Lazabemide hydrochloride (Ro 19-6327 hydrochloride) is a selective, reversible inhibitor ofmonoamine oxidaseB (MAO-B)(IC₅₀=0.03 μM) but less active forMAO-A(IC₅₀>100 μM). Lazabemide inhibits monoamine uptake at high concentrations, the IC₅₀values are 86 μM, 123 μM and >500 μM for noradrenalin, serotonin and dopamine uptake, respectively. Lazabemide can be used for the research of parkinson and alzheimer′s disease^[1].

The in vitro binding characteristics of both radiolabeled inhibitors revealed them to be selective, high-affinity ligands for the respective enzymes. K_Dand B_maxvalues for³H-Ro 19-6327 in rat cerebral cortex are 18.4 nM and 3.45 pmol/mg protein, respectively^[1].
The IC₅₀values for lazabemide are: 86 μM for NA uptake; 123 μM for 5HT uptake; >500 μM for DA uptake, respectively^[1].
. Lazabemide (5 μM) inhibits human MAO-B and MAO-A with IC₅₀of 6.9 nM and >10 nM, respectively. And it inhibits rat MAO-B and MAO-A with IC₅₀of 37 nM and >10 μM, respectively ina enzymatic assay^[2].
Lazabemide differs from L-deprenyl in their ability to induce release of endogenous monoamines from synaptosomes. Thus, Lazabemide (500 μM) induces a greater 5 HT release than does L-deprenyl, but is less effective than L-deprenyl in releasing DA. On the contrary, lazabemide was almost completely inactive on either 5 HT and DA release^[2].
Lazabemide (250 nM) results in a clear inhibition of DOPAC formation, while does not increase the accumulation of newly-formed DA in those tubular epithelial cells loaded with 50 microM L-DOPA^[3].

Lazabemide (3 mg/kg) attenuates ichemia reperfusion-induced hydroxyl radical generation and pretreatment with Lazabemide showed decreased DOPAC levels in comparison with those of their respective vehicle-treated control groups^[4].

236.10

C₈H₁₁Cl₂N₃O

103878-83-7

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