Amthamine dihydrobromide - CAS 142457-00-9
Category: Inhibitor
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Histamine Receptor
Amthamine dihydrobromide is the dihydrobromide salt of amthamine, which is a highly selective histamine H2 receptor agonist. It is a weak antagonist at H3 and has no activity at H1 receptors. It decreases myogenic tone and induces vasodilation of cerebral arteries in vitro. It can be used in the suppression of the release of serotonin and H2 receptor-mediated eosinophil peroxidase (EPO). It has been used to study the effect of mast cells on T regulatory cell function.
≥99% by HPLC
5-(2-Aminoethyl)-4-methylthiazol-2-amine Dihydrobromide; A 4730 Dihydrobromide; 2-Amino-4-methyl-5-thiazoleethanamine dihydrobromide; 2-Amino-5-(2-aminoethyl)-4-methylthiazole dihydrobromide
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1.Mast cells down-regulate CD4+CD25+ T regulatory cell suppressor function via histamine H1 receptor interaction.
Forward NA;Furlong SJ;Yang Y;Lin TJ;Hoskin DW J Immunol. 2009 Sep 1;183(5):3014-22. doi: 10.4049/jimmunol.0802509. Epub 2009 Aug 10.
Mast cells promote both innate and acquired immune responses, but little is known about the effect of mast cells on T regulatory (T(reg)) cell function. In this study, we show for the first time that the capacity of murine CD4(+)CD25(+) T(reg) cells to suppress in vitro proliferation by CD4(+)CD25(-) T responder (T(resp)) cells in response to anti-CD3/anti-CD28 mAb-coated beads was reduced in the presence of syngeneic bone marrow-derived mast cells (BMMC) activated by FcepsilonR cross-linking. Activated BMMC culture supernatants or exogenous histamine also inhibited T(reg) cell suppressor function while the histamine H1 receptor-specific antagonist loratadine, but not the H2 receptor-specific antagonist famotidine, restored T(reg) cell suppressor function in the presence of activated BMMC or activated BMMC culture supernatants. Moreover, treatment of T(reg) cells with loratadine, but not famotidine, rescued T(reg) cell suppressor function in the presence of exogenous histamine. In addition, the H1 receptor-specific agonist 2-pyridylethylamine dihydrochloride inhibited T(reg) cell suppressor function to an extent that was comparable to histamine, whereas the H2 receptor-specific agonist amthamine dihydrobromide was without effect.
2.The role of histamine in the regulation of the viability, proliferation and transforming growth factor β1 secretion of rat wound fibroblasts.
Wolak M;Bojanowska E;Staszewska T;Ciosek J;Juszczak M;Drobnik J Pharmacol Rep. 2017 Apr;69(2):314-321. doi: 10.1016/j.pharep.2016.11.006. Epub 2016 Nov 15.
BACKGROUND: ;Inflammation mediators play a regulatory role in repair processes. The study will examine the influence of histamine on wound fibroblast metabolic activity, viability, proliferation, and TGFβ1 secretion. The study also will identify the histamine receptor involved in regulation of the tested repair processes.;METHODS: ;Fibroblasts were obtained from the granulation tissue of wounds or intact dermis of rats. The MTT and BrdU assays were used to examine the effect of histamine (10;-8;M-10;-4;M) on the viability and metabolic activity of fibroblasts, and on their proliferative capacity. The influence of histamine receptor antagonists (i.e., ketotifen, ranitidine, ciproxifan and JNJ7777120) and agonists (2-pyridylethlamine dihydrochloride, amthamine dihydrobromide) was also investigated. The TGFβ1 and histamine receptors H1 were evaluated by enzyme-linked immunosorbent assay.;RESULTS: ;Histamine significantly increased granulation tissue fibroblast viability and metabolic activity at 10;-8; and 10;-6;M but did not change their proliferative activity. Only the blockade of the H1 receptor removed this effect of histamine. H1 receptor agonist (2-pyridylethlamine dihydrochloride) increased cell viability, thereby mimicking histamine action.
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CAS 142457-00-9 Amthamine dihydrobromide

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