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| Other names | 18-MC; Zolunicant; MM-110; MM110 |
| Routes of administration | Oral |
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| Formula | C22H28N2O3 |
| Molar mass | 368.477 g·mol−1 |
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18-Methoxycoronaridine (18-MC; developmental code name MM-110), also known aszolunicant (INNTooltip International Nonproprietary Name), is a derivative ofibogaine invented in 1996 by the research team around the pharmacologist Stanley D. Glick from theAlbany Medical College and the chemists Upul K. Bandarage and Martin E. Kuehne from theUniversity of Vermont. In animal studies it has proven to be effective at reducing self-administration ofmorphine,cocaine,methamphetamine,nicotine, andsucrose.[1][2] It has also been shown to produceanorectic effects in obese rats, most likely due to the same actions on thereward system which underlie its anti-addictive effects against drug addiction.[3]
18-MC was in the early stages of human testing by the California-based drug development company Savant HWP before being acquired byMindMed, a Canadian pharmaceutical company.[4][5] In 2002 the research team began raising funds for human trials, but were unable to secure the estimated $5 million needed.[6] In 2010, Obiter Research, a chemical manufacturer inChampaign, Illinois, signed a patent license withAlbany Medical College and theUniversity of Vermont, allowing them the right to synthesize and market 18-MC and othercongeners. In 2012 theNational Institute on Drug Abuse gave a $6.5 million grant to Savant HWP for human trials.[5] In 2017 it went into Phase-II trials in Brazil for treatment ofLeishmaniasis at theEvandro Chagas Institute,[7] but not for approval for use as a treatment for drug addiction. A phase 2a study of MM-110 treatment in patients experiencingopioid withdrawal happened in Q2 of 2022.[8]
18-MC is aα3β4nicotinic antagonist and, in contrast to ibogaine, has no affinity at theα4β2 subtype nor atNMDA-channels nor at theserotonin transporter,[9] and has significantly reduced affinity forsodium channels and for theσ receptor, but retains modest affinity forμ-opioid receptors where it acts as an agonist,[10] andκ-opioid receptors.[11] The sites of action in the brain include themedial habenula,interpeduncular nucleus,[12][13][14] dorsolateraltegmentum andbasolateral amygdala.[2] (±)-18-MC competitively inhibits α9α10nAChRs with potencies higher than that at α3β4 and α4β2 nAChRs and directly blocksCaV2.2.[15]
A number of derivatives of 18-MC have been developed, with several of them being superior to 18-MC itself, the methoxyethyl congenerME-18-MC being more potent than 18-MC with similar efficacy, and the methylamino analogue18-MAC being more effective than 18-MC with around the same potency. These compounds were also found to act as selectiveα3β4 nicotinic acetylcholine antagonists, with little or no effect on NMDA receptors.[16][17]
