Mesalazine (5-ASA)

製品コードS1681 バッチS168103

化学情報

	Synonyms	Mesalamine, 5-Aminosalicylic acid	Storage (From the date of receipt)	3 years -20°C powder 1 years -80°C in solvent
	化学式	C₇H₇NO₃
	分子量	153.14	CAS No.	89-57-6
Solubility (25°C)*	体外	DMSO	31 mg/mL (202.42 mM)
		Water	Insoluble
		Ethanol	Insoluble
* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

溶剤液（一定の濃度）を調合する

生物活性

製品説明	Mesalazine (5-ASA) is a specific inhibitor of TNFα-induced IKK activity, used to treat inflammatory bowel disease.
in vitro	Mesalamine inhibits the enzyme 3-hydroxysteroid dehydrogenase, involved in the reversible conversion between DHP and THP, and therefore may affect the local actions of DHP and THP in the brain. Mesalamine, an anti-inflammatory aminosalicylate, dose-dependently inhibits IL-1-stimulated NF-kappaB-dependent transcription without preventing IkappaB degradation or nuclear translocation and DNA binding of the transcriptionally active NF-kappaB proteins, RelA, c-Rel, or RelB. Mesalamine is found to inhibit IL-1-stimulated RelA phosphorylation. ^[1] Mesalamine increases cell adhesion which is measured by cell adhesion assay and transcellular-resistance measurement. Mesalamine treatment restores membranous expression of adhesion molecules E-cadherin and β-catenin. ^[2] Mesalamine or sulfasalazine (2 mM), but not sulfapyridine, significantly reduces the expression of the TC22 transcript and significantly reduces the expression of TC22 protein in a dose-dependent and reversible manner. ^[3] Mesalamine induces membranous expression of E-cadherin and increases intercellular adhesion. Mesalamine activity modulates E-cadherin glycosylation and increases both mRNA and protein levels of GnT-III and its activity as detected by increased E4-lectin reactivity. ^[4] Mesalamine (0.1-1 mM) shows considerable inhibition of peroxynitrite-mediated luminol chemiluminescence in a dose-dependent fashion, suggesting that Mesalamine is able to directly scavenge the peroxynitrite. Mesalamine only at higher concentration (1 mM) inhibits the hydroxyl radical adduct while shifting Electron paramagnetic resonance (EPR) spectra. ^[5]
in vivo	5-ASA exerts potent antineoplastic effects that are mediated through PPARγ in an aberrant crypt mice model.

製品説明

Mesalazine (5-ASA) is a specific inhibitor of TNFα-induced IKK activity, used to treat inflammatory bowel disease.

in vitro

Mesalamine inhibits the enzyme 3-hydroxysteroid dehydrogenase, involved in the reversible conversion between DHP and THP, and therefore may affect the local actions of DHP and THP in the brain. Mesalamine, an anti-inflammatory aminosalicylate, dose-dependently inhibits IL-1-stimulated NF-kappaB-dependent transcription without preventing IkappaB degradation or nuclear translocation and DNA binding of the transcriptionally active NF-kappaB proteins, RelA, c-Rel, or RelB. Mesalamine is found to inhibit IL-1-stimulated RelA phosphorylation. ^[1]

Mesalamine increases cell adhesion which is measured by cell adhesion assay and transcellular-resistance measurement. Mesalamine treatment restores membranous expression of adhesion molecules E-cadherin and β-catenin. ^[2]

Mesalamine or sulfasalazine (2 mM), but not sulfapyridine, significantly reduces the expression of the TC22 transcript and significantly reduces the expression of TC22 protein in a dose-dependent and reversible manner. ^[3]

Mesalamine induces membranous expression of E-cadherin and increases intercellular adhesion. Mesalamine activity modulates E-cadherin glycosylation and increases both mRNA and protein levels of GnT-III and its activity as detected by increased E4-lectin reactivity. ^[4]

Mesalamine (0.1-1 mM) shows considerable inhibition of peroxynitrite-mediated luminol chemiluminescence in a dose-dependent fashion, suggesting that Mesalamine is able to directly scavenge the peroxynitrite. Mesalamine only at higher concentration (1 mM) inhibits the hydroxyl radical adduct while shifting Electron paramagnetic resonance (EPR) spectra. ^[5]

in vivo

5-ASA exerts potent antineoplastic effects that are mediated through PPARγ in an aberrant crypt mice model.

プロトコル(参考用のみ)

細胞アッセイ	細胞株	BVECs
	濃度	1 mM
	反応時間	1 h
	実験の流れ	Cells were treated with indicated concentration of drug for an hour.
動物実験	動物モデル	A/JOlaHsd mic
	投薬量	200 mg/kg
	投与方法	p.o.

参考

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Selleckの高級品が、幾つかの出版された研究調査結果（以下を含む）で使われた：

Effect of Lactobacillus johnsonii Strain SQ0048 on the TLRs-MyD88/NF-κB Signaling Pathway in Bovine Vaginal Epithelial Cells [ Front Vet Sci, 2021, 8:670949]	PubMed: 34447797
The NF-κB inhibitor, SC75741, is a novel antiviral against emerging tick-borne bandaviruses [ Antiviral Res, 2020, 185:104993]	PubMed: 33296695

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人間や獣医の診断であるか治療的な使用のためにでない。

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