SRI-37264
SRI-37264 is a HIV-1 Nef inhibitor with a Kd value of 162 nM. SRI-37264 binds directly to HIV-1 Nef, disrupts the Nef·MHC-I·AP-1 μ1 complex, and inhibits the Nef-dependent enhancement of HIV-1 infectivity. SRI-37264 restores MHC-I expression on the surface of HIV-infected primary cells. SRI-37264 inhibits HIV-1 replication in primary macrophages. SRI-37264 is applicable to research related to HIV-1 infection.
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- CAS No.: 2358714-71-1
- 화학식: C17H14ClN3O3S
- 분자량:375.83
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
In Vitro
SRI-37264 (3-48 h) inhibits Nef-dependent HIV-1 infectivity in TZM-bl cells with an IC50 of 0.32 μM and has no detectable cytotoxicity (CC50 > 100 μM)[1].
SRI-37264 (1.0 μM; 24 h) partially restores cell-surface MHC-I expression by 15.9% in HIV-1-infected primary HLA-A2+ CD8-depleted PBMCs[1].
SRI-37264 (125 μM; 25 min) at a 5-fold molar excess disrupts preformed recombinant Nef-CD·AP-1 μ1 complexes in solution[1].
SRI-37264 has excellent metabolic stability with a half-life > 2 h in mouse and human liver microsomes[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
| Species | Dose | Route | T1/2 |
|---|---|---|---|
| Mice[1] | 1 mg/kg | i.v. | 40 min |
Chemical Information
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CAS No. 2358714-71-1
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분자량 375.83
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화학식 C17H14ClN3O3S
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SMILES
O=C1C2=CC=CN=C2SN1C3=CC=C(C(C(N4CCOCC4)=O)=C3)Cl
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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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.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)