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Oral bioavailability and brain penetration of (−)‐stepholidine, a tetrahydroprotoberberine agonist at dopamine D 1 and antagonist at D 2 receptors, in rats
Author(s) -
Sun Yan,
Dai Jieyu,
Hu Zheyi,
Du Feifei,
Niu Wei,
Wang Fengqing,
Liu Fei,
Jin Guozhang,
Li Chuan
Publication year - 2009
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.2009.00393.x
Subject(s) - bioavailability , glucuronidation , pharmacology , chemistry , pharmacokinetics , metabolite , dopamine receptor d2 , dopamine , medicine , receptor , in vitro , biochemistry , microsome
Background and purpose:  (−)‐Stepholidine has high affinity for dopamine D 1 and D 2 receptors. The aims of the present study were to examine the oral bioavailability and brain penetration of (−)‐stepholidine and to gain understanding of mechanisms governing its transport across the enterohepatic barrier and the blood–brain barrier. Experimental approach:  The pharmacokinetics of (−)‐stepholidine was studied in rats and microdialysis was used to measure delivery to the brain. These studies were supported by biological measurement of unbound (−)‐stepholidine. Membrane permeability was assessed using Caco‐2 cell monolayers. Metabolite profiling of (−)‐stepholidine in rat bile and plasma was performed. Finally, in vitro metabolic stability and metabolite profile of (−)‐stepholidine were examined to compare species similarities and differences between rats and humans. Key results:  Orally administered (−)‐stepholidine was rapidly absorbed from the gastrointestinal tract; two plasma concentration peaks were seen, and the second peak might result from enterohepatic circulation. Due to extensive pre‐systemic metabolism, the oral bioavailability of (−)‐stepholidine was poor (<2%). However, the compound was extensively transported across the blood–brain barrier, demonstrating an AUC (area under concentration–time curve) ratio of brain : plasma of ∼0.7. (−)‐Stepholidine showed good membrane permeability that was unaffected by P‐glycoprotein and multidrug resistance‐associated protein 2. In vitro (−)‐stepholidine was metabolized predominantly by glucuronidation and sulphation in rats and humans, but oxidation of this substrate was very low. Conclusions and implications:  Although (−)‐stepholidine exhibits good brain penetration, future development efforts should aim at improving its oral bioavailability by protecting against pre‐systemic glucuronidation or sulphation. In this regard, prodrug approaches may be useful.

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