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6-APDB (also known as 6-(2-aminopropyl)-2,3-dihydrobenzofuran or 4-Desoxy-MDA) is a stimulant and entactogenic research chemical of the phenethylamine and benzofuran classes. It is a closely related synthetic analogue of MDA and 6-APB and broadly shares the characteristics of serotonin-selective triple monoamine releasers and reuptake inhibitors associated with other entactogenic or empathogenic compounds.

6-APDB was first synthesized and studied along with 5-APDB in 1993 by David E. Nichols as a potential non-neurotoxic alternative to MDMA. It did not come into popular recreational use until over a decade later, where it briefly entered the rave scene and global research chemicals market, in particular the “legal highs” market in the U.K., before its sale and import were subsequently banned.

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Because 6-APDB and other substituted benzofurans have not been explicitly outlawed in some countries, they are often technically legal, contributing to their popularity as a substitute or replacement for serotonergic entactogens like MDMA or MDA, and are typically distributed through the online research chemicals grey market.

6-APDB, also known as 6-(2-aminopropyl)-2,3-dihydrobenzofuran, is a synthetic molecule of the benzofuran family. Molecules of this class contain a phenethylamine core bound to an amino (NH2) group through an ethyl chain with an additional methyl substitution at Rα.

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6-APDB does not contain a methyl substitution on RN, a motif which it shares with MDA. It is an analogue of MDA where the heterocyclic 4-position oxygen from the 3,4-methylenedioxy ring has been replaced with a methylene bridge. 6-APDB shares this furan ring with 5-APDB, 5-MAPDB and 6-MAPDB.

6-APDB acts as a releasing agent and triple reuptake inhibitor of the monoamine neurotransmitters known as serotonin, dopamine and noradrenaline which are the global neurotransmitters that modulate the brain’s ability to feel pleasure, motivation, reward, planning, attention and focus. This is done by promoting the release and inhibiting the reuptake and reabsorption of the neurotransmitters after they have performed their function of transmitting a neural impulse through release into the synaptic cleft, essentially allowing them to accumulate and render them liable for immediate reuse.

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