ODN 2216 

ODN 2216 is a type A CpG oligodeoxynucleotide vaccine adjuvant and a TLR9 agonist. ODN 2216 interacts with TLR9 in the lysosomes of CD4⁺ T cells and activates feedback-dependent signaling pathways. ODN 2216 induces the production of type I interferons, IL-6 and TGF-β via the IRAK4/IRF7 axis, while increasing intracellular ATP levels. ODN 2216 not only induces the differentiation of CD4⁺ T cells into anti-inflammatory Th3-like regulatory phenotypes to inhibit autologous proliferation, but also enhances the specific CD8⁺ T cell-mediated cytotoxicity against Mammaglobin-A in breast cancer cells. ODN 2216 is widely used in studies related to breast cancer and systemic lupus erythematosus^[1][2][3].

ODN 2216 (10 μM; 16 h pre-treatment, 9 days co-culture, 48 h cytotoxicity assay) does not significantly enhance MamA2.1-specific activation of primary HLA-A2⁺ CD8⁺ T cells or subsequent MamA-specific cytotoxicity against AU565 breast cancer cells compared to MamA2.1 peptide alone^[1].
ODN 2216 (3 μM; 24 h) induces TLR9-mediated IFN-α secretion by human PBMCs after 24 hours of incubation at a concentration of 3 μM^[2].
ODN 2216 (0.5-10 μM; 4 days) dose-dependently increases intracellular ATP and IL-6 levels in human PBMCs^[2].
ODN 2216 (500 ng/mL; 14 hours) physically interacts with intracellular TLR9 in lysosomes of human CD4⁺ CD25^- T cells following 14-hour incubation with 500 ng/mL ODN 2216 FITC^[3].
ODN 2216 (500 ng/mL; 72 hours) induced increased proliferation of human CD4⁺ CD25^- T cells, which is dependent on TLR9 signaling via TLR9, MyD88, IRAK1, and TRAF3, but not IRF7^[3].
ODN 2216 (500 ng/mL; 48 hours) treated human CD4⁺ CD25^- T cells acquire dose-dependent suppressive activity against untreated autologous CD4⁺ T cells, with maximum suppression (48.57%) at a 4:1 suppressor:responder ratio^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

ODN 2216 (100 μg/mouse; i.p.; 4 total doses at 2-week intervals) acts as an adjuvant to MamA2.1 peptide vaccination in HLA-A2/C57BL/6J mice, enhancing peritoneal macrophage IL-12p70, TLR9, and TLR6 expression, and increasing MamA2.1-specific CD8⁺ T cell activation, but does not significantly reduce AU565 breast tumor growth in SCID/beige mice following adoptive T cell transfer^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

6432.00

332437-00-0

Solid

White to off-white

DNA, d(G-sp-G-sp-G-G-G-A-C-G-A-T-C-G-T-C-G-sp-G-sp-G-sp-G-sp-G-sp-G)

[DNA, d(G-sp-G-sp-G-G-G-A-C-G-A-T-C-G-T-C-G-sp-G-sp-G-sp-G-sp-G-sp-G)]

Room temperature in continental US; may vary elsewhere.

-20°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

• [1]. Krug A, et al. Identification of CpG oligonucleotide sequences with high induction of IFN-alpha/beta in plasmacytoid dendritic cells. Eur J Immunol. 2001 Jul;31(7):2154-63.  [Content Brief]

  [2]. Okada T, et al. Murine thymic plasmacytoid dendritic cells. Eur J Immunol. 2003 Apr;33(4):1012-9.  [Content Brief]

  [3]. Huang L, et al. CpG-based immunotherapy impairs antitumor activity of BRAF inhibitors in a B-cell-dependent manner. Oncogene. 2017 Jul 13;36(28):4081-4086.  [Content Brief]

  [4]. He Y, et al. Hepatic mitochondrial DNA/Toll-like receptor 9/MicroRNA-223 forms a negative feedback loop to limit neutrophil overactivation and acetaminophen hepatotoxicity in mice. Hepatology. 2017 Jul;66(1):220-234.  [Content Brief]

  [5]. Li Y, et al. A novel antagonist of TLR9 blocking all classes of immunostimulatory CpG-ODNs. Vaccine. 2011 Mar 3;29(11):2193-8.  [Content Brief]