DOB (4-Bromo-2,5-dimethoxyamphetamine; brolamfetamine; bromo-DMA;1-(4-Bromo-2,5-dimethoxyphenyl)-2-aminopropane) – is a synthetic substance of phenylethylamine class, which causes predominantly psychedelic effects. It is a part of a DOx –series, which also includes DOET, DOF, DOC, DOB, DOI, DON. It is different from other psychedelic substances because of its more pronounced effect, duration of effects, dangerous and frequent overdoses. It is not recommended for use by people unfamiliar with such psychedelics as lysergic acid and psilocybin. DOB molecule fundamentally is a substituted phenylethylamine, characterized by presence of methoxyfunctional groups of H3, attached to the carbon atoms in R2 and R5, as well as bromine, attached to the carbon atom in R4 of the phenyl ring. The substance itself is not stable enough, since at a temperature of 40 degrees Celsius, or more up to 40% of the substance is lost. It has a high sensitivity to oxygen, as well as chlorine and ultraviolet radiation; it decomposes at room temperature, which causes a decrease in the severity and duration of effects. When dissolved in water, DOB is a transparent liquid with moderate fluidity, low viscosity and density, more than average tensile strength and more than average surface tension, the melting point is about 63-65 C, most often the blotters are impregnated with the concentrate of the substance.
The most common form of DOB is Blotter – which is a small square sheet of perforated "blotting" paper, submerged in the solution of DOB. These blotters are placed on the tongue or under the tongue with a temporary exposure, chewed or swallowed. Sometimes the solution of DOB is used, which can be taken with a pipette and dripped on the mucous membrane of the mouth or nose. Tablets or microdots are usually intended for oral use, which can be swallowed or chewed. If DOB is in the form of powder, it is best diluted in a liquid solution and put on a blotter to control the dose. Another form of this substance is "gel tablets", which are taken orally and are elements of gelatin containing DOB.
Pharmacokinetics and Pharmacodynamics.
At the moment, there is a very small number of studies on the pharmacological properties of DOB. There are theories that, when ingested, its primary metabolism occurs in the lungs, where it accumulates, so it enters the brain from there, which causes a gradual and slow onset of effects with a high duration (18-30 hours). Also, there is a hypothesis that it's not DOB, but some active metabolite that may be responsible for the main psychedelic effects. The main metabolite of this substance is 2-methoxy-5-hydroxy-4-bromoamphetamine. Biotransformation into this metabolite is quite fast and takes about two hours (in the liver through the demethylation stage) together with the distribution in the tissues. Then the elimination process begins, which takes 32 hours, and the peak concentration of distribution in the tissues (brain, liver, lungs) takes about 1 hour, while the highest level is initially registered in the lungs, then in the brain, then in the liver. The maximum concentration in the blood plasma is reached after 1.2 hours. After 32 hours, another 15% concentration of metabolites can be detected in the blood. The medium lethal dose of the substance has not been established in studies, but there are theoretical grounds to assume that it is about 0.6 mg/kg. In experimental studies, it has been proved that the right-sided enantiomer of DOB has more pronounced psychedelic properties at a low dose than its mirror molecule.
In terms of pharmacodynamics, brolamfetamine affects 5-hydroxytryptamine receptors, mainly of type 2,(which determines its main psychedelic properties), and TAAR1. After DOB use the greatest activity is detected in the following areas of the brain: the neocortex (mainly the postcentral gyrus responsible for "bodily sensations"), the olfactory tubercle, and the apical dendrites of the pyramidal cells of the 5th layer of the cerebral cortex. When the 5-HT2a receptor is activated, the beta and gamma subunits "release" the Gq subunit that activates phospholipase C (PLC), which, in turn, cleaves phosphatidylinositol bisphosphate (PIP2) into diacylglycerol (DAG) and inositol triphosphate (IP3). DAG activates protein kinase C (PC), and PS3 triggers a calmodulin-dependent mechanism for the release of calcium from the endoplasmic reticulum. There are also side biochemical pathways associated with the formation of arachidonic acid from DAG. This pathway is engaged as a result of the presence of a methyl group in the alpha position on the side chain of brolamfetamine. Interestingly, the participation of serotonin in the processes of inflammation(not only neurogenic one) was discovered relatively recently. The well-known hallucinogen DOI in dosages that do not affect the mental status showed the ability to suppress TNF-induced inflammation. Lysergic acid was discovered to have that same property, so it can be assumed that DOB also takes part in the inflammation processes. When 5-HT2A receptors are activated in the hypothalamus, the level of oxytocin, prolactin, ACTH, corticosterone and renin increases in the blood.
