Pharmacodynamics Similarly to
MDMA, 5-IAI acts as a
serotonin–norepinephrine–dopamine releasing agent (SNDRA). Its values for induction of monoamine release have not been reported. In any case, its relative
potency for monoamine release is serotonin > dopamine > norepinephrine. In addition, 5-IAI's
affinity (Ki) values for the
monoamine transporters are 879nM for the
serotonin transporter (SERT), 311nM for the
norepinephrine transporter (NET), and 992nM for the
dopamine transporter (DAT), whereas its values in terms of
functional inhibition have been reported to be 241nM or 2,500nM at the SERT, 612nM or 760nM at the NET, and 992nM or 2,300nM at the DAT in two different respective studies. In addition to its interactions with the monoamine transporters, 5-IAI shows high affinity for the
serotonin 5-HT1A,
5-HT2A,
5-HT2B, and
5-HT2C receptors, as well as affinity for the
α2A-,
α2B-, and
α2C-adrenergic receptors. The high affinity for the
serotonin receptors is in contrast to
MDAI. 5-IAI and MDAI fully substitute for MDMA in
drug discrimination tests in rodents. This suggests that they produce MDMA-like subjective and entactogenic effects in rodents. Unlike related
2-aminoindane derivatives like MDAI and
MMAI, 5-IAI causes some
serotonergic neurotoxicity in rats (15% or less reduction of serotonergic markers), but is less neurotoxic than its corresponding
amphetamine homologue
para-iodoamphetamine (pIA) and the doses employed have been described as "extremely high". In any case, regular high-dose 5-IAI has been found to produce
cognitive and
memory deficits in rodents. ==History==