反応 #534889

ord-eae22b0c7c294073beeb048fda45eec6

反応方程式

NCCc1ccc(O)c(O)c1
DA
NCCc1ccc(O)cc1
tyramine
COc1ccc(CC2c3cc(O)c(OC)cc3CCN2C)cc1O
reticuline
COc1ccc2c3c1O[C@H]1[C@@H](O)C=C[C@H]4[C@@H](C2)N(C)CC[C@@]341
codeine
NCCc1ccc(O)c(O)c1
dopamine
NCCc1ccc(O)cc1
tyramine
NCCc1ccc(O)cc1
Tyramine
C=C[C@H]1CN2CCC1C[C@@H]2[C@@H](O)c1ccnc2ccc(OC)cc12
quinidine
C=C[C@H]1CN2CCC1C[C@@H]2[C@@H](O)c1ccnc2ccc(OC)cc12
quinidine
NCCc1ccc(O)c(O)c1
dopamine
NCCc1ccc(O)c(O)c1
DA
NCCc1ccc(O)c(O)c1
DA
CN1CC[C@]23c4c5ccc(O)c4O[C@H]2[C@@H](O)C=C[C@H]3[C@H]1C5
morphine

反応条件

詳細条件
See reaction.notes.procedure_details.

実験手順

To examine the tyramine to dopamine step, dopamine (DA) levels in ganglia and hemolymph were examined before and after tyramine addition followed by CYP2D6 inhibition by quinidine. Tyramine injection significantly increased ganglionic (4.98±0.27 μg/g to 9.17±1.21 μg/g wet weight; P<0.01) and hemolymph (10.13±1.24 μg/mL to 16.47±1.28 μg/mL, P<0.05) DA levels (FIGS. 19 and 20). The ganglionic and hemolymph DA level increases were blocked by quinidine exposure, demonstrating that the CYP2D6 enzyme was mediating this step. Ganglia were also exposed to THP, reticuline, DA, or codeine. Each resulted in significantly enhanced morphine levels, a phenomenon that was also significantly blocked by quinidine exposure, again demonstrating a role for CYP2D6 in the second part of the morphine biosynthetic pathway (FIGS. 15 and 20).

出典

DOI: 10.6084/m9.figshare.5104873.v1特許: US08481559B2uspto-grants-2013_07