H-Gly-Pro-Gly-NH2
H-Gly-Pro-Gly-NH2 is a tripeptide that inhibits HIV-1 replication. H-Gly-Pro-Gly-NH2 inhibits the activity of HIV-1 IIIB and HIV-2 ROD with EC50 values of 35 µM and 30 µM, respectively. H-Gly Pro Gly NH2 inhibits HIV-1 replication in vitro by interfering with capsid formation. H-Gly Pro Gly NH2 has antiviral activity and can be used for virus research.
For research use only. We do not sell to patients.
- CAS No.: 141497-12-3
- Formula: C9H16N4O3
- Molecular Weight:228.25
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Storage:
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
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[3]|
HIV (IIIB) 35 μM (EC50) |
HIV-2 (ROD) 30 μM (EC50) |
In Vitro
H-Gly-Pro-Gly-NH2 (5, 20 and 100 µM) shows antiviral activities in HUT78 cells infected with HIV-1 SF-2[1].
H-Gly-Pro-Gly-NH2 (100 µM) destroys the capsid of HIV-1 virus particles in ACH-2 cells[1].
Antiviral activity of H-Gly-Pro-Gly-NH2 against clinical HIV-1[2]
| T215Y/F | K70R | M184V | L74V | T69D | |||||||||
| Mean IC50 (µM) | 16 | 17 | 20 | 12 | 17 | ||||||||
| K103N | Y181C | G48V | L90M | V82A/T | M46I/L | |
| Mean IC50 (µM) | 13 | 21 | 16 | 18 | 16 | 17 |
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. 141497-12-3
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Molecular Weight 228.25
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Formula C9H16N4O3
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Sequence
H-Gly-Pro-Gly-NH2
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Sequence Shortening
GPG-NH2
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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]. Höglund S, et al. Tripeptide interference with human immunodeficiency virus type 1 morphogenesis. Antimicrob Agents Chemother. 2002 Nov;46(11):3597-605. [Content Brief]
[3]. Balzarini J, et al. Obligatory involvement of CD26/dipeptidyl peptidase IV in the activation of the antiretroviral tripeptide glycylprolylglycinamide (GPG-NH(2)). Int J Biochem Cell Biol. 2004 Sep;36(9):1848-59. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
H-Gly-Pro-Gly-NH2 Related Classifications
HY-P4292 Related Classifications
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