ODN 2007

Name: ODN 2007
SKU: CGON-10
Availability: InStock

For research use only. Not intended for any clinical use.

Cat. No. : CGON-10

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Product Information

Cat. No.	CGON-10
Description	CpG oligodeoxynucleotides (or CpG ODNs) are synthetic oligonucleotides that contain unmethylated CpG motifs. CpG ODN can bind to and activate a Toll-like receptor 9 (TLR9) and leading to strong immunostimulatory effects. So far 3 major classes of CpG ODNs have been identified, based on their structural and biological characteristics, and are designated Type A, Type B, and Type C. Type A ODNs, which feature a central palindromic CpG-containing phosphodiester (PO) structure followed by a phosphorothioate (PS) homopolymeric G-stretch, are robust inducers of interferon-α (IFN-α) production and dendritic cell maturation. Type B ODNs, in contrast, contain a full phosphorothioate backbone with one or more CpG dinucleotides. They strongly activate B cells but stimulate weakly IFN-α secretion. Type C ODNs, combine the properties of both Type A and B, and are characterized by their complete PS backbone and palindromic CpG-containing motifs. Type C ODNs induce strong IFN-α production from pDC and B cell stimulation. ODN 2007 is a type B CpG ODN specific for bovine / porcine TLR9.
Features	• Classification: Type B • Product format: Lyophilized product • Sequence: 5'-tcgtcgttgtcgttttgtcgtt-3' (lower case letters are phosphorothioate) • Specificity: Bovine, Porcine
Storage	Store lyophilized product at -20°C. Upon reconstitution, aliquots should be stored at -20°C and are stable for 6 months. Avoid repeated freeze-thaw cycles.

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In the context of innate immunity modulation, how does ODN 2007 differ in its interaction with TLR9 compared to other CpG oligodeoxynucleotides?

A: ODN 2007 belongs to the class of suppressive or inhibitory oligodeoxynucleotides. Unlike stimulatory CpG ODNs, ODN 2007 is designed to antagonize the effects of TLR9 activation, leading to a dampened immune response by blocking the interaction of stimulatory motifs with TLR9.

Can ODN 2007 influence the polarization of dendritic cells, and if so, what is the anticipated impact on T-helper cell differentiation?

A: Yes, ODN 2007 can impact dendritic cell maturation and function, leading to a potential shift towards a more tolerogenic dendritic cell phenotype. This, in turn, might favor the differentiation of T cells into regulatory T cell phenotypes rather than pro-inflammatory T-helper cell subsets.

What are the potential therapeutic applications of ODN 2007 in autoimmune diseases, and how does its efficacy compare with other TLR9 modulators?

A: ODN 2007 holds promise in autoimmune conditions by suppressing overactive immune responses. Its efficacy may vary based on disease context, but its unique sequence and modifications allow it to dampen immune reactions potentially more effectively than some other TLR9 modulators.

When looking at in vivo administration, what are the pharmacokinetic properties of ODN 2007, especially in terms of distribution, half-life, and excretion?

A: The pharmacokinetics of ODN 2007 would depend on various factors, including the route of administration and the species studied. Generally, ODNs have a relatively short half-life in the bloodstream but can be modified to improve stability. Biodistribution would often favor immune-rich organs, and renal excretion is common for oligonucleotides.

Given its inhibitory nature, how does ODN 2007 impact the cytotoxic activity of natural killer (NK) cells upon TLR9 stimulation?

A: ODN 2007 is likely to reduce the activation and subsequent cytotoxic activity of NK cells in response to TLR9 stimulation by inhibiting the TLR9 signaling pathway, leading to decreased production of activating cytokines and chemokines.

How does ODN 2007 modulate B cell receptor signaling, especially concerning B cell activation and differentiation?

A: ODN 2007, by suppressing TLR9-mediated signals, can modulate B cell receptor signaling to dampen B cell activation. This can lead to reduced antibody production and might influence the differentiation pathway of B cells into specific effector subsets.

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