JRT — Safety, Research, Risks & Legal Status

Not medical advice. JRT is discussed here for informational and harm-reduction purposes only. We do not endorse use, and any dosing context is informational, not a protocol.

Also known as	(+)-JRT; isotryptamine-LSD; Tuck compound (informal)
Category	Research Chemical
Molecular formula	C₂₀H₂₅N₃O (323.44 g/mol); constitutional isomer of LSD
Structural class	Indolonaphthyridine; created by carbon-nitrogen transposition in the LSD scaffold
5-HT2A Emax	81% (partial agonist); dissociates from 5-HT2A ~10-fold faster than LSD
Preclinical neuroplasticity	46% increase in dendritic spine density, 18% increase in synapse density in rodent mPFC (single dose)
Development stage (mid-2026)	Phase 2 clinical trials underway; FDA IND cleared; developer: Delix Therapeutics
Named after	Jeremy R. Tuck, co-developer at UC Davis; first formally described in Lee Dunlap's 2022 PhD dissertation
US legal status	Not currently listed on DEA Schedule I-V. However, as a structural isomer of LSD (a Schedule I controlled substance), it may be subject to prosecution under the Federal Analogue Act if intended for human consumption outside of an approved clinical context. An FDA Investigational New Drug (IND) application has been cleared, and JRT is advancing through regulated clinical trials under Delix Therapeutics. It is not approved for any indication and is not legally available for human use outside of authorized clinical research settings.

What is JRT?

JRT is a synthetic indolonaphthyridine compound and constitutional isomer of LSD, created by transposing a single carbon-nitrogen bond in the LSD scaffold via a 12-step de novo synthesis. It was designed as a "non-hallucinogenic psychoplastogen" - a compound intended to promote neuroplasticity and psychiatric benefit while lacking the hallucinogenic properties of classical psychedelics. It is under active clinical development by Delix Therapeutics in partnership with academic groups at UC Davis, the Salk Institute, Harvard Medical School/McLean Hospital, and Weill Cornell Medicine.

How it works

JRT acts as a potent partial agonist at serotonin 5-HT2A receptors (81% Emax) and a near-full agonist at 5-HT2C receptors, with comparatively reduced activity at 5-HT2B. The key design feature is disruption of an indole N-H hydrogen bond interaction with serotonin receptors while preserving downstream Gq protein signaling, which is believed to mediate neuroplasticity. JRT dissociates from 5-HT2A approximately 10-fold faster than LSD, a kinetic property hypothesized to underlie its reduced hallucinogenic potential. It does not appear to have significant affinity for dopamine, histamine, or adrenergic receptors in preclinical profiling.

Background & history

JRT was first formally described in a 2022 PhD dissertation by Lee E. Dunlap at UC Davis, under the mentorship of David Olson's lab (known for psychoplastogen research). The compound is named informally after Jeremy R. Tuck, one of its co-developers. A peer-reviewed paper describing its molecular design and preclinical characterization was published in PNAS in April 2025. Delix Therapeutics, the commercial development partner, received FDA IND clearance and completed Phase 1 trials; Phase 2 trials - including studies of at-home administration - were underway as of mid-2026.

What the research says

All efficacy and mechanism data as of mid-2026 derive from in vitro studies and rodent models; no published human efficacy data exist. In murine models, a single dose produced a 46% increase in dendritic spine density and an 18% increase in synapse density in the medial prefrontal cortex. JRT was reported to be approximately 100-fold more potent than ketamine in the forced-swim test (a rodent model of depression), and reversed stress-induced cognitive deficits and anhedonia in mice. Critically, JRT did not induce the head-twitch response (HTR) in mice - a standard surrogate marker for hallucinogenic activity - and actively blocked LSD-induced HTR. It did not impair prepulse inhibition, and gene expression analysis showed no enrichment for schizophrenia-associated loci (in contrast to LSD). ADME profiling was favorable, including absence of hERG channel inhibition, a common cardiac safety disqualifier. Phase 1 human trial results were characterized as positive for safety and biomarker endpoints, but the detailed adverse event profile has not been released in the public literature as of this writing.

Reported effects

Promoted dendritic spine and synapse density in rodent prefrontal cortex (preclinical only)
Antidepressant-like effects in murine forced-swim and stress models (preclinical only)
Reversal of stress-induced anhedonia and cognitive deficits in mice (preclinical only)
No hallucinogenic effects observed in rodent HTR assay; actively blocked LSD-induced HTR
Did not impair sensory gating (prepulse inhibition) in animal models
Favorable ADME profile in preclinical studies, including absence of cardiac hERG liability
Human effects profile unknown pending publication of Phase 1/2 trial data

Dosing & administration (informational)

Dose ranges used in preclinical rodent studies are reported in the primary PNAS publication (PubMed: "JRT neuroplastogen LSD analog Olson PNAS 2025"). Phase 1 human dosing data, if released, would appear in ClinicalTrials.gov trial records under Delix Therapeutics. No clinically established or recommended human dose exists. This information is provided for reference only and does not constitute a protocol or recommendation. Anyone considering participation in JRT research should consult a licensed clinician and enroll only through authorized clinical trial channels.

