SeDMA

Last updated
SeDMA
SeDMA.svg
Clinical data
Other namesSelenadiazolylmethamphetamine; Selenadiazolyl-N-methylamphetamine
Drug class Serotonin–norepinephrine–dopamine releasing agent; Entactogen; Stimulant
Identifiers
  • 1-(2,1,3-benzoselenadiazol-5-yl)-N-methylpropan-2-amine
CAS Number
Chemical and physical data
Formula C10H13N3Se
Molar mass 254.206 g·mol−1
3D model (JSmol)
  • N1[Se]N=C2C=CC(=CC=12)CC(C)N([H])C
  • InChI=1S/C10H13N3Se/c1-7(11-2)5-8-3-4-9-10(6-8)13-14-12-9/h3-4,6-7,11H,5H2,1-2H3
  • Key:RWTXADPLGLKHLV-UHFFFAOYSA-N

SeDMA is a bioisosteric analogue of 3,4-methylenedioxy-N-methylamphetamine (MDMA) which was developed in an attempt to create an improved MDMA alternative for potential clinical use. [1] It is the analogue of MDMA in which the 1,3-benzodioxole ring has been replaced with a 2,1,3-benzoselenadiazole ring. [1] ODMA and TDMA are closely related analogues. [1] ODMA, TDMA, and SeDMA are releasing agents of serotonin, norepinephrine, and dopamine similarly to MDMA. [1] However, they are less potent and efficacious in activating the serotonin 5-HT2A, 5-HT2B, and 5-HT2C receptors than MDMA and show differing and potentially improved metabolic and pharmacokinetic properties in comparison. [1] ODMA, TDMA, and SeDMA were first described in the scientific literature in June 2024. [1]

Contents

MDMA and 3,4-methylenedioxyamphetamine (MDA) are well-known serotonergic neurotoxins that damage serotonergic neurons in the brain. [2] [3] [4] [5] [6] However, MDMA and MDA injected directly into the brain have been found to not produce serotonergic neurotoxicity in rodents. [2] [7] [8] This suggests that peripherally formed metabolites of MDMA and MDA may be the actual mediators of the neurotoxicity rather than MDMA and MDA themselves. [2] [7] [8] ODMA, TDMA, and SeDMA, with the exception of N-demethylation, do not share any of the phase I or phase II metabolic pathways of MDMA. [1] Notably, in contrast to MDMA, methylenedioxy ring opening and consequent formation of catechol metabolites, which have been linked with free radical generation, does not occur. [1] As a result, ODMA, TDMA, and SeDMA might not share the serotonergic neurotoxicity of MDMA and MDA. [1] However, more research is needed to assess this possibility. [1] Moreover, other studies have found that slow infusion of MDMA directly into the brain does produce signs of serotonergic neurotoxicity. [9]

See also

Related Research Articles

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<span class="mw-page-title-main">Empathogen</span> Class of psychoactive drugs that produce empathic experiences

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<span class="mw-page-title-main">3,4-Methylenedioxyamphetamine</span> Empathogen-entactogen, psychostimulant, and psychedelic drug of the amphetamine family

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<span class="mw-page-title-main">MBDB</span> Chemical compound

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<span class="mw-page-title-main">Methylone</span> Group of stereoisomers

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<span class="mw-page-title-main">EDMA</span> Chemical compound

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<span class="mw-page-title-main">1,3-Benzodioxolylbutanamine</span> Enactogenic drug of the phenethylamine class

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<span class="mw-page-title-main">MDAI</span> Chemical compound

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<span class="mw-page-title-main">MMAI</span> Chemical compound

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α-Methyldopamine Chemical compound

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<span class="mw-page-title-main">4-Chlorophenylisobutylamine</span> Entactogen and stimulant drug of the phenethylamine class

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<span class="mw-page-title-main">DFMDA</span> Chemical compound

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<span class="mw-page-title-main">5-MAPB</span> Chemical compound

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<span class="mw-page-title-main">2,3-Methylenedioxymethamphetamine</span> Chemical compound

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<span class="mw-page-title-main">Monoamine neurotoxin</span> Compounds that damage or destroy monoaminergic neurons

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<span class="mw-page-title-main">ODMA (drug)</span> MDMA analogue

ODMA is a bioisosteric analogue of 3,4-methylenedioxy-N-methylamphetamine (MDMA) which was developed in an attempt to create an improved MDMA alternative for potential clinical use. It is the analogue of MDMA in which the 1,3-benzodioxole ring has been replaced with a 2,1,3-benzoxadiazole ring. TDMA and SeDMA are closely related analogues. ODMA, TDMA, and SeDMA are releasing agents of serotonin, norepinephrine, and dopamine similarly to MDMA. However, they are less potent and efficacious in activating the serotonin 5-HT2A, 5-HT2B, and 5-HT2C receptors than MDMA and show differing and potentially improved metabolic and pharmacokinetic properties in comparison. ODMA, TDMA, and SeDMA were first described in the scientific literature in June 2024.

<span class="mw-page-title-main">TDMA (drug)</span> MDMA analogue

TDMA is a bioisosteric analogue of 3,4-methylenedioxy-N-methylamphetamine (MDMA) which was developed in an attempt to create an improved MDMA alternative for potential clinical use. It is the analogue of MDMA in which the 1,3-benzodioxole ring has been replaced with a 2,1,3-benzothiadiazole ring. ODMA and SeDMA are closely related analogues. ODMA, TDMA, and SeDMA are releasing agents of serotonin, norepinephrine, and dopamine similarly to MDMA. However, they are less potent and efficacious in activating the serotonin 5-HT2A, 5-HT2B, and 5-HT2C receptors than MDMA and show differing and potentially improved metabolic and pharmacokinetic properties in comparison. ODMA, TDMA, and SeDMA were first described in the scientific literature in June 2024.