DOB has a low affinity for 5-HT2B and 5-HT2C receptors. However, clinical effects caused by agonism to these receptors are usually manifested and can be identified. For instance, when the central 5HT-2B receptor is affected by DOB, increased motor arousal is observed, and when exposed to the same receptor type located outside the brain, there is blood vessel spasm and an increase in blood pressure. According to the research data, this effect is direct, not mediated, since the administration of beta-adrenomimetics to rats with 5-HT2B receptors already blocked did not lead to an increase in blood pressure. In addition, it was found that 5-HT2B agonists can cause cardiac fibrosis with prolonged use – this, again, is due to the direct participation of 5-HT2B receptors in triggering the process of fibroblast proliferation. The occurrence of a massive arterial spasm may also be associated with the effect on this subtype of receptors. This fact can be one of the causes of acute intoxication development, or lethal outcome, associated with DOB. In addition to the direct proliferative effect on fibroblasts, the activation of these receptors can also help the regeneration of liver cells. The activation of this type of receptors has a protective effect in patients with serotonin syndrome. The least affinity of DOB to 5-НТ2C is the reason why the effects associated with the agonism to this receptor type remain impossible to register due to the poor presentation of clinical symptoms.
Methods of use and doses.
The most important thing while using DOB is not the dose of the substance, but preparation for this act. It is necessary that the following principles of preparation are observed:
The most common form of DOB is Blotter – which is a small square sheet of perforated "blotting" paper, submerged in the solution of DOB. These blotters are placed on the tongue or under the tongue with a temporary exposure, chewed or swallowed. Sometimes the solution of DOB is used, which can be taken with a pipette and dripped on the mucous membrane of the mouth or nose. Tablets or microdots are usually intended for oral use, which can be swallowed or chewed. If DOB is in the form of powder, it is best diluted in a liquid solution and put on a blotter to control the dose. Another form of this substance is "gel tablets", which are taken orally and are elements of gelatin containing DOB.
Pharmacokinetics and Pharmacodynamics.
At the moment, there is a very small number of studies on the pharmacological properties of DOB. There are theories that, when ingested, its primary metabolism occurs in the lungs, where it accumulates, so it enters the brain from there, which causes a gradual and slow onset of effects with a high duration (18-30 hours). Also, there is a hypothesis that it's not DOB, but some active metabolite that may be responsible for the main psychedelic effects. The main metabolite of this substance is 2-methoxy-5-hydroxy-4-bromoamphetamine. Biotransformation into this metabolite is quite fast and takes about two hours (in the liver through the demethylation stage) together with the distribution in the tissues. Then the elimination process begins, which takes 32 hours, and the peak concentration of distribution in the tissues (brain, liver, lungs) takes about 1 hour, while the highest level is initially registered in the lungs, then in the brain, then in the liver. The maximum concentration in the blood plasma is reached after 1.2 hours. After 32 hours, another 15% concentration of metabolites can be detected in the blood. The medium lethal dose of the substance has not been established in studies, but there are theoretical grounds to assume that it is about 0.6 mg/kg. In experimental studies, it has been proved that the right-sided enantiomer of DOB has more pronounced psychedelic properties at a low dose than its mirror molecule.
