Source: PsychonautWiki. Duration View duration charts in the KnowDrugs app. Effects light visual effects with open eyes strong visual effects with closed eyes a sense of well-being and contentedness stimulation unpleasant bodyload sedation Source: Tripsit. NBOMe has a quick onset with an initial rush, and then strong effects that typically last hours. These effects can include:. This can have serious consequences as it greatly increases the risk of overdose.
Internationally, there have been multiple deaths linked to NBOMe, mostly due to accidental overdoses. This is because it is very hard to get an accurate dose. It is very easy for someone estimating NBOMe doses to get this wrong and take too much. It is a vasoconstrictor, which means it tightens blood vessels.
These results suggest that in rats effects of 25I-NBOMe on dopaminergic and serotoninergic transmission depend not only on the brain structure but also strain and sex. An important question that remains to be fully resolved is whether NBOMe compounds are endowed with an abuse potential. Two behavioral tests, conditioned place preference CPP and self-administration SA , are widely used in studies examining the abuse potential of drugs by analyzing their rewarding and reinforcing effects.
The 25B-NBOME-elicited CPP was blocked by antagonists of D 1 - and D 2 -dopamine receptors, SCH and haloperidol, respectively, but was not affected by ketanserin, an observation indicating an important role of dopaminergic transmission in this phenomenon Custodio et al.
Results of these studies are, however, not uniform. Among several factors that might contribute to the above discrepancies, different dosing protocols appears to play an important role. Recent studies demonstrated that NBOMes exhibit neurotoxic and cardiotoxic activity. Acute 30 min and prolonged 5 h exposure of primary rat cortical cultures to 25B-NBOMe decreased spontaneous neuronal activity, measured as firing rate and burst rate Zwartsen et al.
The compound was fold more potent than its precursor, 2C-B. Both compounds used at doses of 0. Other less common routes of administration include oral, rectal, vaginal, intravenous or intramuscular injection, and smoking EMCDDA, ; World Health Organization, a , b.
Doses and duration of action depend on the route of administration see Table 1. According to information given on drug fora, users may find that LSD has a slight metallic taste or no taste at all, while 25I-NBOMe will have a bitter taste.
Importantly, the use of serotoninergic drugs, e. Visuals are crazy, and the music is intense — waves of 3D objects have taken over my living room and everything looks beautiful! My perception of myself is erased. NBOMes produce an array of adverse effects Hill et al. Severe agitation, agitated delirium, intensive unpleasant hallucinations, aggression that sometimes progresses to violent and self-destructive behavior, paranoia, suicidal attempts, psychosis with delusions, dysphoria, irritability, fear, and panic attacks.
Hyperthermia, convulsions, clonus, motor incoordination, mouth numbing and impaired speech, insomnia, blurred vision, and leucoencephalopathy.
Loss of location and time, confusion, short-term memory deficits, cognitive impairment, mental fatigue, altered mental state, loosening of association, and disorganized thoughts.
Srisuma et al. In general, the features of NBOMe toxicity are also induced by other psychedelics. The main difference is an intensity and frequency of severe intoxication symptoms. The incidence of seizures is higher with NBOMes compared with other psychedysleptics, whereas muscle spasms, hyperreflexia, and tremors are rarely noted in cases of intoxication with NBOMes.
The progression from rhabdomyolysis to metabolic acidosis, anuria, and acute renal failure is a common complication of severe NBOMe toxicity, but this is reported less frequently in cases of intoxication with other drugs. By analogy to other NPSs, except for opioids and benzodiazepines, at present there are no specific antidotes for NBOMes, and all treatments used are symptomatic. Clinical management of acute toxicity resulting from the use of NBOMe compounds consists of monitoring, including fluids, electrolytes, acid-base balance, and supportive treatment: mechanical ventilation and intravenous administration of fluids; benzodiazepines e.
Patients with hematological disturbances require transfusion s of blood preparations frozen plasma, frozen erythrocytes, or platelet concentrate. Severely aggressive patients may require antipsychotic drugs in addition to benzodiazepines Hill et al. Table 2 presents clinical fatality cases due to intoxication with NBOMes. In recent years, biotransformation studies have been carried out for many NBOMe compounds. The metabolites have mainly been identified via in vitro study with microsomes and polled human hepatocytes or by the analysis of mouse or rat urine or authentic human samples of blood and urine collected from drug users.
An accumulating body of data clearly indicates that NBOMes undergo extensive biotransformation that results in the production of numerous metabolites. For example, Caspar et al. The reported biotransformation steps include oxidative deamination, oxidative N -dealkylation also in combination with hydroxylation, oxidative O -demethylation possibly combined with hydroxylation, oxidation of secondary alcohols, mono- and dihydroxylation, oxidation of primary alcohols, and carboxylation of primary alcohols Figure 2.