<span class="mw-page-title-main">3,4-Dihydroxymethamphetamine</span> MDMA metabolite

3,4-Dihydroxymethamphetamine, or 3,4-dihydroxy-N-methylamphetamine, also known as α-methylepinine or α,N-dimethyldopamine, is the major metabolite of 3,4-methylenedioxy-N-methylamphetamine (MDMA). It is formed from MDMA by O-demethylation via cytochrome P450 enzymes including CYP2D6 as well as CYP1A2 and CYP3A4. Like MDMA, HHMA is a monoamine releasing agent.

<span class="mw-page-title-main">Borax combo</span> Designer drug combination mimicking MDMA

The Borax combo, also known by the informal brand names Blue Bliss and Pink Star, is a combination recreational and designer drug described as an MDMA-like entactogen.

<span class="mw-page-title-main">3,4-Isopropylidenedioxyamphetamine</span> Pharmaceutical compound

3,4-Isopropylidenedioxyamphetamine (IDA) is a monoamine releasing agent (MRA) of the amphetamine family related to 3,4-methylenedioxyamphetamine (MDA). It is considerably less potent than MDA as an MRA in vitro. IDA fully substituted for MDMA and LSD in animal drug discrimination tests, albeit with 5- to 7-fold lower potency than MDA.

References

  1. 1 2 3 4 5 6 7 8 9 10 Alberto-Silva AS, Hemmer S, Bock HA, da Silva LA, Scott KR, Kastner N, Bhatt M, Niello M, Jäntsch K, Kudlacek O, Bossi E, Stockner T, Meyer MR, McCorvy JD, Brandt SD, Kavanagh P, Sitte HH (June 2024). "Bioisosteric analogs of MDMA: Improving the pharmacological profile?". J Neurochem. 168 (9): 2022–2042. doi:10.1111/jnc.16149. PMC  11449655. PMID   38898705.
  2. 1 2 3 Costa G, Gołembiowska K (January 2022). "Neurotoxicity of MDMA: Main effects and mechanisms". Exp Neurol. 347: 113894. doi:10.1016/j.expneurol.2021.113894. hdl: 11584/325355 . PMID   34655576.
  3. ↑ Kostrzewa RM (2022). "Survey of Selective Monoaminergic Neurotoxins Targeting Dopaminergic, Noradrenergic, and Serotoninergic Neurons". Handbook of Neurotoxicity. Cham: Springer International Publishing. pp. 159–198. doi:10.1007/978-3-031-15080-7_53. ISBN   978-3-031-15079-1.
  4. ↑ Parrott AC (September 2013). "MDMA, serotonergic neurotoxicity, and the diverse functional deficits of recreational 'Ecstasy' users". Neurosci Biobehav Rev. 37 (8): 1466–1484. doi:10.1016/j.neubiorev.2013.04.016. PMID   23660456.
  5. ↑ Aguilar MA, García-Pardo MP, Parrott AC (January 2020). "Of mice and men on MDMA: A translational comparison of the neuropsychobiological effects of 3,4-methylenedioxymethamphetamine ('Ecstasy')". Brain Res. 1727: 146556. doi:10.1016/j.brainres.2019.146556. PMID   31734398.
  6. ↑ Montgomery C, Roberts CA (January 2022). "Neurological and cognitive alterations induced by MDMA in humans" (PDF). Exp Neurol. 347: 113888. doi:10.1016/j.expneurol.2021.113888. PMID   34624331.
  7. 1 2 Monks TJ, Jones DC, Bai F, Lau SS (April 2004). "The role of metabolism in 3,4-(+)-methylenedioxyamphetamine and 3,4-(+)-methylenedioxymethamphetamine (ecstasy) toxicity". Ther Drug Monit. 26 (2): 132–136. doi:10.1097/00007691-200404000-00008. PMID   15228153.
  8. 1 2 Esteban B, O'Shea E, Camarero J, Sanchez V, Green AR, Colado MI (March 2001). "3,4-Methylenedioxymethamphetamine induces monoamine release, but not toxicity, when administered centrally at a concentration occurring following a peripherally injected neurotoxic dose". Psychopharmacology (Berl). 154 (3): 251–260. doi:10.1007/s002130000645. PMID   11351932.
  9. ↑ Baggott, Matthew; Mendelson, John (2001). "Does MDMA Cause Brain Damage?". In Holland, J. (ed.). Ecstasy: The Complete Guide: A Comprehensive Look at the Risks and Benefits of MDMA. Inner Traditions/Bear. pp. 110–145, 396–404. ISBN   978-0-89281-857-0 . Retrieved 24 November 2024. While a single injection of MDMA into the brain (intracerebroventricularly) had no effect on TPH activity, slow infusion of 1 mg/kg MDMA into the brain over 1 hr produced enough oxidative stress to acutely reduce TPH activity (Schmidt and Taylor 1988). The acute decrease in TPH activity is an early effect of MDMA and can be measured at post 15 min (Stone et al. 1989b). TPH inactivation can also be produced by non-neurotoxic MDMA doses (Schmidt and Taylor 1988; Stone et al. 1989a; Stone et al. 1989b). It therefore appears that MDMA rapidly induces oxidative stress but only produces neurotoxicity when endogenous free radical scavenging systems are overwhelmed.
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