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Buy MDAI Drug Online

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5,6-Methylenedioxy-2-aminoindane (also known as MDAI) is a lesser-known novel entactogen substance of the aminoindane class. Notably, this compound primarily produces the non-stimulating effects of prototypical entactogens like MDMA such as sedation, muscle relaxation, and tactile enhancement.

MDAI was developed in the 1990s by a team led by David E. Nichols at Purdue University. It acts as a putatively non-neurotoxic and highly selective serotonin releasing agent (SSRA) with neglible effects on dopamine and norepinephrine. This reportedly limits its potential at producing overtly invigorating, prosocial or euphoric effects.

MDAI has been marketed alongside research chemical entactogens like 5-MAPB, 5-APB, and 6-APB as a legal, grey-market alternative to MDMA.

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Very little data exists about the pharmacological properties, metabolism, and toxicity of MDAI, and it has a limited history of human use. It is highly advised to use harm reduction practices if using this substance.

MDAI, or 5,6-methylenedioxy-2-aminoindane, is a synthetic molecule of the aminoindane class with structural similarity to amphetamines. It features the R3 terminal carbon of the propane chain of amphetamine bound to the benzene ring. This creates an indane group, a bicyclic moeity containing a benzene ring fused to a pentane ring. MDAI contains an amino group NH2 bound to R2 of the indane ring. MDAI also contains two oxygen substitutions at R5 and R6 joined by a methylene bridge to form a methylenedioxy group.

MDAI is structurally related to 2-AI, differing by a methylenedioxy ring.

MDAI has been shown to inhibit the reuptake of serotonin and has a selective affinity for the serotonin receptor. Studies have shown that the brains of animals treated with MDAI have greater extracellular concentrations of monoamine neural transmitters, most significantly serotonin.

For comparison, MDAI is similar in potency with releasing serotonin to MDA, but significantly less potent than MDMA. This is done by inhibiting the reuptake and reabsorption of the neurotransmitters after they have performed their function of transmitting a neural impulse, essentially allowing them to accumulate, be reused and cause entactogenic effects.

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