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LSM-775
lysergic acid morpholide
LSM-775 (lysergic acid morpholide) is a synthetic psychedelic of the lysergamide class. It is a close structural relative of LSD, but far less potent. It activates serotonin receptors in two opposing ways — generating and simultaneously suppressing psychedelic signals — producing a body-heavy, muted result.[1][2]
LSM-775 (lysergic acid morpholide) is a semi-synthetic psychedelic of the lysergamide class. It is a structural derivative of LSD, distinguished by markedly lower potency and a heavier somatic profile. LSM-775 activates both 5-HT₁A and 5-HT₂A serotonin receptors, producing its effects through a dual action in which 5-HT₁A agonism actively suppresses its own psychedelic signaling.[1][2]
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Albert Hofmann synthesized LSM-775 at Sandoz Laboratories in the mid-1950s, searching for new lysergic acid derivatives.[3] Three small human studies confirmed it was 5 to 10 times weaker than LSD with a heavier side-effect profile; Sandoz abandoned development, and the compound lay dormant until it resurfaced on the research chemical market in 2013.[1] It remains unscheduled in most countries and circulates in small quantities among research chemical users.
Subjective effects include nausea, sedation, mild geometric visual patterns, mood shifts, and pervasive bodily heaviness. The experience is defined by somatic weight — a nauseogenic, heavy baseline through which faint perceptual changes emerge, less a psychedelic journey than a body burden with psychedelic undertones.[4] Vomiting, rapid heart rate, heavy sweating, and cardiovascular discomfort are characteristic unwanted effects.
LSM-775 produces no physical dependence, and no lethal dose has been established — rapid tolerance makes compulsive redosing self-limiting.[5] The dominant hazard is the pronounced body load: severe nausea, vomiting, and cardiovascular stress at effective doses, plus a theoretical risk of heart valve damage with repeated use.[1] Understanding rests on a single 2018 pharmacological study and sparse user reports — no clinical trials or toxicity data exist.
History[edit]
Discovery
Albert Hofmann synthesized LSM-775 at Sandoz Laboratories in Basel in the mid-1950s, as part of a systematic exploration of lysergic acid derivatives.[1][6] The first human data appeared in 1957: 75 µg produced roughly the same effect as 50 µg of LSD, but with shorter duration.[3] Two further small studies confirmed it was 5 to 10 times less potent than LSD and unable to produce more than threshold psychedelic effects.[1]
Institutional trajectory
Sandoz did not pursue LSM-775 further. Unlike LSD, which the company marketed as Delysid for psychiatric research, LSM-775's weak potency and unfavorable profile — sedation and nausea at effective doses — made it unsuitable for clinical development.
Modern era
LSM-775 reappeared in 2013 on the research chemical market, presumably based on historical reports of weak LSD-like effects.[1] This prompted the first modern pharmacological characterization by Brandt and colleagues in 2018 — the only published study specific to the compound.[1] It remains unscheduled in most jurisdictions and circulates in small quantities.
The designation "LSM" comes from the German Lysergsäure-Morpholid (lysergic acid morpholide), and "775" is its Sandoz compound number — the same naming convention as LSD-25. It is known mainly among research chemical enthusiasts as an example of how a small structural change to LSD can dramatically alter the character of the experience.
