|Lazabemide (Ro 19-6327) Catalog No.GC30979|
Sample solution is provided at 25 µL, 10mM.
GlpBio Products Cited In Reputable Papers
|Cas No.||103878-84-8||SDF||Download SDF|
|Solubility||DMSO : ≥ 34 mg/mL (170.31 mM)||Storage||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.Stock solution can be stored below -20℃ for several months.|
|Shipping Condition||Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
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. 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. 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.
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.
. 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. . 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. . Guimaraes J, et al. The activity of MAO A and B in rat renal cells and tubules. Life Sci. 1998;62(8):727-37. . 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.