Elkader Alexander, Sproule Beth
Centre for Addiction and Mental Health, Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada.
Clin Pharmacokinet. 2005;44(7):661-80. doi: 10.2165/00003088-200544070-00001.
Buprenorphine is a semi-synthetic opioid derived from thebaine, a naturally occurring alkaloid of the opium poppy, Papaver somniferum. The pharmacology of buprenorphine is unique in that it is a partial agonist at the opioid mu receptor. Buprenorphine undergoes extensive first-pass metabolism and therefore has very low oral bioavailability; however, its bioavailability sublingually is extensive enough to make this a feasible route of administration for the treatment of opioid dependence. The mean time to maximum plasma concentration following sublingual administration is variable, ranging from 40 minutes to 3.5 hours. Buprenorphine has a large volume of distribution and is highly protein bound (96%). It is extensively metabolised by N-dealkylation to norbuprenorphine primarily through cytochrome P450 (CYP) 3A4. The terminal elimination half-life of buprenorphine is long and there is considerable variation in reported values (mean values ranging from 3 to 44 hours). Most of a dose of buprenorphine is eliminated in the faeces, with approximately 10-30% excreted in urine. Naloxone has been added to a sublingual formulation of buprenorphine to reduce the abuse liability of the product. The presence of naloxone does not appear to influence the pharmacokinetics of buprenorphine. Buprenorphine crosses the placenta during pregnancy and also crosses into breast milk. Buprenorphine dosage does not need to be significantly adjusted in patients with renal impairment; however, since CYP3A activity may be decreased in patients with severe chronic liver disease, it is possible that the metabolism of buprenorphine will be altered in these patients. Although there is limited evidence in the literature to date, drugs that are known to inhibit or induce CYP3A4 have the potential to diminish or enhance buprenorphine N-dealkylation. It appears that the interaction between buprenorphine and benzodiazepines is more likely to be a pharmacodynamic (additive or synergistic) than a pharmacokinetic interaction. The relationship between buprenorphine plasma concentration and response in the treatment of opioid dependence has not been well studied. The pharmacokinetic and pharmacodynamic properties of buprenorphine allow it to be a feasible option for substitution therapy in the treatment of opioid dependence.
丁丙诺啡是一种半合成阿片类药物,由蒂巴因衍生而来,蒂巴因是罂粟(Papaver somniferum)中天然存在的生物碱。丁丙诺啡的药理学特性独特,它是阿片μ受体的部分激动剂。丁丙诺啡经历广泛的首过代谢,因此口服生物利用度非常低;然而,其舌下生物利用度足够高,使这种给药途径成为治疗阿片类药物依赖的可行方法。舌下给药后达到最大血浆浓度的平均时间各不相同,范围从40分钟到3.5小时。丁丙诺啡分布容积大,且与蛋白质高度结合(96%)。它主要通过细胞色素P450(CYP)3A4经N-脱烷基化广泛代谢为去甲丁丙诺啡。丁丙诺啡的终末消除半衰期很长,报告值存在相当大的差异(平均值范围为3至44小时)。丁丙诺啡的大部分剂量经粪便排出,约10 - 30%经尿液排泄。纳洛酮已被添加到丁丙诺啡的舌下制剂中,以降低该产品的滥用可能性。纳洛酮的存在似乎不影响丁丙诺啡的药代动力学。丁丙诺啡在孕期可穿过胎盘,也可进入母乳。肾功能损害患者的丁丙诺啡剂量无需显著调整;然而,由于严重慢性肝病患者的CYP3A活性可能降低,这些患者体内丁丙诺啡的代谢有可能发生改变。尽管目前文献中的证据有限,但已知抑制或诱导CYP3A4的药物有可能减少或增强丁丙诺啡的N-脱烷基化。丁丙诺啡与苯二氮䓬类药物之间的相互作用似乎更可能是药效学方面的(相加或协同),而非药代动力学相互作用。丁丙诺啡血浆浓度与阿片类药物依赖治疗反应之间的关系尚未得到充分研究。丁丙诺啡的药代动力学和药效学特性使其成为阿片类药物依赖替代治疗的可行选择。