Chemistry[edit]
Structural class
LSM-775 belongs to the lysergamide family, sharing the same four-ring ergoline core as LSD, 1P-LSD, and AL-LAD. The defining difference from LSD is a morpholine ring in place of LSD's two flexible ethyl groups — a structural change that constrains the molecule's shape and alters how it fits into serotonin receptor binding sites.[7]
Molecular identity
| Molecular formula | C₂₀H₂₃N₃O₂ |
| Molecular weight | 337.4 g/mol |
The morpholine ring contains an oxygen atom absent in LSD, making LSM-775 slightly less lipophilic. The absolute configuration of its two stereocenters has been confirmed by X-ray crystallography of the hemitartrate salt.[1]
Pharmacology[edit]
Mechanism of action
LSM-775 acts at two serotonin receptor types simultaneously, with opposing effects.[1] One generates psychedelic activity; the other — more potently activated — produces sedation and actively suppresses that psychedelic signal. Psychedelic-type behavior only appears in animal models when the suppressive pathway is blocked first[1][2] — a pattern also seen with 5-MeO-DMT and the non-hallucinogenic drug lisuride.[2][8][9]
Pharmacokinetics
No pharmacokinetic studies have been published for LSM-775. Absorption, distribution, and elimination are entirely uncharacterized. By analogy with LSD, liver enzymes likely handle metabolism, and slow metabolizers probably experience stronger and longer effects.[10]
Historical reports describe the duration as shorter than LSD at comparable doses.[3][4] Community data suggest onset at 10–30 minutes and total duration of 6–10 hours.[11] inferred
Neuroscience[edit]
No direct neuroimaging, electrophysiological, or neuroplasticity data have been published for LSM-775. The following draws on class-level evidence from serotonergic psychedelics and LSM-775's specific pharmacological profile. inferred
Where it acts
Classical serotonergic psychedelics produce their effects by activating receptors on neurons in the prefrontal cortex, disrupting the brain's normal filtering of sensory input.[12] LSM-775 engages this pathway partially, while simultaneously fully activating a second receptor type that slows neuronal firing and dampens arousal — introducing a powerful brake on the psychedelic signal.
The behavioral result is stark: no psychedelic response in animals unless the suppressive pathway is blocked first.[1] The likely experience is a partially loosened perceptual state — far less disruption than LSD or psilocybin. The sedation and nausea users report[4] likely reflect the suppressive pathway acting on arousal and nausea circuits in the brainstem.
Why it matters
Psychedelics are thought to work partly by loosening rigid thinking patterns — increasing the brain's flexibility through serotonin receptor activation. LSM-775's suppression of that activation would constrain this effect, predicting mild perceptual loosening without the deeper dissolution seen with LSD or psilocybin. Whether it promotes new brain connections, as other serotonergic psychedelics do, is unknown.
- Does LSM-775 promote new brain connections at pharmacologically relevant doses, and are these proportional to its partial receptor activation?
- What happens to the morpholine ring when metabolized — does it produce active breakdown products?
- Does LSM-775 affect dopamine systems, as its shared structure with LSD would predict?
Subjective Effects[edit]
The LSM-775 experience is built on a heavy, nauseogenic foundation. Physical weight, bodily discomfort, and cardiovascular awareness persist throughout, with faint psychedelic shifts — mild visuals, mood changes — emerging through that baseline rather than dominating it. The body is the foreground; altered perception is the background.
Relative to LSD, LSM-775 is notably less visual and more sedating, characterized by somatic burden rather than cognitive or perceptual expansion. Within the lysergamide family, it most closely resembles a low-dose experience of ergine (LSA) — muted and body-heavy — though the underlying mechanisms differ.
Synthesized by Albert Hofmann at Sandoz Laboratories in the mid-1950s as part of a systematic exploration of lysergic acid amide derivatives, LSM-775 was one of hundreds of ergoline compounds screened for psychoactive potential.[3] Three small human studies found it markedly weaker than LSD and incapable of producing more than threshold psychedelic effects, and Sandoz abandoned further development.[1] The compound resurfaced on the research chemical market in 2013, prompting its first modern pharmacological characterization in 2018.[1]
Subjective effects include nausea, sedation, mild geometric visual patterns, and mood alteration. The experience is defined by its somatic weight — a heavy, nauseogenic baseline through which muted psychedelic shifts emerge, more bodily burden than perceptual expansion.[4] Vomiting, tachycardia, excessive sweating, and cardiovascular discomfort are characteristic unsought effects.
LSM-775 produces no physical dependence, and no lethal dose has been established — rapid tolerance makes compulsive redosing self-limiting.[5] The primary risk is pronounced body load at effective doses: nausea, vomiting, and cardiovascular stress dominate, and repeated use raises a theoretical concern for heart valve damage through 5-HT₂B activation.[1] The current understanding rests on a single 2018 pharmacological study and sparse user reports — no clinical trials, toxicity data, or human pharmacokinetic measurements exist.