In terms of pharmacodynamics, brolamfetamine affects 5-hydroxytryptamine receptors, mainly of type 2,(which determines its main psychedelic properties), and TAAR1. After DOB use the greatest activity is detected in the following areas of the brain: the neocortex (mainly the postcentral gyrus responsible for "bodily sensations"), the olfactory tubercle, and the apical dendrites of the pyramidal cells of the 5th layer of the cerebral cortex. When the 5-HT2a receptor is activated, the beta and gamma subunits "release" the Gq subunit that activates phospholipase C (PLC), which, in turn, cleaves phosphatidylinositol bisphosphate (PIP2) into diacylglycerol (DAG) and inositol triphosphate (IP3). DAG activates protein kinase C (PC), and PS3 triggers a calmodulin-dependent mechanism for the release of calcium from the endoplasmic reticulum. There are also side biochemical pathways associated with the formation of arachidonic acid from DAG. This pathway is engaged as a result of the presence of a methyl group in the alpha position on the side chain of brolamfetamine. Interestingly, the participation of serotonin in the processes of inflammation(not only neurogenic one) was discovered relatively recently. The well-known hallucinogen DOI in dosages that do not affect the mental status showed the ability to suppress TNF-induced inflammation. Lysergic acid was discovered to have that same property, so it can be assumed that DOB also takes part in the inflammation processes. When 5-HT2A receptors are activated in the hypothalamus, the level of oxytocin, prolactin, ACTH, corticosterone and renin increases in the blood.
DOB has a low affinity for 5-HT2B and 5-HT2C receptors. However, clinical effects caused by agonism to these receptors are usually manifested and can be identified. For instance, when the central 5HT-2B receptor is affected by DOB, increased motor arousal is observed, and when exposed to the same receptor type located outside the brain, there is blood vessel spasm and an increase in blood pressure. According to the research data, this effect is direct, not mediated, since the administration of beta-adrenomimetics to rats with 5-HT2B receptors already blocked did not lead to an increase in blood pressure. In addition, it was found that 5-HT2B agonists can cause cardiac fibrosis with prolonged use – this, again, is due to the direct participation of 5-HT2B receptors in triggering the process of fibroblast proliferation. The occurrence of a massive arterial spasm may also be associated with the effect on this subtype of receptors. This fact can be one of the causes of acute intoxication development, or lethal outcome, associated with DOB. In addition to the direct proliferative effect on fibroblasts, the activation of these receptors can also help the regeneration of liver cells. The activation of this type of receptors has a protective effect in patients with serotonin syndrome. The least affinity of DOB to 5-НТ2C is the reason why the effects associated with the agonism to this receptor type remain impossible to register due to the poor presentation of clinical symptoms.
Methods of use and doses.
The most important thing while using DOB is not the dose of the substance, but preparation for this act. It is necessary that the following principles of preparation are observed:
- Make sure that you can spend the following hours in a calm and comforting environment. DOB-trip lasts a while, for 1.75 mg – up to 15-24 hours. After that, the effects remain and decrease for another couple of hours. Sort out your affairs in advance to be sure that you will not need to rush somewhere and that no one will bother you. It is better to use DOB no later than 12 hours before going to sleep because there may be problems with falling asleep. Buy some light food in advance to eat after. During the trip, food will not be especially enjoyable, however it will not be repulsive either.
- Calculate the correct dose for yourself. If it is your first time using, start with a minimum dose, if you have positive experience using DOB at a certain dose – you can repeat it with increasing the dose by 10-15% (100-200 mcg) of the initial one, but no more! If you want to try, but you are worried about the process, you can try the dose of 100 mcg, you will feel light but distinctive change in mood and perception, but your consciousness will not be altered.
Low dose - 500-750 mcg; medium dose- 750-1100 mcg; high dose- more than 1100 mcg.
- Place the blotter on your tongue and leave for 10 minutes until it dissolves or until you feel that you have achieved the desired effect for the trip.
- It is necessary for the first trip to be accompanied by a setter (there should only be positive interactions between this person and you, there shouldn't be any conflict or negative emotions about them because, otherwise, it can induce negative thoughts about the setter during the trip).
- When the effects manifest, there will be distinct changes in your world perception, your vision can change: rainbow halos around lights, trails behind moving objects, geometric shapes with closed eyes, moving, twisting, crawling patterns on the surface of objects. These effects can be entertaining, but don't let them distract you from your sense of self, your life and the world around you.
