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AF 12198 is a potent and selective antagonist for the human type I interleukin-1 (IL-1) receptor (IC50 values are 8 nM, > 6.7 mM and > 200 mM for human type I, human type II and murine type I IL-1 receptors respectively). Blocks IL-1-induced expression of ICAM-1 and E-selectin in HUVECs and IL-1β induction of IL-8 in human dermal fibroblasts. Reduces IL-1β-induced IL-6 production and exhibits anti-inflammatory activity in vivo.
(Modifications: Phe-1 = N-terminal Ac, X = Aze, Leu-15 = C-terminal amide)
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solubility||Soluble to 1 mg/ml in 10% ethanol/PBS|
References are publications that support the biological activity of the product.
Aimbire et al (2008) Low level laser therapy (LLLT) decreases pulmonary microvascular leakage, neutrophil influx and IL-1β levels in airway and lung from rat subjected to LPS-induced inflammation. Inflammation 31 189 PMID: 18421573
Akeson et al (1996) AF12198, a novel low molecular weight antagonist, selectively binds the human type I interleukin (IL)-1 receptor and blocks in vivo responses to IL-1. J.Biol.Chem. 271 30517 PMID: 8940020
If you know of a relevant reference for AF 12198, please let us know.
Keywords: AF 12198, AF 12198 supplier, Potent, selective, human, type, I, IL-1, receptors, antagonists, IL, Interleukins, Cytokines, AF12198, Cytokine, Receptors, 1793, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for AF 12198 include:
Lin et al (2010) Interleukin-1β expression is required for lysophosphatidic Acid-induced lymphangiogenesis in human umbilical vein endothelial cells. J Psychopharmacol 2011 351010 PMID: 21151531
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The antagonist for the human type I interleukin-1 (IL-1) receptor was used in studies exploring immunogenic cell death induced by chemotherapeutics. Results were consistent.
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Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.