History[edit]
Discovery
LSM-775 was synthesized by Albert Hofmann at Sandoz Laboratories in Basel during the mid-1950s, part of a systematic program exploring lysergic acid amide structure-activity relationships.[1][6] The first published human data appeared in 1957, when Gogerty and Dille reported that 75 µg produced roughly the same subjective response as 50 µg of LSD in two subjects, with shorter duration.[3] Two additional small studies confirmed LSM-775 as approximately 5- to 10-fold less potent than LSD by weight and incapable of producing more than threshold psychedelic effects.[1]
Institutional trajectory
Sandoz did not pursue LSM-775 commercially. Unlike LSD, which the company marketed as Delysid for psychiatric research, LSM-775's attenuated potency and unfavorable side-effect profile — sedation and nausea at effective doses — rendered it unsuitable for clinical development. No pharmaceutical company has investigated the compound in any therapeutic context, and it produced no discernible scientific or cultural impact during its initial era.
Modern era
LSM-775 reappeared in 2013 on the new psychoactive substances market, sold as a research chemical — presumably motivated by historical reports suggesting weak LSD-like effects.[1] This emergence prompted the first modern pharmacological characterization by Brandt and colleagues in 2018, published as part of the "Return of the Lysergamides" research series — the only published investigation specific to LSM-775.[1] The compound remains unscheduled in most jurisdictions and circulates in small quantities among research chemical users.
The designation "LSM" derives from the German Lysergsäure-Morpholid (lysergic acid morpholide), and "775" is its Sandoz laboratory compound number — following the same naming convention as LSD-25. The compound occupies a footnote in lysergamide history, known primarily among research chemical enthusiasts as an example of how small structural modifications to the LSD molecule can dramatically alter the character of the experience.
Chemistry[edit]
Structural class
LSM-775 belongs to the lysergamide family of ergoline derivatives, sharing the tetracyclic ergoline core with LSD, 1P-LSD, and AL-LAD. The defining structural modification is the replacement of LSD's N,N-diethylamide group at C-9 with a morpholine ring, forming a cyclic amide. This rigid ring constrains the spatial orientation of the amide nitrogen, directly altering how the molecule fits into serotonin receptor binding pockets.[7]
Molecular identity
| Molecular formula | C₂₀H₂₃N₃O₂ |
| Molecular weight | 337.4 g/mol |
The core structure consists of four fused rings — the indole moiety (rings A and B), the cyclohexane ring (C), and the piperidine ring (D) — with a morpholine substituent at C-9. The morpholine ring contains an oxygen atom that introduces an additional hydrogen-bond acceptor site absent in LSD, contributing to the compound's somewhat lower lipophilicity.
Stereochemistry
LSM-775 has two chirality centers at C-6a and C-9, both in the R-configuration: (6aR,9R). This matches the pharmacologically active d-isomer series shared by LSD and other active lysergic acid derivatives. The absolute configuration has been confirmed by X-ray crystallography of the hemitartrate salt.[1]
Structure-activity relationships
The morpholine substitution is the key structural determinant of LSM-775's pharmacological profile. LSD's flexible diethyl groups adopt specific conformations to optimally occupy the 5-HT₂A binding pocket;[8] the rigid morpholine ring disrupts these interactions, reducing psychedelic potency while leaving 5-HT₁A activity relatively intact.[7] The result is a compound that retains strong serotonergic activity but shifts the balance from hallucinogenic to sedative-somatic effects.
Pharmacology[edit]
Mechanism of action
LSM-775 acts simultaneously at two serotonin receptor types with opposing functional consequences.[1] At 5-HT₂A — the receptor responsible for psychedelic effects — it functions as a partial agonist, activating the receptor with reduced efficacy compared to LSD or serotonin. At 5-HT₁A, it functions as a full agonist with high potency, producing sedation and dampening the excitatory outputs of 5-HT₂A activation.
