5-Aminolevulinic acid hydrochloride

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抑制剂描述：

产品名称：5-Aminolevulinic acid hydrochloride

产品别名：见爱必信官网

英文别名：5-Aminolevulinic acid hydrochloride

靶点：Endogenous Metabolite;Mitophagy;Autophagy

CAS：5451-09-2

纯度：>98%

外观：见爱必信官网

保存方法：store at -20℃ for one year（Powder）； in DMSO or others solvent store at 2-4℃ for two weeks, at -20℃ for six months.

描述：

5-Aminolevulinic acid is an intermediate in heme biosynthesis in the body and the universal precursor of tetrapyrroles, such as chlorophyll and heme. In mammals, yeast, fungi and the purple bacteria, 5-aminolevulinic acid is formed by the Shemin pathway. Then it is used in the synthesis of hemes, vitamin B12 and bacteriochlorophyll. Two molecules of 5-aminolevulinic acid are condensed to form porphobilinogen. It is the first step compound in the porphyrin synthesis. Aminolevulinic acid hydrochloride (5-aminolevulinic acid hydrochloride) is a prodrug that is metabolized intracellularly to form the photosensitizing molecule protoporphyrin (PpIX). When PpIX is activated by light, cytotoxic reactive oxygen species and free radicals are generated. ALA can diffuse through skin and preferentially localizes in tumors and dysplasic tissue. Subsequent exposure of PpIX-loaded tumor cells to light can destroy the tumor.

溶解性：Ethanol ：6mg/mL(35.8mM)
DMSO ：34 mg/mL (202.87 mM)
Water ：34 mg/mL (202.87 mM)

体外研究：

5-aminolevulinic acid (5-ALA)-Photodynamic therapy (PDT) results in down regulation of nuclear factor kappa B (NFkappaB) and baculovirus inhibitor-of-apoptosis repeat containing-3 (BIRC-3) protein. 5-aminolevulinic acid (5-ALA)-Photodynamic therapy (PDT) causes increase in Bax:Bcl-2 ratio and mitochondrial release of cytochrome c and apoptosis-inducing factor (AIF). 5-aminolevulinic acid yields reactive oxygen species upon metal-catalyzed oxidation and causes in vivo and in vitro impairment of rat liver mitochondria and DNA damage. 5-aminolevulinic acid induces a dose-dependent damage in nuclear and mitochondrial DNA in human SVNF fibroblasts and rat PC12 cells. 5-aminolevulinic acid dose-dependently decreases cAMP levels (maximal inhibition of 38%, at 1 mM), due to an inhibition of basaladenylate cyclase activity. 5-aminolevulinic acid also inhibits fluoride- and Gpp(NH)p-stimulated, but not the forskolin-stimulated adenylate cyclase activity. 5-aminolevulinic acid also inhibits the activity of adenylate cyclase in membranes isolated from rat cortex and striatum and from human cortex. 5-aminolevulinic acid (0-3mM) dose-dependently inhibits glutamate uptake by astrocyte cultures. 5-aminolevulinic acid significantly reduces both the K(m) and V(max) of glutamate uptake indicating an uncompetitive inhibition. 5-aminolevulinic acid significantly increases astrocyte lipoperoxidation in astrocytes incubated under these conditions. 5-aminolevulinic acid mediated sonodynamic therapy exhibits synergistic apoptotic effects on THP-1 macrophages, involving excessive intracellular reactive oxygen species generation and MMP loss.

体内研究：

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