577-59-2
-
Masse moléculaire 498.64
-
Formule C25H34N6O3S
-
SMILES
O=C(N1CCC(CC1)N(C)C2=NC=CC=C2NC(C)(C)C)C3=CC4=C(N3)C=CC(NS(=O)(C)=O)=C4
-
Livraison
Room temperature in continental US; may vary elsewhere.
-
Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
-
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.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)