This is general research/context information, not medical advice or a recommended protocol.

Safety & side effects

No human safety or efficacy data published as of mid-2026; Phase 1 results described as positive but not released in detail
No hallucinogenic effects or head-twitch response in rodent models
No serotonin syndrome-like responses at therapeutic doses in preclinical work
Did not affect locomotion or motor behavior in animal studies
Theoretical 5-HT2B-mediated cardiac valvulopathy risk with chronic use - a concern raised by analogy with other partial 5-HT2B agonists; not yet reported in JRT clinical use
Lacks dopamine, histamine, and adrenergic receptor activity, which may reduce off-target risk relative to LSD
Not for human use outside of authorized clinical trials; regulatory, purity, and long-term safety profiles are unknown outside the clinical development program

Drug & supplement interactions

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Who should avoid it

Use outside of authorized clinical trial protocols
Combination with MAOIs, serotonergic drugs, or other 5-HT2A ligands without medical supervision
Use by individuals with personal or family history of psychotic disorders (precaution consistent with all 5-HT2A-active agents pending human data)
Chronic self-administration given unresolved 5-HT2B cardiac valvulopathy signal
Sourcing from non-pharmaceutical channels where identity and purity cannot be confirmed
Use during pregnancy or lactation - no safety data exist

How it is commonly combined

No stacking data exist for JRT in humans. Preclinical design intent was to isolate neuroplastic 5-HT2A Gq signaling from hallucinogenic effects; any combination with other serotonergic, psychedelic, or neuroactive compounds is untested and potentially hazardous. No combination protocols can be recommended.

Legal & regulatory. Not currently listed on DEA Schedule I-V. However, as a structural isomer of LSD (a Schedule I controlled substance), it may be subject to prosecution under the Federal Analogue Act if intended for human consumption outside of an approved clinical context. An FDA Investigational New Drug (IND) application has been cleared, and JRT is advancing through regulated clinical trials under Delix Therapeutics. It is not approved for any indication and is not legally available for human use outside of authorized clinical research settings.

Quality & harm reduction

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Frequently asked questions

Is JRT the same as LSD?

No. JRT is a constitutional isomer of LSD, meaning it shares the same molecular formula but has a different arrangement of atoms - specifically a carbon-nitrogen transposition in the indole ring system. This structural change appears to substantially alter receptor binding kinetics and eliminates hallucinogenic activity in rodent models, though human effects have not been published.

Has JRT been tested in humans?

Phase 1 clinical trials have been completed with results described as positive for safety and biomarker endpoints as of mid-2026, but the detailed data have not been published in peer-reviewed literature. Phase 2 trials including at-home administration studies were underway. No published human efficacy or safety data are available.

What dose should I take?

No dose recommendation can be made. JRT is an unapproved investigational drug with no established human dosing. All human exposure has occurred within controlled, FDA-authorized clinical trials. If you are interested in access, consult a clinician and inquire about participation in authorized trials via ClinicalTrials.gov.

Is JRT legal to possess or buy?

JRT is not listed on the DEA controlled substance schedules as of mid-2026, but it is not legal for human use outside of authorized clinical research. As an LSD structural isomer, it may fall under Federal Analogue Act jurisdiction if sold or possessed with intent for human consumption. It is not commercially available; any material sold outside the clinical program cannot be verified as authentic.

What is JRT being developed to treat?

Based on published preclinical data and trial descriptions, development targets include depression, schizophrenia, and potentially other psychiatric conditions involving synaptic deficits. The emphasis in published literature is on treating psychiatric diseases associated with reduced neuroplasticity. No indication has been approved.

What makes JRT different from ketamine or psilocybin for depression?

JRT targets serotonin 5-HT2A/2C receptors rather than NMDA receptors (ketamine) or broadly activating 5-HT2A (psilocybin with hallucinogenic effects). Its proposed advantage over both is the combination of neuroplastic Gq signaling and the absence of subjective hallucinogenic effects, which in preclinical models appears to be separable from antidepressant-like activity. Whether this translates to clinical differentiation is not yet established from human data.

References & further reading

PubMed: "JRT neuroplastogen LSD analog Olson PNAS 2025" (primary molecular design paper)
PubMed: "isotryptamine psychoplastogen 5-HT2A non-hallucinogenic" (mechanism studies)
PubMed: "5-HT2A partial agonist dendritic spine neuroplasticity" (broader psychoplastogen context)
ClinicalTrials.gov: search "Delix Therapeutics" or "JRT depression" for Phase 1/2 trial records
PNAS April 2025: doi.org/10.1073/pnas.2416106122 (Molecular design of a therapeutic LSD analogue with reduced hallucinogenic potential)