Rpi-856 A
Rpi-856 A is a competitive inhibitor of HIV-1 protease and HTLV-I protease, with an IC50 of 37 nM against HIV-1 protease and an IC50 of 27 nM against HTLV-I protease. Rpi-856 A inhibits Pepsin with an IC50 of 1.9 μM. Rpi-856 A does not inhibit chymosin, trypsin, chymotrypsin, papain, bromelain, thermolysin, prolyl endopeptidase, carboxypeptidase A or carboxypeptidase B. Rpi-856 A can be used in the research of acquired immunodeficiency syndrome (AIDS) and related diseases, as well as HIV infection.
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- CAS No.: 157381-54-9
- 화학식: C43H61N7O13
- 분자량:883.98
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocol
- 순도&문서
- References
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Help & FAQs
Biological Activity
제품 설명
In Vitro
Rpi-856 A (3 h) competitively inhibits recombinant HIV-1 protease (expressed in Escherichia coli MM294 (DE3)/pHIV7004), with a Ki of 13 nM and an IC50 of 37 nM[1].
Rpi-856 A (3 h) competitively inhibits recombinant HTLV-I protease (expressed in Escherichia coli MM294 (DE3)/pHTI7707) with an IC50 of 27 nM[1].
Rpi-856 potently inhibits HIV-1 protease in cell-free biochemical assays, with an IC50 value of 37 nM[2].
Rpi-856 A inhibits porcine pepsin with an IC50 of 1.9 μM, and its activity is weaker than that against retroviral protease[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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CAS No. 157381-54-9
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분자량 883.98
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화학식 C43H61N7O13
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Sequence
Val-{Gly(2-(3,5-dihydroxyphenyl))}-Leu-{2-oxo-4-phenyl-3-aminobutanoyl}-Val-Val-Asp
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Sequence Shortening
V-{Gly(2-(3,5-dihydroxyphenyl))}-L-{2-oxo-4-phenyl-3-aminobutanoic acid}-VVD
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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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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)
Rpi-856 A Related Classifications
HY-P1981 Related Classifications
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