Molecular Formula | C8H10ClN3O.HCl |
Molar Mass | 236.1 |
Melting Point | 193-195° |
pKa | 8.9(at 25℃) |
Storage Condition | Desiccate at RT |
In vitro study | 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 3 H-Ro 19-6327 in rat cerebral cortex are 18.4 nM and 3.45 pmol/mg protein, respectively. The IC 50 values for lazabemide are: 86 μM for NA uptake; 123 μM for 5HT uptake; > 500 μM for DA uptake, respectively.. Lazabemide (5 μM) inhibits human MAO-B and MAO-A with IC 50 of 6.9 nM and >10 nM, respectively. And it inhibits rat MAO-B and MAO-A with IC 50 of 37 nM and >10 μM, respectively ina enzymatic assay.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. 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. |
In vivo study | 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. |
Toxicity | LD50 orally in mice: 1000-2000 mg/kg (Imhof, Kyburz, 1986) |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 4.235 ml | 21.177 ml | 42.355 ml |
5 mM | 0.847 ml | 4.235 ml | 8.471 ml |
10 mM | 0.424 ml | 2.118 ml | 4.235 ml |
5 mM | 0.085 ml | 0.424 ml | 0.847 ml |