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Markus R Meyer

34 papers in the library · 768 citations · publishing 2009-2026

Papers

In vivo and in vitro toxicokinetics including metabolism, isozyme mapping, and monoamine oxidase inhibition of three (2-aminopropyl)benzo[b]thiophene (APBT) psychedelics.

Toxicology March 1, 2026 Lea Wagmann, Simon D. Brandt, Pierce V. Kavanagh et al.

Three recently identified psychedelics and entactogens—3-APBT, 5-APBT, and 6-APBT—activate serotonin 2 receptor subtypes and cause head-twitch responses in mice. Their toxicokinetics, metabolism, and monoamine oxidase (MAO) inhibition were characterized using liquid chromatography-high-resolution tandem mass spectrometry. Metabolites were identified in urine from male Wistar rats over 24 hours after oral administration (2 mg/kg) and in incubations with pooled human liver S9 fraction (25 µM). Hydroxylation, primarily catalyzed by CYP1A2, CYP2D6, CYP3A4, and CYP3A5, was the main phase I biotransformation; phase II reactions included N-acetylation, glucuronidation, and sulfation. All three isomers strongly inhibited MAO-A (IC50: 5-APBT 0.4 µM, 6-APBT 0.6 µM, 3-APBT 4 µM) but only weakly inhibited MAO-B (IC50 23-49 µM). Clinically relevant MAO-A inhibition and associated interaction risks cannot be excluded.

Toxicometabolomics Characterization of Two N1-Sulfonated Dimethyltryptamine Derivatives in Zebrafish Larvae and Human Liver S9 Fractions Using Liquid Chromatography-High-Resolution Mass Spectrometry.

Metabolites February 14, 2026 Prajwal Punnamraju, Sascha K. Manier, Selina Hemmer et al.

A liquid chromatography–high-resolution mass spectrometry workflow was used to investigate the metabolism of two N1-sulfonated N,N-dimethyltryptamine derivatives, which have potential for both therapeutic use and recreational abuse. Zebrafish larvae and pooled human liver S9 fractions revealed key phase I and phase II biotransformations. Untargeted metabolomics showed significant downregulation of L-threonine associated with compound exposure. These findings advance the understanding of tryptamine metabolism and highlight the value of toxicometabolomics for evaluating novel psychoactive substances.

Next-Generation MDMA Analogue SDMA: Pharmacological and Metabolic Insights

ACS Chemical Neuroscience December 2, 2025 Nina Kastner, Núria Nadal‐gratacós, Selina Hemmer et al.

Replacing the 1,3-benzodioxole group in MDMA (ecstasy) with a 1,3-benzoxathiole yields two analogues, SDA and SDMA, that interact with monoamine transporters similarly to MDMA but with key differences. SDA and SDMA inhibit dopamine and norepinephrine transporters more potently than MDMA and act as partial releasers at serotonin and dopamine transporters. Metabolism studies show SDA and SDMA are cleared faster, while MDMA and MDA degrade only weakly. In mice, SDMA does not produce rewarding effects, unlike MDMA, and SDA only shows a preference for the drug-paired compartment at the lowest dose. SDMA shares similar locomotor and hyperthermic profiles with MDMA, whereas SDA induces increased hyperlocomotion and more sustained hyperthermia. SDMA may be a safer candidate for further study.

Bioisosteric analogs of MDMA with improved pharmacological profile.

bioRxiv : the preprint server for biology April 11, 2024 Ana Sofia Alberto-Silva, Selina Hemmer, Hailey A. Bock et al. preprint

Three new chemical variants of MDMA—ODMA, TDMA, and SeDMA—show similar activity at serotonin and dopamine transporters but reduced activity at serotonin 5-HT2A/2B/2C receptors, which may lower the risk of off-target side effects. They also differ from MDMA in how they are broken down by the liver, with fewer metabolic pathways and no phase II metabolites. The analogs interact more weakly with certain organic cation transporters. These findings suggest the new compounds could be promising therapeutic alternatives to MDMA for conditions like PTSD, though further research is needed to confirm whether they pose lower risks.

In vitro metabolic fate of nine LSD-based new psychoactive substances and their analytical detectability in different urinary screening procedures

Analytical and Bioanalytical Chemistry July 19, 2019 Lea Wagmann, Lilian H. J. Richter, Tobias Kehl et al.

