G2-Peptide
G2-Peptide is a 3-O-sulfated heparan sulfate (3-OS HS) binder and antiviral agent. G2-Peptide blocks herpesvirus attachment, entry, cell-to-cell spread and syncytium formation, and reduces viral protein translocation. G2-Peptide exhibits antiviral activity against both HSV-1 and HSV-2. G2-Peptide inhibits neural activity and impairs synapse assembly. G2-Peptide can be used in the research of genital herpes, ocular herpes infection and keratitis.
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- CAS No.: 361443-81-4
- 화학식: C90H155N13O54
- 분자량:2283.25
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
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HSV-2 |
HSV-1 |
In Vitro
G2-Peptide specifically binds to HS on the surface of Vero cells, which is confirmed by the reduced binding observed after heparinase III-mediated HS removal[1].
G2-Peptide (2.5-20 mg/mL; 24 h) shows no cytotoxicity to Vero cells and HCE cells at concentrations of 2.5 mg/mL or lower, while cytotoxicity occurs at higher concentrations[1].
The G2 peptide binds to discrete sites on the axonal surface of mature primary mouse hippocampal neurons[3].
The G2 peptide specifically binds to sites on mouse synaptosomes, which is confirmed by dose-dependent competition assays with unlabeled G2 peptide[3].
G2 peptide (0.1-10 μM) acutely and reversibly suppresses the electrical firing activity of mature primary mouse hippocampal neuron networks in a dose-dependent manner, achieving near-complete silencing at 10 μM[3].
G2-Peptide (0.15-10 mg/well; 1 h) inhibits HSV-2 entry into HeLa cells, with the inhibitory effect reaching its peak at a concentration of 2.5 mg/well[1].
G2-Peptide (2 mg/mL; 30 min) reduces the ability of HSV-2 to invade HeLa cells by approximately 80%, a result confirmed by detecting the decrease in VP16 protein levels[1].
G2-Peptide (0.15-10 mg/mL; 1 h) inhibits plaque formation of HSV-2 in Vero cells, with an IC50 of 1 mg/mL, and reaches the maximum inhibitory effect at a concentration of 2.5 mg/mL[1].
G2-Peptide (0.03125-2 mg/mL; 1 h) dose-dependently inhibits HSV-2-induced cell-cell fusion in CHO-K1 cells expressing HSV-2 entry factors[1].
G2-Peptide (0-0.25 mM; 60 min) potently inhibits HSV-1 entry into CHO-K1 cells expressing 3-OST-3, nectin-1 or HVEM, with an IC50 of 0.02-0.03 mM, and shows no cytotoxicity at concentrations up to 0.5 mM[2].
The G2 peptide significantly reduces glutamate exocytosis evoked at synapses of primary mouse hippocampal neurons[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:HeLa cells
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Concentration:2 mg/mL
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Incubation Time:30 min pretreatment
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Result:Reduced VP16 protein levels by approximately 80% compared to untreated infected cells, indicating significantly reduced viral entry.
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Cell Line:Vero cells, human corneal epithelial (HCE) cells
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Concentration:2.5-20 mg/mL
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Incubation Time:24 h
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Result:Exhibited cytotoxic effects at concentrations above 2.5 mg/mL in both Vero and HCE cells, with reduced viable cell counts and altered cell morphology observed at higher concentrations.
Showed no cytotoxicity at concentrations ≤2.5 mg/mL.
In Vivo
G2-Peptide (0.5 mM) completely blocks the replication and spread of HSV-1 in mouse corneas and maintains corneal epithelial integrity[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c (female)[1]
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Dosage:2 mg/mL
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Administration:intravaginal; single pretreatment dose 1 hour before infection
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Result:Reduced average number of genital HSV-2-infected cell colonies from 15 to 1, representing a ~93% reduction.
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Animal Model:BALB/c mice[2]
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Dosage:0.5 mM
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Administration:single prophylactic dose prior to viral inoculation
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Result:Detected virtually no HSV-1 gD protein expression in corneas at 4 and 7 days post-infection.
Maintained intact corneal epithelium at both 4 and 7 days post-infection.
Chemical Information
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CAS No. 361443-81-4
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분자량 2283.25
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화학식 C90H155N13O54
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Sequence
KVA-{Asn(Galβ(1-4)GlcNAcβ(1-2)Manα(1-3)[Galβ(1-4)GlcNAcβ(1-2)Manα(1-6)]Manβ(1-4)GlcNAcβ(1-4)GlcNAc)}-KT
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Sequence Shortening
Lys-Val-Ala-{Asn(Galβ(1-4)GlcNAcβ(1-2)Manα(1-3)[Galβ(1-4)GlcNAcβ(1-2)Manα(1-6)]Manβ(1-4)GlcNAcβ(1-4)GlcNAc)}-Lys-Thr
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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
[1]. Ali MM, et al. A 3-O-sulfated heparan sulfate binding peptide preferentially targets herpes simplex virus 2-infected cells. Journal of virology. 2012 Jun;86(12):6434-43. [Content Brief]
[2]. Tiwari V, et al. Anti-heparan sulfate peptides that block herpes simplex virus infection in vivo. The Journal of biological chemistry. 2011 Jul 15;286(28):25406-15. [Content Brief]
[3]. Maïza A,, et al. 3-O-sulfated heparan sulfate interactors target synaptic adhesion molecules from neonatal mouse brain and inhibit neural activity and synaptogenesis in vitro. Sci Rep. 2020 Nov 5;10(1):19114. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)