Hydromorphone-3-glucuronide: Biochemical synthesis and preliminary pharmacological evaluation
References (36)
- et al.
J. Pain. symptom. Manage.
(1995) - et al.
Pain
(1997) - et al.
J. Pharm. Sci.
(1977) - et al.
Biochem. Pharmacol.
(1973) - et al.
Brain Res.
(1979) - et al.
Life Sci.
(1990) - et al.
Life Sci.
(1994) - et al.
Pain
(1989) - et al.
Pain
(1991) - et al.
Pain
(1992)
Pain
Pain
Pain
J. Pain. Symptom. Manage.
J. Pain. Symptom. Manage.
Pain
J. Biol. Chem.
Neurosci. Lett.
Cited by (51)
Which Opioids Are Safest and Most Effective in Patients With Renal or Hepatic Failure?
2023, Evidence-Based Practice of Palliative Medicine, Second EditionHydromorphone: Evolving to Meet the Challenges of Today's Health Care Environment
2013, Clinical TherapeuticsCitation Excerpt :H6G, to which hydromorphone is largely metabolized, seems to lack analgesic activity, whereas the analgesic activity of the other metabolites of hydromorphone is uncertain.13,16 Animal studies have shown that H3G causes neuroexcitatory effects.17,18 This mechanism may be responsible for the occurrence of myoclonus and seizures, which have been described in a small number of patients who received extremely high doses of parenteral hydromorphone.19,20
Evidence that intrathecal morphine-3-glucuronide may cause pain enhancement via toll-like receptor 4/MD-2 and interleukin-1β
2010, NeuroscienceCitation Excerpt :The implications of TLR4 signaling activation by M3G's interaction with these and other residues in the absence of LPS deserves further investigation as it has implications for TLR4 signaling activation by other endogenous small molecules, environmental or pharmacological xenobiotics. For example, other 3-glucuronide opioid metabolites have been shown to neuroexcitatory or pain enhancing properties, including hydromorphone-3-glucuronide (Wright et al., 1998) and normorphone-3-glucuronide (Smith and Smith, 1998). The studies presented here would predict that glial and inflammatory activity could contribute to these responses.
Opioid metabolism
2009, Mayo Clinic ProceedingsCitation Excerpt :Although the affinities of morphine and M6G for the μ1-opioid receptor are similar, a study of low-dose morphine, M6G, and M3G found that morphine had greater analgesic efficacy.67 The M3G metabolite of morphine lacks analgesic activity, but it exhibits neuroexcitatory effects in animals and has been proposed as a potential cause of such adverse effects as allodynia, myoclonus, and seizures in humans.68–70 In a clinical trial, however, low-dose M3G exhibited no analgesic effects, did not potentiate the analgesic effects of morphine or M6G, and did not produce adverse effects.67
The Rational Use of Intrathecal Opioid Analgesics
2009, NeuromodulationChapter 1 Opioids: methods of forensic analysis
2008, Handbook of Analytical SeparationsCitation Excerpt :The limits of quantitation (2.5 ng/ml for hydromorphone and 1.2 ng/ml for morphine) were sufficient for pharmacokinetic studies. Wright et al.[356] synthesized hydromorphone-3-glucuronide (H3G) from hydromorphone, using rat liver microsomes. The crude product was purified by semi-preparative HPLC with UV detection.
- 1
Tel: 61-7-33652554, Fax: 61-7-33651688.