HIV-IN-16
HIV-IN-16 is a HIV replication inhibitor with an EC50 of 25 pM, and shows no activity in inducing CYP2B6. HIV-IN-16 inhibits HIV replication. HIV-IN-16 can be used in studies related to HIV infection and human immunodeficiency diseases.
For research use only. We do not sell to patients.
- CAS No.: 2570323-59-8
- Formula: C37H29ClF9N9O5S
- Molecular Weight:918.19
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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]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
HIV 25 pM (EC50) |
In Vitro
HIV-IN-16 (Example 1) (1 μM; up to 60 min) exhibits high stability in liver microsomes, with a half-life of >120 minutes in human, rat and monkey liver microsomes, and a half-life of 105 minutes in dog liver microsomes[1].
HIV-IN-16 exhibits high stability in human hepatocytes, with a half-life of over 480 min and an intrinsic clearance rate of 0.312 mL/min/g liver[1].
HIV-IN-16 does not induce CYP2B6 expression in primary human hepatocytes and shows no cytotoxicity at the highest concentration of 30 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
Chemical Information
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CAS No. 2570323-59-8
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Molecular Weight 918.19
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Formula C37H29ClF9N9O5S
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SMILES
O=C1C2=C(N=C(C(CC3=CC(F)=CC(F)=C3)NC(CN4N=C(C(F)F)C5=C4C(F)(C6CC56)F)=O)N1C7=CC=C(C8=C7N(C)N=C8NS(=O)(C)=O)Cl)N=C(OCCC(F)(F)F)C=C2
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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)
HIV-IN-16 Related Classifications
HY-184864 Related Classifications
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