This dual action creates an unusual self-suppressing pharmacology: LSM-775's 5-HT₁A activity actively masks the psychedelic effects mediated by its own 5-HT₂A activity. In the standard animal model for hallucinogenic potential, LSM-775 alone produces no significant response — hallucinogenic-type behavior emerges only when 5-HT₁A receptors are pharmacologically blocked.[1][2] This masking phenomenon parallels observations with 5-MeO-DMT[2][9] and is analogous to the non-hallucinogenic 5-HT₂A agonist lisuride.[10]
Despite sharing the ergoline scaffold with LSD — which binds dopamine D₂ receptors with high affinity[8] — no published binding data confirm dopamine receptor activity for LSM-775.[1] Dopamine receptor engagement is plausible but remains experimentally unconfirmed. inferred
Pharmacokinetics
No pharmacokinetic studies have been published for LSM-775 in any species. Absorption, distribution, metabolism, and elimination parameters are entirely uncharacterized.
By structural analogy with LSD, metabolism likely involves hepatic cytochrome enzymes, and poor metabolizers of related compounds show substantially higher plasma concentrations and prolonged effects.[11] LSD's principal urinary metabolite is 2-oxo-3-hydroxy-LSD,[12] and a similar pathway is plausible for LSM-775 but unmeasured.
Historical reports describe LSM-775's duration as shorter than LSD at equivalent subjective doses,[3][4] suggesting either faster elimination or shorter receptor residence time, but neither parameter has been determined. Community-derived data suggest total duration of 6–10 hours with onset at 10–30 minutes by the oral route.[13] inferred
Neuroscience[edit]
No direct neuroimaging, electrophysiological, or neuroplasticity data have been published for LSM-775. The following discussion draws on class-level evidence from serotonergic psychedelics and LSM-775's specific pharmacological profile. inferred
Where it acts
Classical serotonergic psychedelics produce their effects through 5-HT₂A activation on pyramidal neurons in the prefrontal cortex, disrupting the brain's default filtering of sensory and cognitive input.[14] LSM-775's partial 5-HT₂A agonism engages this pathway, but its concurrent full 5-HT₁A agonism introduces a countervailing brake — reducing neuronal firing rates in the cortex and dampening arousal circuits in the brainstem.
The behavioral evidence is stark: LSM-775 produces no head-twitch response in mice unless 5-HT₁A receptors are blocked first.[1] The neural prediction is a partially engaged psychedelic state — some disruption of default mode network integrity and cortical synchronization, but substantially attenuated compared to compounds like LSD or psilocybin. The prominent sedation and nausea reported by users[4] likely reflect 5-HT₁A-driven suppression of arousal and activation of brainstem emetic circuits.
Why it matters
The REBUS model (relaxed beliefs under psychedelics) predicts that psychedelics loosen rigid cognitive patterns by increasing cortical entropy through 5-HT₂A activation. LSM-775's 5-HT₁A suppression of 5-HT₂A output would constrain this entropy increase, predicting mild perceptual loosening without the full dissolution of conceptual boundaries seen with LSD or psilocybin.
Whether LSM-775 promotes neuroplasticity — dendritic growth and synapse formation, as documented for other 5-HT₂A agonists — is unknown. Whether partial agonists produce proportionally reduced neuroplastic effects is an open question in the field, and LSM-775 could serve as a useful test case.
- Does LSM-775 produce neuroplastic effects at pharmacologically relevant doses, and are these proportional to its partial 5-HT₂A efficacy?
- What is the metabolic fate of the morpholine ring in vivo — does ring-opening produce active metabolites?
- Does LSM-775 bind dopamine D₂ receptors, as the shared ergoline core with LSD would predict?
Subjective Effects[edit]
The LSM-775 experience is shaped less by psychedelic intensity than by the pharmacological tension between its two primary receptor actions. A sedative, somatically heavy foundation — nausea, bodily heaviness, cardiovascular awareness — persists across dose ranges, with attenuated perceptual shifts emerging through this baseline rather than dominating it. Set and setting influence the psychological dimension, but the somatic burden remains a near-constant feature that compresses the experiential window relative to most lysergamides.
