Lazabemide (hydrochloride)

Lazabemide hydrochloride (Ro 19-6327 hydrochloride) is a selective, reversible inhibitor of monoamine oxidase B (MAO-B) (IC₅₀=0.03 μM) but less active for MAO-A (IC₅₀>100 μM). Lazabemide ?inhibits monoamine uptake at high concentrations, the IC₅₀ values 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]. In Vitro: The in vitro binding characteristics of both radiolabeled inhibitors revealed them to be selective, high-affinity ligands for the respective enzymes. K_D and B_max values for ³H-Ro 19-6327 in rat cerebral cortex are 18.4 nM and 3.45 pmol/mg protein, respectively^[1].
The IC₅₀ values 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 IC₅₀ of 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].
In Vivo: 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].