ODN 1668 sodium
Based on 2 publication(s) in Google Scholar
ODN 1668 sodium, a class B CpG ODN (oligodeoxynucleotide), is a TLR-9 agonist. ODN 1668 sodium has strong immune regulatory properties, can enhance the level of antibody IgG2 subtype, promote the immune response of T cells and B cells, and can be used in the study of vaccine adjuvants. In addition, CpG ODN 1668 sodium induces an antimicrobial immune response via a CaTLR9 dependent pathway in groupers. Sequence: 5'-tccatgacgttcctgatgct-3’.
For research use only. We do not sell to patients.
- Purity : 98.79%
- Molecular Weight:6364.1 (free acid)
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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)
Publications Citing Use of MedChemExpress (MCE) ODN 1668 sodium
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Biological Activity
Description
IC50 & Target
[4]|
TLR9 |
In Vitro
Non-salt dose:
ODN 1668 (6-60 µg/mL; 12-72 h) increases the synthesis of S100A8/A9, IL-6 and β-galactosidase in mouse bone marrow derived macrophages[1].
ODN 1668 (24 h) promotes the activation and proliferation of B cells and increases the expression of CD86 and CD25[2].
ODN 1668 (0.3-3.0 μM; 4 days) promotes cell growth in anti-CD3-treated CD8+ T cells in a dose-dependent manner[2].
ODN 1668 (0.25-32 μg/mL; 12 h) promotes the proliferation of head kidney lymphocytes and enhances the expression of immune genes[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:Head kidney lymphocytes
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Concentration:2 μg/mL
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Incubation Time:12 h
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Result:Increased the mRNA levels of TLR9, IL-1β, IL-6, IL-8, TNF-α, IFN-γ, MHC-Iα and MHC-IIα.
In Vivo
ODN 1668 (10 nmol ≈ 63.6 μg; injection into the hind footpads; single dose) significantly enhances antibody response in OVA treated mice and increases titers of IgG2a and IgG2b[2].
ODN 1668 (15 μg; intramuscular injection; single dose) improves the antibacterial immunity of Epinephelus laminatus infection, and has the most significant antibacterial activity in liver, spleen and kidney[3].
ODN 1668 (1-5 mg/kg; intraperitoneal/subcutaneous injection; single dose) can cause fever, anorexia and brain inflammation in rats[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male Wistar rats (175-200 g)[4]
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Dosage:1 and 5 mg/kg
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Administration:Intraperitoneal and subcutaneous injection, single dose
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Result:Caused moderate fever and anorexia.
Induced a significant increase of IL-6.
Increased expression of inflammatory genes in the hypothalamus (SOCS3, PGE2, COX-2 and mPGES).
Activated inflammatory transcription factors in the rat brain (STAT3 and NF-IL6).
Chemical Information
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Appearance Solid
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Molecular Weight 6364.1 (free acid)
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Color White to off-white
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SMILES
[DNA, d(P-thio)(T-C-C-A-T-G-A-C-G-T-T-C-C-T-G-A-T-G-C-T), sodium salt]
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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)
Publications (2)
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Journal Impact Factor
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Most Recent
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Nat Methods
Genetically encoded biosensor for monitoring spatiotemporal dynamics of CCR2 ligands in culture and in vivo. [Abstract]2025 Aug;22(8):1731-1741. PMID: 40665002 -
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 (270 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2242 KB)
References
[1]. Rattanaprukskul K, et al. TLR9 Mediates Periodontal Aging by Fostering Senescence and Inflammaging. J Dent Res. 2022 Dec;101(13):1628-1636. [Content Brief]
[2]. Lipford GB, et al. CpG-containing synthetic oligonucleotides promote B and cytotoxic T cell responses to protein antigen: a new class of vaccine adjuvants. Eur J Immunol. 1997 Sep;27(9):2340-4. [Content Brief]
[4]. Damm J, et al. Intraperitoneal and subcutaneous injections of the TLR9 agonist ODN 1668 in rats: brain inflammatory responses are related to peripheral IL-6 rather than interferons. J Neuroimmunol. 2014 Dec 15;277(1-2):105-17. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)