In the case of 25N-NBOMe, reduction of the aromatic nitro group and N -acetylation of the primary aromatic amine have also been reported. The dominant phase I biotransformation was O -demethylation, followed by O -di-demethylation and hydroxylation; accordingly, the most abundant metabolites were the O -demethylated and hydroxylated forms.
Phase I metabolites subsequently undergo glucuronidation and sulfation Caspar et al. Poklis et al. However, it is also possible that 25H-NBOMe is not formed during metabolic processes in the body but, more likely, is already present in the consumed product as a contaminant. Assuming that the halogenation step performed during synthesis in a clandestine laboratory was incomplete and the unreacted material was not adequately removed by purification, it appears likely that 25H-NBOMe could be present in the final drug product.
This makes the signals of the parent compounds approximately fold lower than those of the most abundant metabolites Stellpflug et al. The significantly greater intensity of glucuronated metabolites when compared to the parent compounds in plasma make them prime candidates to be used as markers for NBOMe intoxication Leth-Petersen et al.
An important issue worth pointing out is the fact that metabolites can also be responsible for the toxic effects of NBOMes Leth-Petersen et al. Two other groups of active formed compounds, which are also sold on the drug market, include 2C phenethylamines or NBOH derivatives Pasin et al. For all investigated NBOMes, the corresponding 2,5-dimethoxyphenethylamine 2C-X metabolite formed during N -demethoxybenzylation was detected; however, they were mostly seen at low levels Temporal et al.
Hence, only sensitive and specific analytical methods can be used for the detection, identification, and determination of NBOMes in biological materials Kyriakou et al. Even in post-mortem cases, the reported blood concentrations of NBOMe compounds also tend to be low and are often below 0. Although the compounds are generally present at higher concentrations in urine than in blood, detection methods should be targeted to the metabolites rather than the parent compounds.
The analysis of NBOMes can be a challenging task, even for laboratories equipped with sensitive modern methods, and popular immunochemical tests are not effective. Common analytical methods used in laboratories, such as gas chromatography coupled with mass spectrometry GC-MS or high-performance liquid chromatography with diode array detection HPLC-DAD without derivatization of the sample, are also inadequate for identifying NBOMe compounds due to insufficient sensitivity.
This latter technique allows for accurate determination of molecular and fragmentation ions, which in turn makes it possible to elucidate the chemical structure of compounds and consequently unambiguously identify not only the parent substance but also many metabolites. Sometimes, a simple precipitation or just a dilution of a sample is sufficient. Although many methods have been developed for the detection of NBOMe analogs in biological materials, both in metabolic studies and authentic forensic sample analyses, only a few screening methods covering more than one or two NBOMe compounds have been published.
Caspar et al. A diethyl ether:ethyl acetate mixture was applied for a two-step extraction. The approach allowed the detection of these analytes down to concentrations of 0.
Pasin et al. Temporal et al. A Q-Trap apparatus was used in multiple reaction monitoring MRM acquisition mode, which allowed the compounds to be detected at a level of 0. The method, characterized by LODs as low as 0.
Urine samples were analyzed directly after dilution. Mass spectrometers were operated in positive ionization mode using full scan FS data and a subsequent data-dependent acquisition DDA mode. Both applied systems were comparable, but nanoLC allowed much lower eluent consumption: flow rate of 0. Wohlfarth et al. Yu et al. The resulting MS-MS spectral data was used to establish a molecular networking map for different NBOMes, as these compounds generally showed similar product ion spectral patterns.
The map was applied to spiked urine samples, confirming that it can be used for the rapid detection and identification of unknown NBOMes. In addition to body fluids, other biological materials have also been analyzed for NBOMe compounds, including post-mortem tissues. Ameline et al. The hairs were collected 6. As a result of the analyses, the presence of 25I-NBOMe was demonstrated in two of five 2 cm hair segments at concentrations of 1.
GC-MS is used less frequently but it can be a great tool in screening analyses when used in combination with a derivatization step. In recent years, NBOMe derivatives, a specific set of psychedelic phenylalkylamines, have been encountered on the drugs of abuse market.
NBOMe drugs are highly toxic and their intake has been associated with severe adverse reactions including deaths. The analysis of NBOMes and their metabolites is a challenging task; only sensitive and specific analytical methods can be used for their detection, identification, and determination in biological materials.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Abiero, A. Brain Res. Aghajanian, G. Serotonin and hallucinogens.
Neuropsychopharmacology 21 Suppl. Al-Iman, A. NBOMe compounds: systematic review and data crunching of the surface web. Health Sci. Google Scholar. Ameline, A. Symptoms of overdose may include: intense confusion severe agitation seizure kidney failure nausea and vomiting rapid heart rate rapid or difficulty breathing overheating attempted suicide coma death.
Read more about overdose. Long-term effects As the use of NBOMes is relatively new, long term effects are still being determined.
Getting help If your use of NBOMes is affecting your health, family, relationships, work, school, financial or other life situations, you can seek help and support. You can also search our list of Support Services for services in your local area:.
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