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Deconstructing the Iboga Alkaloid Skeleton: Potentiation of FGF2-induced Glial Cell Line-Derived Neurotrophic Factor Release by a Novel Compound.

Madalee M Gassaway, Teresa L Jacques, Andrew C Kruegel, Richard J Karpowicz, Xiaoguang Li, Shu Li, Yves Myer, Dalibor Sames

ACS Chemical Biology January 15, 2016 DOI: 10.1021/acschembio.5b00678 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Laboratory study Peer reviewed
Population C6 glioma cells
Interventions XL-008 FGF2
Topics Addiction Ibogaine
Keywords Neuroprotection Brain protection Neurological protection Neuroprotective mechanisms Brain health Neuropsychiatric disorders Mental health Brain disorders Neurological disorders Substance abuse Drug discovery Drug development Pharmaceutical research Novel compounds Therapeutic compounds Pharmacology Drug research Xl-008 Neurotrophic factors Growth factors Brain signaling Gdnf Fgf2 Neurotrophins Brain pathways
Citations 23
Key points XL-008 induces GDNF release and potentiates FGF2-induced GDNF release in C6 glioma cells via MEK and PI3K pathways.

Abstract

Modulation of growth factor signaling pathways in the brain represents a new experimental approach to treating neuropsychiatric disorders such as depression, anxiety, and addiction. Neurotrophins and growth factors exert synaptic, neuronal, and circuit level effects on a wide temporal range, which suggests a possibility of rapid and lasting therapeutic effects. Consequently, identification of small molecules that can either enhance the release of growth factors or potentiate their respective pathways will provide a drug-like alternative to direct neurotrophin administration or viral gene delivery and thus represents an important frontier in chemical biology and drug design. Glial cell line-derived neurotrophic factor (GDNF), in particular, has been implicated in marked reduction of alcohol consumption in rodent addiction models, and the natural product ibogaine, a substance used traditionally in ritualistic ceremonies, has been suggested to increase the synthesis and release of GDNF in the dopaminergic system in rats. In this report, we describe a novel iboga analog, XL-008, created by unraveling the medium size ring of the ibogamine skeleton, and its ability to induce release of GDNF in C6 glioma cells. Additionally, XL-008 potentiates the release of GDNF induced by fibroblast growth factor 2 (FGF2), another neurotrophin implicated in major depressive disorder, increasing potency more than 2-fold (from 7.85 ± 2.59 ng/mL to 3.31 ± 0.98 ng/mL) and efficacy more than 3-fold. The GDNF release by both XL-008 and the FGF2/XL-008 mixture was found to be mediated through the MEK and PI3K signaling pathways but not through PLCγ in C6 glioma cells.

Comparable studies

Other experimental studies on ibogaine for addiction, most cited first.

Study Year Design Participants
Noribogaine is a G-protein biased κ-opioid receptor agonist. 2015 Experimental study with binding experiments, functional assays, and computational simulations
Anti-addiction drug ibogaine inhibits hERG channels: a cardiac arrhythmia risk. Human cells 2014 Experimental study
Anti-addiction drug ibogaine inhibits voltage-gated ionic currents: a study to assess the drug's cardiac ion channel profile. Heterologously expressed human ion channels and guinea pig cardiomyocytes 2013 Experimental study
Ibogaine signals addiction genes and methamphetamine alteration of long-term potentiation. Rat brain models 2002 Review with experimental data
Anti-addiction Drug Ibogaine Prolongs the Action Potential in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes. Human ventricular-like cardiomyocytes derived from induced pluripotent stem cells 2017 Experimental study

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