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Lazabemide (Ro 19-6327)

  • 產(chǎn)品貨號:CS-01Y76679
  • 產(chǎn)品價格:電議
  • 產(chǎn)品產(chǎn)地:進口、國產(chǎn)
  • 包裝類型:10mM*1mLinDMSO 10mg 50mg
  • 采購熱度:226
  • 庫存:100
  • CAS號:103878-84-8
  • 方法:
  • 含量:>99.50%
  • 品牌名稱:莼試
  • 分子式:C8H10ClN3O
  • 分子量:199.64

簡介內(nèi)容:質(zhì)量保證、價格優(yōu)惠

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標簽:Lazabemide (Ro 19-6327) 

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化學性質(zhì):                                                                                                             

規(guī)格

10mM*1mLinDMSO 10mg 50mg

CAS

103878-84-8

別名

N/A

化學名

N/A

分子式

C8H10ClN3O

分子量

199.64

溶解度

DMSO : 34 mg/mL (170.31 mM)

儲存條件

Store at -20°C

General tips

For obtaining a higher solubility , please warm the tube at 37 and shake it in the ultrasonic bath for a while.

Shipping Condition

Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

 

產(chǎn)品描述:                                                                                                            

Lazabemide(Ro 19-6327) is selective, reversible monoamine oxidase B (MAO-B) inhibitor (IC50 values are 0.03 and > 100 μM for MAO-B and MAO-A respectively).

The in vitro binding characteristics of both radiolabeled inhibitors revealed them to be selective, high-affinity ligands for the respective enzymes. KD and Bmax values for 3H-Ro 41-1049 in rat cerebral cortex were 10.7 nM and 7.38 pmol/mg protein, respectively, and for 3H-Ro 19-6327 were 18.4 nM and 3.45 pmol/mg protein, respectively[1]. The IC50 values for lazabemide and Ro 16-6491, respectively, were: 86 microM and 90 microM for NA uptake; 123 microM and 90 microM for 5HT uptake; > 500 microM and > 1000 microM for DA uptake. Lazabemide and Ro 16-6491 also differed from L-deprenyl in their ability to induce release of endogenous monoamines from synaptosomes. Thus, Lazabemide(Ro 19-6327) (500 microM) induced a greater 5 HT release than did L-deprenyl, but was less effective than L-deprenyl in releasing DA. On the contrary, lazabemide was almost completely inactive on either 5 HT and DA release[2]. a clear inhibition of DOPAC formation was observed with Lazabemide(Ro 19-6327) (250 nM), while 250 nM lazabemide was found not to increase the accumulation of newly-formed DA in those tubular epithelial cells loaded with 50 microM L-DOPA[3].

The ischemia reperfusion-induced hydroxyl radical generation was attenuated by 3 mg/kg of clorgyline and lazabemide. Furthermore, mice pretreated with these MAO inhibitors showed decreased DOPAC levels in comparison with those of their respective vehicle-treated control groups; recovery of the reduced DOPAC level was also delayed[4].

[1]. Saura J, et al. Quantitative enzyme radioautography with 3H-Ro 41-1049 and 3H-Ro 19-6327 in vitro: localization and abundance of MAO-A and MAO-B in rat CNS, peripheral organs, and human brain. J Neurosci. 1992 May;12(5):1977-99. [2]. Bondiolotti GP, et al. In vitro effects on monoamine uptake and release by the reversible monoamine oxidase-B inhibitors lazabemide and N-(2-aminoethyl)-p-chlorobenzamide: a comparison with L-deprenyl. Biochem Pharmacol. 1995 Jun 29;50(1):97-102. [3]. Guimaraes J, et al. The activity of MAO A and B in rat renal cells and tubules. Life Sci. 1998;62(8):727-37. [4]. Suzuki T, et al. MAO inhibitors, clorgyline and lazabemide, prevent hydroxyl radical generation caused by brain ischemia/reperfusion in mice. Pharmacology. 1995 Jun;50(6):357-62.

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原創(chuàng)作者:上海莼試生物技術(shù)有限公司

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