Bromo-DragonFLY

Bromo-DragonFLY was first synthesized by Matthew Parker in the laboratory of David E. Nichols in 1998. As with the earlier and less potent dihydrofuran series of compounds nicknamed FLY, Bromo-DragonFLY was named after its superficial structural resemblance to a dragonfly.

Bromo-DragonFLY also has a high binding affinity for the 5-HT_2B and 5-HT_2C serotonin receptors, and is most accurately described as a non-subtype selective 5-HT₂ agonist, as it is actually twice as potent an agonist for 5-HT_2C receptors as for 5-HT_2A, as well as being less than 5x selective for 5-HT_2A over 5-HT_2B.[4][5] Bromo-DragonFLY is also a MAO-A inhibitor,[6] and thus strongly inhibits oxidative deamination of 5-HT, increasing its risk profile.

The first synthesis of racemic Bromo-DragonFLY was reported by David E. Nichols in 1998 and was an expansion upon earlier research into the tetrahydrobenzodifuran analogue of DOB.[7] The 1998 synthesis of racemic Bromo-DragonFLY starts from hydroquinone, which is dialkylated with 1-bromo-2-chloroethane, brominated, and treated with n-butyllithium to yield the tetrahydrobenzodifuran ring system. After formylation of the ring system, the nitropropene derivative was obtained by condensation with nitroethane under ammonium acetate catalysis. The nitropropene derivative was then reduced with lithium aluminum hydride to yield the amine intermediate, which was protected with trifluoroacetic anhydride. Following para-bromination with elemental bromine and oxidation of the tetrahydrobenzodifuran ring system with DDQ, the trifluoroacetyl protecting group of the amine was removed to give Bromo-DragonFLY as a racemic mixture of the R and S enantiomers.

In 2001, David E. Nichols reported an enantiospecific synthesis of Bromo-DragonFLY which allowed the individual R and S enantiomers to be studied.[8] Further research determined that (R)-(-)-Bromo-DragonFLY possessed greater binding affinity at the 5-HT_2A and 5-HT_2C receptors than (S)-(-)-Bromo-DragonFLY. To synthesize the more active R enantiomer, a derivative of D-alanine was reacted with 2,3,6,7-tetrahydrobenzodifuran in a Friedel–Crafts acylation, yielding an intermediate containing a β-keto moiety which was removed by treatment with triethylsilane in trifluoroacetic acid. After para-bromination and oxidation of the ring system with DDQ, the amine was deprotected yielding (R)-(-)-Bromo-DragonFLY.

The 1997 synthesis of Bromo-DragonFLY by Nichols et al.[9]

The 2001 enantiospecific synthesis of (R)-(-)-Bromo-DragonFLY by Nichols et al.[10]

The typical dose of Bromo-DragonFLY is not known, however it has varied from 500 μg to 1 mg.[3] It has about 300 times the potency of mescaline, or 1/3 the potency of LSD. It has been sold in the form of blotters, similar to the distribution method of LSD, which has led to confusion and reports of mistakenly consuming Bromo-DragonFly. It has a much longer duration of action than LSD and can last for up to 2–3 days[3] following a single large dose, with a slow onset of action that can take up to 6 hours before the effects are felt.

4BDF powder. The pink color is most likely due to an impurity. The color of pure BDF is usually white to off-white, similar to most recreational drugs, so there is no way to distinguish between them by eye.

The toxicity of Bromo-DragonFLY appears to be fairly high for humans, with reports of at least five deaths believed to have resulted from Bromo-DragonFLY reported in Norway,[11] Sweden,[12][13] Denmark,[14][15] Finland[16] and the United States. Laboratory testing has confirmed that in October 2009, a batch of Bromo-Dragonfly was distributed, mislabeled as the related compound 2C-B-FLY, which is around 20x less potent than BDF by weight. This mistake is believed to have contributed to several lethal overdoses and additional hospitalizations. The batch implicated in these deaths also contained significant synthesis impurities, which may have contributed to the toxicity.[17]

Vasoconstrictive action resulting from severe overdose of Bromo-DragonFLY is known to have caused tissue necrosis of the extremities in at least one case. In September 2007, a 35-year-old Swedish male required amputation of the front part of his feet and several fingers on one hand after taking a massive (but unknown) overdose; reportedly, the compound acted as a long-acting efficacious vasoconstrictor, leading to necrosis and gangrene which became apparent several weeks after the overdose occurred. Treatment was of limited efficacy in this case, although tolazoline is reportedly an effective treatment where available.[18][19]

Overdose-associated disturbing experiences and health problems have been described. One case in 2008 in England involved inhalation of vomit, causing nearly fatal asphyxia.[20] Seizures have also been reported.[21]

On October 3, 2009, a 22-year-old male from Copenhagen died after ingesting Bromo-dragonfly. His friend described the trip saying, "It was like being dragged to hell and back again. Many times. It is the most evil [thing] I've ever tried. It lasted an eternity." [22]

On May 7, 2011, in the United States, two young adults died after overdosing on Bromo-DragonFLY, which they thought was 2C-E, and several others were hospitalized during the same incident. Because they took a dosage appropriate for 2C-E, those who took the drug received, in some cases, 100x the normal dose. Both deaths followed seizures, vomiting blood, and terrifying hallucinations. Several surviving victims are reportedly still suffering from its physical effects.[23]

• 2C-B
• DOB
• 2C-B-FLY
• 5-HT_2A receptor
• PiHKAL
• Ergotism