Clinical effects of DOB use.
Desirable/positive effects: stimulation (motor, research, speech, behavioral activity) - is pronounced, sometimes corresponds with that of synthetic psychostimulants-cathinone derivatives; spontaneous bodily sensations – body high, euphoria and empathy; enhanced tactile feelings; increased physical performance and endurance; a sense of increased "body control", when it seems that one has a complete control of every cell of the body in the physical aspect; moderate visual illusions, auditory illusions, increased brightness of color, improved visual acuity, the appearance of "new color shades"; the desire to communicate, perform various routine work; analysis enhancement – which is described as expressed ability to creatively analyze information, deep contemplation and the appearance of various ideas; positive emotions; positive suggestibility; high frequency of thought processes, high speed of information processing; the appearance of "conceptual" thinking.
Undesirable negative effects: disorder of temperature regulation with an increase in body temperature; muscle spasm, fine tremor; increased heart rate; increased blood pressure; heart rhythm disturbances; nausea, rarely - vomiting; decreased appetite up to its complete absence; difficulty of urination up to the complete impossibility of emptying the bladder; peripheral vasospasm; bruxism; "restless legs" syndrome; mydriasis; dehydration; rarely-diarrhea; headache; pain, tingling, discomfort in sternum area; increased salivation and increased sweating; paranoia, constant anxiety; impairment of short-term memory; hypophasia; a sense of" flowing time", distortion of time frames; " thought loop; internal and external hallucinations up to terrible, hysterical representations, leading to a panic attack with syncope; hppd-syndrome.
DOB – is a very powerful substance, which effects last significantly longer comparing to other psychedelics. DOB overdose is a serious and extremely dangerous condition. Exceeding recommended dosages can be life-threatening! DOB barely causes addiction. Desire to use it can be present as a regular thought without mania or sense of addiction. Tolerance is moderate; it disappears when DOB is not used in 7-15 days. Also, there is cross tolerance between DOB and all representatives of the phenylethylamine class.
DOB overdose and first aid.
The most common symptoms of an DOB overdose (with each increase in the starting average dose by 10%, the probability of occurrence of one of the following symptoms increases by 25%): panic attack, paranoia, delusions of persecution, anxiety, disorientation, small-scale tremor, shortness of breath, respiratory arrhythmia, increased sweating.Desirable/positive effects: stimulation (motor, research, speech, behavioral activity) - is pronounced, sometimes corresponds with that of synthetic psychostimulants-cathinone derivatives; spontaneous bodily sensations – body high, euphoria and empathy; enhanced tactile feelings; increased physical performance and endurance; a sense of increased "body control", when it seems that one has a complete control of every cell of the body in the physical aspect; moderate visual illusions, auditory illusions, increased brightness of color, improved visual acuity, the appearance of "new color shades"; the desire to communicate, perform various routine work; analysis enhancement – which is described as expressed ability to creatively analyze information, deep contemplation and the appearance of various ideas; positive emotions; positive suggestibility; high frequency of thought processes, high speed of information processing; the appearance of "conceptual" thinking.
Undesirable negative effects: disorder of temperature regulation with an increase in body temperature; muscle spasm, fine tremor; increased heart rate; increased blood pressure; heart rhythm disturbances; nausea, rarely - vomiting; decreased appetite up to its complete absence; difficulty of urination up to the complete impossibility of emptying the bladder; peripheral vasospasm; bruxism; "restless legs" syndrome; mydriasis; dehydration; rarely-diarrhea; headache; pain, tingling, discomfort in sternum area; increased salivation and increased sweating; paranoia, constant anxiety; impairment of short-term memory; hypophasia; a sense of" flowing time", distortion of time frames; " thought loop; internal and external hallucinations up to terrible, hysterical representations, leading to a panic attack with syncope; hppd-syndrome.
DOB – is a very powerful substance, which effects last significantly longer comparing to other psychedelics. DOB overdose is a serious and extremely dangerous condition. Exceeding recommended dosages can be life-threatening! DOB barely causes addiction. Desire to use it can be present as a regular thought without mania or sense of addiction. Tolerance is moderate; it disappears when DOB is not used in 7-15 days. Also, there is cross tolerance between DOB and all representatives of the phenylethylamine class.