Nine LSD derivatives—ALD-52, 1P-LSD, 1B-LSD, ETH-LAD, 1P-ETH-LAD, AL-LAD, ECPLA, LSZ, and LSM-775—are metabolized in pooled human liver S9 fractions primarily through N-dealkylation and hydroxylation, mainly catalyzed by CYP1A2 and CYP3A4. ALD-52, 1P-LSD, and 1B-LSD undergo deacylation to LSD. Many metabolites are structurally identical, complicating differentiation in urinalysis. However, after administering expected recreational doses to rats, neither parent drugs nor metabolites were detectable in urine using standard screening approaches.

Human cytochrome P450 kinetic studies on six N-2-methoxybenzyl (NBOMe)-derived new psychoactive substances using the substrate depletion approach.

Toxicology Letters March 15, 2018 Achim T. Caspar, Markus R Meyer, Hans H Maurer

Six NBOMe-derived new psychoactive substances (25B-, 25C-, 25I-, 3,4-DMA-, 4-EA-, and 4-MMA-NBOMe) are metabolized by multiple cytochrome P450 enzymes, primarily CYP2D6 and CYP2C19. Michaelis-Menten kinetic constants were determined using the substrate depletion approach; Km values ranged from 0.010 μM (CYP2D6, 4-MMA-NBOMe) to 13 μM (CYP2B6, 4-EA-NBOMe). CYP2D6 contributed most to hepatic net clearance for five compounds (61–89%), while CYP2C19 dominated for 4-MMA-NBOMe (64%). Because multiple isoforms are involved, the risk of drug-drug interactions may be low, but inter-individual variation in metabolism is possible for substances highly dependent on polymorphic CYP2C19 or CYP2D6.

In vitro monoamine oxidase inhibition potential of alpha-methyltryptamine analog new psychoactive substances for assessing possible toxic risks.

Toxicology Letters April 15, 2017 Lea Wagmann, Simon D. Brandt, Pierce V. Kavanagh et al.

Thirteen analogs of the psychoactive substance alpha-methyltryptamine (AMT) were tested for their ability to inhibit monoamine oxidase (MAO), an enzyme that breaks down neurotransmitters. All analogs inhibited MAO-A, with IC50 values ranging from 0.049 to 166 μM, and four also inhibited MAO-B (IC50 82–376 μM). 7-Me-AMT was the most potent MAO-A inhibitor, comparable to the known inhibitors harmine and harmaline, and acted competitively. Most analogs also inhibited MAO in human liver S9 fractions. These findings suggest that MAO inhibition by these compounds could contribute to dangerous serotonin- and adrenaline-related effects, especially when combined with other drugs that block monoamine reuptake.

Investigations on the human hepatic cytochrome P450 isozymes involved in the metabolism of 3,4-methylenedioxy-amphetamine (MDA) and benzodioxolyl-butanamine (BDB) enantiomers.

Toxicology Letters October 8, 2009 Markus R Meyer, Frank T. Peters, Hans H Maurer

The human liver enzymes CYP2D6 and CYP3A4 are primarily responsible for breaking down the chiral designer drugs MDA and BDB, which are also metabolites of MDMA (Ecstasy) and related compounds. The enzymes preferentially process the S-enantiomer of these substances. This metabolic step, called demethylenation, converts the drugs into catecholamines. The findings help clarify how these substances are cleared from the body and may inform understanding of their effects and toxicity in recreational users.

Stereoselective differences in the cytochrome P450-dependent dealkylation and demethylenation of N-methyl-benzodioxolyl-butanamine (MBDB, Eden) enantiomers.

Biochemical Pharmacology June 1, 2009 Markus R Meyer, Frank T. Peters, Hans H Maurer

Cytochrome P450 isozymes responsible for metabolizing the designer drug MBDB (Eden) were identified for the first time. The main metabolites produced are DHMBB and BDB. Dealkylation is primarily catalyzed by CYP2B6 and CYP2C19, while demethylenation also involves CYP1A2, CYP2D6, and CYP3A4. After in vitro-in vivo correlation, CYP2D6 is the most abundant isozyme for total MBDB metabolism, and CYP2C19 is the most enantioselective, metabolizing the S-enantiomer at a higher rate at low substrate concentrations. Inhibition studies with quinidine confirmed CYP2D6's dominant role. These findings align with results for similar amphetamines.