✍ Scribed by Gavin J. Kilpatrick; Terry W. Smith
No coin nor oath required. For personal study only.
Morphine‐6‐glucuronide (M6G) appears to show equivalent analgesia to morphine but to have a superior side‐effect profile in terms of reduced liability to induce nausea and vomiting and respiratory depression. The purpose of this review is to examine the evidence behind this statement and to identify the possible reasons that may contribute to the profile of M6G. The vast majority of available data supports the notion that both M6G and morphine mediate their effects by activating the µ‐opioid receptor. The differences for which there is a reasonable consensus in the literature can be summarized as: (1) Morphine has a slightly higher affinity for the µ‐opioid receptor than M6G, (2) M6G shows a slightly higher efficacy at the µ‐opioid receptor, (3) M6G has a lower affinity for the κ‐opioid receptor than morphine, and (4) M6G has a very different absorption, distribution, metabolism, and excretion (ADME) profile from morphine. However, none of these are adequate alone to explain the clinical differences between M6G and morphine. The ADME differences are perhaps most likely to explain some of the differences but seem unlikely to be the whole story. Further work is required to examine further the profile of M6G, notably whether M6G penetrates differentially to areas of the brain involved in pain and those involved in nausea, vomiting, and respiratory control or whether µ‐opioid receptors in these brain areas differ in either their regulation or pharmacology. © 2005 Wiley Periodicals, Inc. Med Res Rev
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This paper provides the ®rst report on stereoselective synthesis and characterization of morphine 6-a-dglucuronide (M6aG), useful as a reference marker for testing the purity and stability of the pharmaceutically important morphine 6-b-d-glucuronide (M6G). The synthesis is based on the glycosylation