DOB overdose and first aid.
In case of an overdose non-pharmacological help includes: identifying anxiety, understanding that everything occurring is no more than the substance effect, and it will stop soon, you can try breathing exercises with deep inhale and slow exhale for a short time; it is necessary to immediately free your head of all the thoughts in the head, and try to think of good moments in your life that are associated with the pleasant tones of the color palette (color-associated model); if you are a setter, it is necessary to have a therapeutic conversation with the tripper, explain the situation, change location, if the negative effects are associated with the environment.
As for pharmacological treatment, initially, it is necessary to consider using bare minimum of medications. In patients with light anxiety and worrying, drinking 50-100 ml. of strong alcohol with herbs (but no more) can help. If the situation is not improving within 30 minutes and anxiety persists, as a rule, it is necessary to use benzodiazepine tranquilizers: alprazolam (0.5-1 mg). In severe cases of overdose, when there is intense anxiety with signs of delusions of persecution, paranoia - it is necessary to use neuroleptics, when using DOB, the drug of choice is chlorpromazine (50 or 100 mg).
Alcohol's central depressant effects can be used to reduce some of the anxiety and tension produced by DOB. However, alcohol can cause dehydration, nausea and physical fatigue which can negatively influence the trip. Users are advised to pace themselves and drink a portion of their usual amount if making the decision to drink on DOB. Benzodiazepines are highly effective at reducing the intensity of DOB's effects through the general suppression of brain activity. DOB enhances the cognitive, visual and general hallucinatory effects of dissociative.
Dissociative-induced holes, spaces, and voids and internal hallucinations become more vivid and intense on DOB. These effects correspond with an increased risk of confusion, delusions, and psychosis.
Antidepressant and antipsychotic drugs may block the effect of DOB by acting on the same receptors and outcompeting their ability to bind. Antidepressants mirtazapine and trazodone act on the 5-HT2A and 5-HT2C receptors, where they block serotonin and other molecules from binding. Atypical antipsychotics also act on these receptors in order to decrease hallucinations and cognitive distortion. Lithium is commonly prescribed in the treatment of bipolar disorder; however, there is a large body of anecdotal evidence that suggests taking it with psychedelics can significantly increase the risk of psychosis and seizures. As a result, this combination should be strictly avoided. Tricyclic antidepressants increase physical, hallucinatory and psychological responses to DOB. Since the symptoms are similar to those induced by lithium and DOB, seizures cannot be excluded.
Tramadol is well documented to lower the seizure threshold in individuals, and DOB also has the potential to induce seizures in susceptible individuals. Cannabis can have an unexpectedly strong and unpredictable synergy with DOB. While it is commonly used to intensify or prolong DOB's effects, caution is highly advised as mixing these substances can significantly increase the risk of negative psychological effects like anxiety, paranoia, panic attacks, and psychosis. Anecdotal reports often describe the ingestion of cannabis as the triggering event for a bad trip or psychosis. It is advised to start off with only a fraction (e.g. 1/4th - 1/3rd) of their typical cannabis dose and space out hits to avoid accidental over intake.
In order to prevent dyspeptic functional disorders of the gastrointestinal tract, 6 hours before they use the consumption of anything other than water is not recommended, and also the consumption of heavy food and large amounts of food is not recommended 12 hours before the use. Pharmacological prevention of dyspeptic functional disorders includes metoclopramide 5-10 mg 2 hours before taking DOB.
DOB interactions with other substances.
- Low risk: alcohol, GHB, benzodiazepines, SSRI, opiates, psilocibines, LSD, DMT (only at minimal doses, in the case of increased doses, joint use can be extremely dangerous).
- Medium risk: DXM, PCP, tramadol, cocaine, amphetamine, ketamine.
- High risk: αMT, mescaline, MAO inhibitors, MDMA, MXE, cannabis, 5-MeO-xxT, 2C-x, 2C-Tx, NBOMes.
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