JRT (drug)
JRT, also known as isoindole-LSD or isotryptamine-LSD, is a serotonin receptor modulator, psychoplastogen, and serotonergic psychedelic related to lysergic acid diethylamide. It is the analogue of LSD in which the embedded tryptamine structure within the ergoline ring system of LSD has been replaced with an isotryptamine structure.
The drug acts as a non-selective serotonin receptor modulator, including as a partial agonist of the serotonin 5-HT2A receptor and as an agonist or antagonist of various other serotonin receptors. The drug has psychedelic-like, psychoplastogenic, antipsychotic-like, antidepressant-like, and pro-cognitive effects in animals and preclinical studies, whilst lacking apparent pro-psychotic-like effects. It has significant but reduced psychedelic-like effects compared to LSD in animals. The drug is a racemic mixture of - and - enantiomers, with -JRT being the active and employed form.
JRT was first described in the scientific literature by 2022 and was described in greater detail in 2025. It was developed by David E. Olson and colleagues in association with Delix Therapeutics. The drug is being investigated as a possible treatment for schizophrenia.
Use and effects
The properties and effects of JRT in humans do not yet appear to be known.Pharmacology
Pharmacodynamics
-JRT is highly selective for a subset of serotonin receptors and does not bind to various dopamine, adrenergic, or histamine receptors, which is in contrast to LSD. It shows high affinity for the serotonin 5-HT2 receptors, with Ki values ranging from 2.0 to 184nM. The drug is a potent partial agonist of the serotonin 5-HT2A and 5-HT2B receptors and a full agonist of the serotonin 5-HT2C receptor. It is also an agonist of the serotonin 5-HT1A and 5-HT7 receptors, an antagonist of the serotonin 5-HT5A and 5-HT7 receptors, and a ligand of the serotonin 5-HT6 receptor. -JRT does not have significant affinity for the serotonin 5-HT1B or 5-HT3 receptors, whereas its affinities for the other serotonin 5-HT1 receptors and the serotonin 5-HT4 receptor were not reported.The drug is 4.4- to 180-fold less potent than LSD as a serotonin 5-HT2A receptor agonist in vitro and is less efficacious than LSD in activating the receptor. It has been found to dissociate from the serotonin 5-HT2A receptor approximately 10-fold more quickly than LSD.
-JRT produces the head-twitch response, a behavioral proxy of psychedelic effects, in rodents, and hence would be expected to be hallucinogenic in humans. However, the drug shows a reduced HTR compared to LSD, producing less than half the maximal number of head twitches. It can also antagonize or diminish the HTR induced by LSD. Hence, -JRT may be less psychedelic than LSD in humans. LSD and -JRT are of similar potency in producing the HTR, with a maximal HTR being achieved at a dose of 0.2mg/kg for both drugs.
-JRT does not affect locomotor activity and does not produce any serotonin behavioral syndrome-type effects. It has been found to inhibit dextroamphetamine-induced hyperlocomotion in female but not male mice, to not exacerbate phencyclidine -induced hyperlocomotion, to not worsen dizocilpine -induced prepulse inhibition, and to not induce PPI deficits itself. Some of these findings are in contrast to reuslts with LSD, and are suggestive that -JRT lacks psychotic-like effects and may have antipsychotic potential.
In addition to its other effects, -JRT has been reported to increase neuroplasticity and hence to act as a psychoplastogen, to produce antidepressant-like effects, and to promote cognitive flexibility. It was equivalent with LSD in terms of producing psychoplastogenic effects.