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Inflammation Peptides

Catalog Go™ peptides

Phospholipase A2s (PLA2) are a family of esterases that initiate the arachidonic acid cascade, resulting in the production of numerous inflammatory mediators. Lipocortins are inhibitors of PLA2. Peptides corresponding to a region of high amino-acid sequence similarity between uteroglobin and lipocortin I have potent PLA2 inhibitory activity. Several synthetic peptides corresponding to the region of highest similarity were designed by Miele, L. et al. The most effective anti-inflammatory nonapeptides, termed antiflammins (AFs) correspond to uteroglobin residues 39–47 and lipocortin-1 residues 246–254. Both peptides are PLA2 inhibitors in-vitro and are effective in a classic model of acute inflammation in carrageenan-induced rat footpad edema. The nonapeptides have anti-inflammatory effects in-vitro and in-vivo. 

The nuclear factor-kappaB, NF-kB/Rel proteins, comprise a family of structurally-related inducible transcription factors which regulate immune and inflammatory responses and apoptosis. These proteins have been linked to numerous diseases, specially cancer, because of the elevated expression of genes encoding antiapoptotic proteins, cytokines, chemokines and cell adhesion molecules. NF-kB family is composed of homo- and heterodimers resulting from the combinatorial association of five polypeptides: p50, p52, p65, cRel and RelB, forming mostly NF-kB1p50/RelAp65 heterodimers. Different combinations of NF-kB/Rel proteins regulate the transcription of different genes and these proteins contain a highly conserved N-terminal DNA-binding/dimerization domain called the Rel Homology Domain (RHD). NF-kB normally resides in the cytoplasm in an inactive form as a complex with IkB kinase, which inhibits NF-kB activity. Phosphorylation of I-kB by IkB kinase (IKK) complex leads to degradation of I-kB and activation of NF-kB allowing NF-kB to translocate to the nucleus and induce target genes. 

Tumor necrosis factor (TNF), a 25 kDa glycoprotein expressed by several types of cells and regulated by lymphocytes, is found in two forms; the TNF-a (cachetin) and TNF-b (lymphotoxin). The cytokine TNF regulates a plethora of vital functions in the whole body, under both physiological and pathophysiological conditions. It is a multifunctional cytokine with effects on anti-tumor activity, immune response, hematopoiesis inflammation, lipid metabolism, coagulation and anorexia. TNF-a is up-regulated in a variety of CNS diseases with diverse etiology and pathological manifestation such as brain trauma, ischemic injury, multiple sclerosis, Alzheimer’s disease, and has been implicated in their pathogenesis. Vascular endothelial cells (EC) are among the principal physiological targets of TNF. In EC, as in other cell types, TNF also elicits a broad spectrum of biological effects. TNF mediates its multiple biological activities through at least two membrane receptors; p55 and p75. p55TNFR plays an exclusive role in mediating TNF-mediated oligodendrocyte apoptosis and primary demyelination.

DescriptionSize Reference USD Qty  
IKKgamma NEMO Binding Domain (NBD) Inhibitory Peptide - 1 mg1 mg AS-61169 176.00Add to cart
NF-kB Inhibitor, SN50 - 1 mg1 mg AS-64660 193.00Add to cart
WP9QY, TNF-a Antagonist - 1 mg1 mg AS-62621 132.00Add to cart
Reference Name Sequence MM (kDa)
AS-62621 WP9QY, TNF-alpha Antagonist YCWSQYLCY (Disulfide bridge: 2-8) 1226,4
AS-61169 IKKg NEMO Binding Domain (NBD) Inhibitory Peptide DRQIKIWFQNRRMKWKKTALDWSWLQTE 3693,3
Reference Name Description
AS-62621 WP9QY, TNF-alpha Antagonist This cyclic peptide is designed to mimic the most critical tumor necrosis factor (TNF) recognition loop on TNF-RI. It prevents interactions of TNF with its receptor. This TNF antagonist is a useful template for the development of small molecular inhibitors to prevent both inflammatory bone destruction and systemic bone loss in rheumatoid arthritis.
AS-61169 IKKg NEMO Binding Domain (NBD) Inhibitory Peptide A cell-permeable synthetic peptide NEMO-binding domain peptide (NBD peptide) corresponding to the NEMO amino-terminal alpha-helical region is shown to block TNF-alpha-induced NF-kB activation. The interaction of IK gammaNEMO with the IKK complex is critical for the activation of the IKK complex and the subsequent activation of NF-kB.
AS-64660 NF-kB Inhibitor, SN50 This is a membrane-translocating peptide sequence consisting of the hydrophobic region of the signal peptide of Kaposi fibroblast growth factor (K-FGF) attached to a NF-kB nuclear localization sequence (NLS).

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