GRL-142
GRL-142 is a potent HIV-1 protease inhibitor capable of crossing the blood-brain barrier. GRL-142 exhibits extremely high inhibitory activity against both wild-type and multidrug-resistant strains (IC50=0.0094 nM). GRL-142 acts synergistically with the P2/P2' segments via a unique scaffold binding mechanism, utilizes fluorine-mediated stable interactions to maintain its bioactive conformation, adapts to p51 HIV-1 protease mutants, and maintains the flap-closed state by directly acting on the flap tip residues. GRL-142 disrupts the flap-water hydrogen bond network of wild-type protease, thereby effectively blocking viral replication. GRL-142 can be used to study HIV-1 infection and the associated neurocognitive disorder (HAND).
For research use only. We do not sell to patients.
- Formula: C34H40F2N4O7S2
- Molecular Weight:718.83
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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
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HIV-1 |
In Vitro
GRL-142 exhibits ultra-potent inhibitory activity against wild-type HIV-1 (Ki=14 pM), and maintains high activity against most drug-resistant HIV-1 strains, but shows a significant reduction in activity against highly drug-resistant p51 strains (with a maximum reduction of 436-fold)[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 718.83
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Formula C34H40F2N4O7S2
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SMILES
[H][C@]1(C2CO[C@@]3(OCC4(C23)CC41)[H])OC(N[C@H]([C@@H](CN(S(=O)(C5=CC6=C(N=C(S6)NC7CC7)C=C5)=O)CC(C)C)O)CC8=CC(F)=CC(F)=C8)=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.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
GRL-142 Related Classifications
HY-181888 Related Classifications
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Keywords
- GRL-142
- GRL142
- GRL 142
- HIV
- HIV Protease
- flap-tip residue
- flap-water hydrogen bonding networks
- p51 HIV-1 protease variant
- drug-resistant HIV-1 strains
- blood-brain barrier
- HIV-associated neurocognitive disorders
- S2/S2' subsites
- multidrug-resistant HIV-1 protease
- HIV-1 infection
- wild-type HIV-1 protease
- Inhibitor
- inhibitor
- inhibit