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Irving W. Wainer

3 papers in the library · 205 citations · publishing 2008-2018

Papers

Simultaneous population pharmacokinetic modelling of ketamine and three major metabolites in patients with treatment‐resistant bipolar depression

British Journal of Clinical Pharmacology February 1, 2012 Xiaochen Zhao, Swarajya Lakshmi Vattem Venkata, Ruin Moaddel et al. 136 citations

Ketamine is metabolized into several compounds, and this study shows that norketamine is not the main metabolite circulating in the blood after a single 40-minute infusion of 0.5 mg/kg ketamine in patients with treatment-resistant bipolar depression. Instead, dehydronorketamine was the major metabolite in four out of nine patients, norketamine in three, and hydroxynorketamine in two. Large inter-patient variation in metabolite levels was observed. The findings suggest that future research on ketamine's effects should measure these downstream metabolites.

d-Serine is a potential biomarker for clinical response in treatment of post-traumatic stress disorder using (R,S)-ketamine infusion and TIMBER psychotherapy: A pilot study.

Biochim Biophys Acta Proteins Proteom March 18, 2018 Basant Pradhan, Ludmil Mitrev, Ruin Moaddell et al. 67 citations

In a pilot study, d-serine levels may serve as a biomarker for clinical response in individuals with post-traumatic stress disorder (PTSD) treated with (R,S)-ketamine infusion combined with TIMBER psychotherapy. The work suggests that changes in d-serine could reflect treatment outcomes, offering a potential biological indicator for monitoring therapeutic efficacy.

Interaction of ibogaine analogs with the nicotinic acetylcholine receptor

The FASEB Journal April 1, 2008 Krzysztof Jozwiak, Ruin Moaddel, Irving W. Wainer et al. 2 citations

Ibogaine analogs, especially 18-methoxycoronaridine (18-MC), bind to a specific site within the ion channel of the nicotinic acetylcholine receptor (AChR) when the receptor is in a desensitized state. The affinity of 18-MC for this site is about 0.17 μM in the desensitized state, much higher than in the resting state (12 μM). The binding site overlaps with the TCP locus, located between valine and leucine rings in the channel. These compounds enhance binding of the agonist cytisine only when the receptor is in a resting but activable state, not when desensitized. The findings suggest that ibogaine analogs inhibit the AChR by promoting receptor desensitization.