NBOMe and 2C substitute phenylethylamine exposures reported to the National Poison Data System

Abstract

Background. Hallucinogenic designer drugs, especially NBOMe and the 2C substitute phenylethylamine series, have been increasing ubiquitous in past years. The purpose of this study is to characterize and compare clinical features of NBOMe and 2C exposures in humans. Method. This is a retrospective cohort study of all single agent exposures to NBOMe and 2C substitute phenylethlamine reported to the National Poison Data System (NPDS) from 1st September 2012 to 30th September 2014. Results. Over the study period, there were a total 341 cases including 148 NBOMe exposures and 193 2C exposures. The majority cases involved men (73.9%); median age was 18 years (Interquartile-range, 16–21). Similar clinical effects were reported in both groups including tachycardia (45.2%), agitation/irritable (44.3%), hallucination/delusion (32.0%), confusion (19.1%) and hypertension (18.5%). There were higher incidences of hallucination/delusion, single episode seizure and benzodiazepine administration in NBOMe exposures (40.5%, 8.8% and 50.0%respectively) than those of 2C exposures (25.4%, 3.1%, and 32.6% respectively). There were 2.3% death; no difference between two groups. Discussion. The higher rate of symptoms in NBOMe is consistent with the higher 5HT2A agonistic effects of NBOMe described in both molecular and animal studies. Conclusion. Common clinical effects of NBOMe and 2C exposures were tachycardia, agitation/irritable, hallucination/delusion, confusion, and hypertension. There were higher incidences of hallucination/delusion, single episode seizure and benzodiazepine administration in NBOMe.     

In vivo release of endogenous dopamine from rat caudate nucleus by phenylethylamine

The in vivo release of endogenous dopamine (DA) from the rat caudate nucleus has been measured in the presence and absence of beta-phenylethylamine. A push-pull cannula was implanted into the brain and the tissue was perfused with artificial cerebrospinal fluid (CSF) containing phenylethylamine in concentrations ranging from 5 X 10(-3) to 5 X 10(-7) M. The DA released into the perfusate was determined radioenzymatically. Dopamine was released at rates significantly greater than its resting rate by concentrations of phenylethylamine of 5 X 10(-3) to 5 X 10(-5)M; 5 X 10(-6)M phenylethylamine caused a slight increase in release, but the difference from the resting rate was not significant. The absence of calcium in the perfusing medium did not significantly alter either the unstimulated release rate of DA or the release rate stimulated by 5 X 10(-5)M phenylethylamine. The concentrations of phenylethylamine required to increase release of DA in vivo are discussed briefly in relation to the doses required to elicit behavioural effects.     

Synthesis of deuterium labeled standards of 5‐methoxy‐N,N‐dimethyltryptamine (5‐Meo‐DMT)

The Batcho‐Leimgruber strategy was employed to synthesize 5‐[²H₃]‐methoxy‐1 H‐indole 4 from commercially available 5‐hydroxy‐2‐nitrotoluene 1 and CD₃I. Compound 4 was treated with oxalyl chloride, dimethylamine and lithium aluminum hydride to yield 5‐[²H₃]‐methoxy‐N,N‐dimethyltryptamine 6 . Copyright © 2006 John Wiley & Sons, Ltd.     

Platelet monoamine oxidase in a pedigree with schizophrenia: an interlaboratory project

Conflicting reports on the association between platelet MAO activity and schizophrenia prompted a critical review and determinations on identical samples at one laboratory in Sweden and one in the USA. Samples originated from eight schizophrenics and 27 relatives belonging to a large pedigree, thus ensuring biological homogeneity.
In the USA laboratory, a significantly lower MAO activity was found in the schizophrenics when benzylamine or β–phenylethylamine was used as substrate (but not with trypt–amine), while a similar result was obtained in the Swedish laboratory when tryptamine was used (but not with benzylamine or (β–phenylethylamine). Comparisons between materials examined in different laboratories do not seem meaningful until differences in methodologies have been clarified. At present there is neither proof nor disproof of MAO being a "genetic marker" for vulnerability to the schizophrenic disorder.     

苯乙胺类物质的滥用危害与管制措施探析

2017年《世界毒品报告》显示:苯乙胺类物质已成为继合成大麻素类、合成卡西酮类之后的第三大合成类毒品.在所有因滥用新精神活性物质导致的临床病例中苯乙胺所占比例高达28.4％[1],苯乙胺类物质因其化学结构灵活多变,由此成为众多非法兴奋剂的演变"载体",加之部分苯乙胺类新精神活性物质兼具兴奋与致幻的双重效应,其危害性较之...     

3-环己烯-1-甲酸的手性拆分研究

目的 研究外消旋3-环己烯-1-甲酸的手性拆分,获得单一构型异构体。方法 通过化学拆分法中的生成非对映异构体拆分法来拆分外消旋3-环己烯-1-甲酸,以手性苯乙胺为手性拆分剂,外消旋3-环己烯-1-甲酸在丙酮中形成非对映体异构体并利用它们的溶解度差别来进行拆分。结果 拆分为(R)-(+)-3-环己烯-1-甲酸（收率28.3%）和(S)-(-)-3-环己烯-1-甲酸（收率28.7%）,光学纯度均大于99%。结论 获得外消旋3-环己烯-1-甲酸的单一构型异构体。     

3-环己烯-1-甲酸的手性拆分研究

目的 研究外消旋3-环己烯-1-甲酸的手性拆分,获得单一构型异构体.方法 通过化学拆分法中的生成非对映异构体拆分法来拆分外消旋3-环己烯-1-甲酸,以手性苯乙胺为手性拆分剂,外消旋3-环己烯-1-甲酸在丙酮中形成非对映体异构体并利用它们的溶解度差别来进行拆分.结果 拆分为(R)-(+)-3-环己烯-1-甲酸(收率28.3％)和(S)-(-)-3-环己烯-1-甲酸(收率28.7％),光学纯度均大于99％.结论 获得外消旋3-环己烯-1-甲酸的单一构型异构体.