RDEA 806
RDEA 806 is an orally effective non-nucleoside reverse transcriptase (NNRT) inhibitor that exhibits potent in vitro inhibitory activity against wild-type HIV-1 (EC50 = 1.7 ng/mL) and NNRTI-resistant HIV-1. RDEA 806 rapidly reduces HIV-1 RNA viral load in vivo. RDEA 806 has a favorable biosafety profile. RDEA 806 can be used for research related to HIV-1 infection.
For research use only. We do not sell to patients.
- CAS No.: 878670-61-2
- Formula: C24H18BrClN4O3S
- Molecular Weight:557.85
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Biological Activity
-
Chemical Information
- Protocols
- Purity & Documentation
- References
-
Help & FAQs
Biological Activity
Description
In Vitro
RDEA 806 exhibits potent in vitro activity against wild-type HIV-1 with an EC50 of 1.7 ng/mL and retains activity against common NNRTI-resistant mutants[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
-
CAS No. 878670-61-2
-
Molecular Weight 557.85
-
Formula C24H18BrClN4O3S
-
SMILES
ClC(C=C(C(O)=O)C=C1)=C1NC(CSC2=NN=C(Br)N2C3=CC=C(C4CC4)C5=C3C=CC=C5)=O
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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)
RDEA 806 Related Classifications
HY-105249 Related Classifications
Powered by Bioz