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Small cyclic amines 8jm ; showed moderate effects with the exception of the pyrrolidine derivative 8i, which was equally active to ; -deprenyl at 109 M. Dibenzo[b, f]oxepines bearing aromatic ring-substituents were generally investigated having either a N-methyl-N-propargylaminomethyl or a pyrrolidinomethyl side-chain in position 10. Small ring substituents, such as a uorine or chlorine atom, in the aromatic positions 1, 2 and 8 led to moderate activities of these compounds 8pr, 8w ; . Introduction of a triuoromethyl group in position 3 8s ; , or chlorine atom in position 6 8tq ; resulted in highly active derivatives. Interestingly, the compound 8u, having a long hexynoic acid side chain in position 7 resulted in an even increased rescuing effect. This derivative has been used as a key-intermediate in the synthesis of tool compounds for the target identication program of 10-aminomethyl-dibenzo[b, f]oxepines [22]. Subsequently, the key-compound CGP 3466 was investigated on other in vitro assays of neuronal cell death and in different animal models, indicative for neurodegenerative diseases. EFFECTS OF CGP 3466 AGAINST MPTP-TOXICITY 1-Methyl-4-phenyl-1, 2, 3, MPTP ; is known to induce parkinsonian symptoms in humans and other primates [25, 26]. MPTP is oxidized by MAO-B to its active metabolite 1-Methyl-4phenylpyridinium MPP ; [27]. MPP is selectively taken up into dopaminergic cells via the dopamine transporter and subsequently accumulated in mitochondria, resulting in energy break-down and cell death. MPTP-toxicity was also demonstrated in mice [13, 28] leading to reduced numbers of tyrosinehydroxylase-positive TH ; cells in the substantia nigra. Finally, MPP-induced apoptotic cell death was reported for different in vitro neuron culture systems [2931]. Currently, MPTP MPP-toxicity is the best-established model-system for Parkinson's disease. Rescue of rat embryonic mesencephalic dopaminergic cells in culture from MPP-induced cell death Rat mesencephalic dopaminergic cells taken at embryonic day 15 were treated on the 4th day in culture with 0.5 mM MPP, the active metabolite of MPTP, in the presence or absence of CGP 3466 free base ; . The compound was re-added after 24 h. After another 24 h in culture, tyrosine-hydroxylase-positive TH ; cells were counted after immunostaining. CGP 3466 at 107 and 109 M rescued about two-thirds of the cells, to a similar extent after both concentrations Fig. 1 ; . Effects of CGP 3466 on survival of dopaminergic cells in mouse substantia nigra after treatment with MPTP MPTP dopaminergic neurotoxicity is an accepted model of Parkinson's disease. C57 B1 6J mice received MPTP twice 30 mg kg s.c., 72 h apart ; and were subsequently treated twice daily for 18 days with 0.00142, and 1.42 mg kg p.o. corresponding to 0.001, and 1 mg kg free base ; CGP 3466B maleate salt ; , beginning 48 h after the second MPTP injection. The animals were sacriced on the last day of treatment and tyrosine hydroxylase-positive TH ; cells were counted in serial sections of the substantia nigra. Data are means of the sums of cells 6 SEM counted in 22 p.o. experiment ; or 17 s.c. experiment ; sections spaced by 50 mm. The substantia nigras of 59 animals were evaluated. Nigral TH cells were signicantly spared, to approximately the same extent, at the doses of 0.0142 and 0.142 mg kg p.o. of the compound Fig. 2, left panel ; . A marginal effect was seen at 0.00142 and none at all at 1.42 mg kg p.o., indicating a biphasic dose-response curve in vivo. In a parallel experiment, a similar and signicant effect of CGP 3466 free base ; administered at 0.1 mg kg s.c. according to the same treatment schedule was observed. Although the comparative compound, ; deprenyl, seemed to have a similar effect, it did not reach statistical signicance Fig. 2, right panel ; . Because nigral TH cells are post-mitotic and therefore do not divide, CGP 3466B was not tested in the absence of MPTP. 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