PGLa
PGLa, a 21-residue peptide, is an antimicrobial peptide. PGLa is a member of the magainin family of antibiotic peptides found in frog skin and its secretions.
For research use only. We do not sell to patients.
- CAS No.: 102068-15-5
- Formula: C88H162N26O22S
- Molecular Weight:1968.45
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Antibiotic Isoforms
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Biological Activity
Description
IC50 & Target
Anti-bacteria[1]
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| CEM-SS | EC50 |
>50.8 μM
Compound: PGLa
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Antiviral activity against HIV1 3B infected in human CEM-SS cells assessed as inhibition of viral replication after 6 days by XTT assay
Antiviral activity against HIV1 3B infected in human CEM-SS cells assessed as inhibition of viral replication after 6 days by XTT assay
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[PMID: 20086159] |
In Vitro
PGLa is a peptide starting with a glycine and ending with a leucine amide[1].
PGLa is bacteriostatic against both Gram-positive and Gram-negative bacteria with MIC values of 64 and 32 mg/L against S. aureus and E. coli, respectively[2].
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. 102068-15-5
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Molecular Weight 1968.45
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Formula C88H162N26O22S
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Sequence
Gly-Met-Ala-Ser-Lys-Ala-Gly-Ala-Ile-Ala-Gly-Lys-Ile-Ala-Lys-Val-Ala-Leu-Lys-Ala-Leu-NH2
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Sequence Shortening
GMASKAGAIAGKIAKVALKAL-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]. Bechinger B, et al. Structure and dynamics of the antibiotic peptide PGLa in membranes by solution and solid-state nuclear magnetic resonance spectroscopy. Biophys J. 1998 Feb;74(2 Pt 1):981-7. [Content Brief]
[2]. Radchenko DS, et al. Does a methionine-to-norleucine substitution in PGLa influence peptide-membrane interactions? Biochim Biophys Acta. 2016 Sep;1858(9):2019-27. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)