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MBDB
MBDB, also known as N-methyl-1,3-benzodioxolylbutanamine or as 3,4-methylenedioxy-N-methyl-α-ethylphenylethylamine, is an entactogen of the phenethylamine, amphetamine, and phenylisobutylamine families related to MDMA. It is known by the nicknames "Eden" and "Methyl-J".
MBDB was first synthesized by pharmacologist and medicinal chemist David E. Nichols and later tested by Alexander Shulgin and described in his book, PiHKAL: A Chemical Love Story. MBDB's dose, according to PiHKAL, is 180 to 210 mg; the proper dosage relative to body mass seems unknown. Its duration is 4 to 8 hours, with noticeable after-effects lasting for 1 to 3 hours.
MBDB was initially developed as a non-psychedelic entactogen. It has lower effects on the dopamine system in comparison to other entactogens such as MDMA. MBDB causes many mild, MDMA-like effects, in particular the lowering of social barriers and inhibitions, pronounced sense of empathy and compassion, and mild euphoria, all of which are present. MBDB tends to produce less euphoria, psychedelia, and stimulation in comparison to MDMA.
Clinical studies have found that MBDB produces similar entactogenic effects to MDMA, but lacks psychedelic and stimulant effects. It enhances mood similarly to MDMA, but lacks the pronounced euphoria of MDMA. MBDB produces prosocial effects similarly to MDMA, although it is said to be moderately less effective.
MBDB acts as a serotonin–norepinephrine releasing agent (SNRA). Its EC50 values for induction of monoamine release are 540 nM for serotonin, 3,300 nM for norepinephrine (6.1-fold lower than for serotonin), and >100,000 for dopamine (>185-fold lower than for serotonin). However, it may still have slight dopamine-releasing actions. MBDB fully substitutes for MDMA in drug discrimination tests in rodents. It increases locomotor activity similarly to but less robustly than MDMA. Likewise, MBDB increases conditioned place preference (CPP) similarly but less efficaciously than MDMA. In contrast to MDMA, which produced hyperthermia, MBDB instead produced dose- and time-dependent hypothermia.
MBDB has similar affinities for the serotonin 5-HT1A and 5-HT2A receptors as MDMA. However, MBDB did not show the head-twitch response, a behavioral proxy of psychedelic effects, at any dose in rodents. On the other hand, it produced a significant head-twitch response at a low dose but not at higher doses in another study in rodents. In any case, MBDB (as well as MDMA) do not substitute for lysergic acid diethylamide (LSD) in drug discrimination tests. The lack of apparent hallucinogenic effects with MBDB is analogous to the case of Ariadne, the α-ethyl homologue of DOM; (R)-Ariadne (BL-3912A) showed no psychedelic effects in humans at doses of up to 270 mg orally, whereas DOM is active as a hallucinogen at doses of 5 to 10 mg orally. This may be due to lower activational efficacy at the serotonin 5-HT2A receptor.
MBDB shows greatly reduced capacity to increase oxytocin levels in rodents compared to MMAI and 4-methylthioamphetamine (4-MTA), for reasons that are unclear.
MBDB is a serotonergic neurotoxin similarly to MDMA. However, MBDB appears to have reduced serotonergic neurotoxicity compared to MDMA at behaviorally equivalent doses. In addition, unlike MDMA, MBDB does not produce dopaminergic neurotoxicity in mice.
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MBDB
MBDB, also known as N-methyl-1,3-benzodioxolylbutanamine or as 3,4-methylenedioxy-N-methyl-α-ethylphenylethylamine, is an entactogen of the phenethylamine, amphetamine, and phenylisobutylamine families related to MDMA. It is known by the nicknames "Eden" and "Methyl-J".
MBDB was first synthesized by pharmacologist and medicinal chemist David E. Nichols and later tested by Alexander Shulgin and described in his book, PiHKAL: A Chemical Love Story. MBDB's dose, according to PiHKAL, is 180 to 210 mg; the proper dosage relative to body mass seems unknown. Its duration is 4 to 8 hours, with noticeable after-effects lasting for 1 to 3 hours.
MBDB was initially developed as a non-psychedelic entactogen. It has lower effects on the dopamine system in comparison to other entactogens such as MDMA. MBDB causes many mild, MDMA-like effects, in particular the lowering of social barriers and inhibitions, pronounced sense of empathy and compassion, and mild euphoria, all of which are present. MBDB tends to produce less euphoria, psychedelia, and stimulation in comparison to MDMA.
Clinical studies have found that MBDB produces similar entactogenic effects to MDMA, but lacks psychedelic and stimulant effects. It enhances mood similarly to MDMA, but lacks the pronounced euphoria of MDMA. MBDB produces prosocial effects similarly to MDMA, although it is said to be moderately less effective.
MBDB acts as a serotonin–norepinephrine releasing agent (SNRA). Its EC50 values for induction of monoamine release are 540 nM for serotonin, 3,300 nM for norepinephrine (6.1-fold lower than for serotonin), and >100,000 for dopamine (>185-fold lower than for serotonin). However, it may still have slight dopamine-releasing actions. MBDB fully substitutes for MDMA in drug discrimination tests in rodents. It increases locomotor activity similarly to but less robustly than MDMA. Likewise, MBDB increases conditioned place preference (CPP) similarly but less efficaciously than MDMA. In contrast to MDMA, which produced hyperthermia, MBDB instead produced dose- and time-dependent hypothermia.
MBDB has similar affinities for the serotonin 5-HT1A and 5-HT2A receptors as MDMA. However, MBDB did not show the head-twitch response, a behavioral proxy of psychedelic effects, at any dose in rodents. On the other hand, it produced a significant head-twitch response at a low dose but not at higher doses in another study in rodents. In any case, MBDB (as well as MDMA) do not substitute for lysergic acid diethylamide (LSD) in drug discrimination tests. The lack of apparent hallucinogenic effects with MBDB is analogous to the case of Ariadne, the α-ethyl homologue of DOM; (R)-Ariadne (BL-3912A) showed no psychedelic effects in humans at doses of up to 270 mg orally, whereas DOM is active as a hallucinogen at doses of 5 to 10 mg orally. This may be due to lower activational efficacy at the serotonin 5-HT2A receptor.
MBDB shows greatly reduced capacity to increase oxytocin levels in rodents compared to MMAI and 4-methylthioamphetamine (4-MTA), for reasons that are unclear.
MBDB is a serotonergic neurotoxin similarly to MDMA. However, MBDB appears to have reduced serotonergic neurotoxicity compared to MDMA at behaviorally equivalent doses. In addition, unlike MDMA, MBDB does not produce dopaminergic neurotoxicity in mice.
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