G3-YSD
Based on 1 Customer Validation
G3-YSD is a cGAS agonist. G3-YSD directly interacts with cGAS to enhance its enzymatic activity, promote the conversion of ATP and GTP into cGAMP, and trigger STING-dependent IFN-α/β secretion. G3-YSD acts as a viral mimic to replace actual viral DNA. G3-YSD is applicable to research related to long COVID and type 1 human immunodeficiency virus infection.
For research use only. We do not sell to patients.
- Purity : 98.37%
- CAS No.: 2780391-08-2
- Molecular Weight:8088.29
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Storage:
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Biological Activity
Description
In Vitro
Stimulation with G3-YSD (1 mg/mL; 24 h) induces significant type I interferon (IFN-I) biological activity in peripheral blood mononuclear cells (PBMCs) from Microx long COVID patients[1].
G3-YSD (0.8 µg/mL; 20 h) potently induces IFN-α secretion from Chloroquine (HY-17589A)-treated human peripheral blood mononuclear cells in a guanosine-dependent manner. It maintains stable activity across a core double-strand length range of 12-28 bp and tolerates small mismatches/bulges in the core double strand[2].
G3-YSD (0.8 µg/mL; 20-36 h) potently induces IFN-α secretion in primary human monocytes and monocyte-derived macrophages, and its activity in macrophages is comparable to that of long-chain HIV-1 ssDNA[2].
G3-YSD (1.3 µg/mL; 20 h) induces IFN-α/β secretion in the human monocyte cell line THP-1 solely via the cGAS-STING signaling axis[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. 2780391-08-2
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Appearance Solid
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Molecular Weight 8088.29
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Color White to off-white
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SMILES
[DNA, d(G-G-G-T-A-T-A-T-A-T-A-T-G-C-A-T-A-T-A-T-A-T-A-G-G-G)]
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
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
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Data Sheet (263 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2242 KB)
References
[1]. Humer B, et al. Exaggerated IFN-I Response in Long COVID PBMCs Following Exposure to Viral Mimics. J Clin Immunol. 2025;46(1):5. Published 2025 Dec 10. [Content Brief]
[2]. Herzner AM, et al. Sequence-specific activation of the DNA sensor cGAS by Y-form DNA structures as found in primary HIV-1 cDNA. Nat Immunol. 2015;16(10):1025-1033. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)