U-75875
U-75875 is a HIV-1 protease inhibitor. U-75875 can block Gag-Pol protein processing and viral maturation and replication. U-75875 can be used for the research of infection.
For research use only. We do not sell to patients.
- CAS No.: 112190-24-6
- Formula: C45H61N7O7
- Molecular Weight:812.01
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| CV-1 | IC50 |
0.2 μM
Compound: U-75875
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Antiviral efficacy measured by a hybrid HIV-l/vaccinia virus infected monkey cell line (HIV- l/vVK-1 infected CV- 1) which produces HIV-1 gag-pol derived polyproteins
Antiviral efficacy measured by a hybrid HIV-l/vaccinia virus infected monkey cell line (HIV- l/vVK-1 infected CV- 1) which produces HIV-1 gag-pol derived polyproteins
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10.1016/S0960-894X(00)80673-3 |
In Vitro
U-75875 shows an IC50 of 100 μM to SIV-infected PBMC cultures[1].
U-75875 (0.1 μM, 2 h) reduces HIV-1 p24 Ag levels in human fetal brain cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Rhesus monkeys infected with SIV Delta B670[1]
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Dosage:7 and 20 mg/kg
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Administration:Intravenously injection, daily for 26 days
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Result:Decreased the level of proviral DNA in peripheral blood mononuclear cells.
Decreased titer of infectious virus.
Chemical Information
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CAS No. 112190-24-6
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Molecular Weight 812.01
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Formula C45H61N7O7
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SMILES
O=C(NCC1=CC=CC=N1)[C@H]([C@@H](C)CC)NC([C@H](C(C)C)[C@@H](O)[C@H](O)[C@H](CC2CCCCC2)NC([C@H](CC3=CN=CN3)NC(COC4=CC=CC5=C4C=CC=C5)=O)=O)=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.
Purity & Documentation
References
[1]. Martin LN, et al. Effects of U-75875, a peptidomimetic inhibitor of retroviral proteases, on simian immunodeficiency virus infection in rhesus monkeys. Antimicrob Agents Chemother. 1994 Jun;38(6):1277-83. [Content Brief]
[2]. Peterson PK, et al. Anti-human immunodeficiency virus type 1 activities of U-90152 and U-75875 in human brain cell cultures. Antimicrob Agents Chemother. 1994 Oct;38(10):2465-8. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)