Relative to LSD, LSM-775 occupies a qualitatively distinct space: less visually immersive, more sedating, and characterized by body load rather than cognitive or perceptual expansion. The closest experiential analogy within the lysergamide family is the muted, body-heavy quality sometimes described with low-dose ergine (LSA), though the underlying pharmacological mechanisms differ.
Effect Grid
A recognizable but attenuated psychedelic state emerges. Color alteration takes on the earthy, sepia-toned quality characteristic of LSM-775. Mild geometry, visual drifting, and internal hallucinations are present but muted relative to LSD at equivalent subjective intensity. Depth perception distortion and perspective distortion may be noticed.
Body load is significant and defines the experience at this tier: nausea is persistent, sedation and dreaminess are prominent, and spontaneous body sensations — sweating, temperature dysregulation, cardiovascular awareness — are common. Pupil dilation is expected. Appetite is strongly suppressed.
Thought connectivity and conceptual thinking are enhanced. Introspection deepens. Time alteration is noticeable. The experience lasts 6–9 hours with residual fatigue afterward.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Holotropic state · Sleep-transition hallucinations · Tracers · Light sensitivity · Visual breathing · Color alteration · Visual morphing · Auditory enhancement · After-images · Visual haze / noise · Sound sensitivity · Brightness alteration · Depth perception distortion · Symmetrical texture repetition · Environmental patterning · Perspective distortion · Touch enhancement · Dreaming enhancement · Spatial disorientation · Proprioceptive distortion · Ganzfeld effect · Auditory distortion · Visual diffraction · Peripheral vision distortion · Synesthesia · Visual melting · Auditory misinterpretation · Vestibular distortion · Peripheral misidentification · Visual acuity enhancement · Taste enhancement · Olfactory enhancement · Visual magnification · Tinnitus · Flashbacks · Object transformations · Internal hallucinations · Object activation · External hallucinations · Visual recursion · Auditory hallucinations · Perspective hallucinations · Visual flipping · Visual scenery slicing · Environmental orbism / cubism · Visual processing suppression · Shadow people · Persisting hallucinations
Visual breathing · Color alteration · Visual morphing · Auditory enhancement · After-images · Visual haze / noise · Sound sensitivity · Brightness alteration · Depth perception distortion · Symmetrical texture repetition · Environmental patterning · Perspective distortion · Touch enhancement · Dreaming enhancement · Spatial disorientation · Proprioceptive distortion · Ganzfeld effect · Auditory distortion · Visual diffraction · Peripheral vision distortion · Synesthesia · Visual melting · Auditory misinterpretation · Vestibular distortion · Peripheral misidentification · Visual acuity enhancement · Taste enhancement · Olfactory enhancement · Visual magnification · Tinnitus · Flashbacks · Object transformations · Internal hallucinations · Object activation · External hallucinations · Visual recursion · Auditory hallucinations · Perspective hallucinations · Visual flipping · Visual scenery slicing · Environmental orbism / cubism · Visual processing suppression · Shadow people · Persisting hallucinations
Stimulation · Spontaneous body sensations · Appetite suppression · Wakefulness · Nausea · Muscle tension · Heart rate perception changes · Tingling / electric sensations · Insomnia · Physical fatigue · Tactile euphoria · Excessive sweating · Dizziness · Restlessness · Vibrations / buzzing · Dry mouth · Laughter fits · Bodily pressures · Bodily lightness · Sexual arousal enhancement · Yawning · Body schema distortion · Trembling · Headache · Bruxism · Involuntary body movements · Bodily heaviness · Dehydration sensation · Nystagmus (eye wobbles) · Motor control impairment · Breathing alteration · Watery eyes · Vomiting · Bodily dissociation · Tactile hallucination
Wakefulness · Nausea · Muscle tension · Heart rate perception changes · Tingling / electric sensations · Insomnia · Physical fatigue · Tactile euphoria · Excessive sweating · Dizziness · Restlessness · Vibrations / buzzing · Dry mouth · Laughter fits · Bodily pressures · Bodily lightness · Sexual arousal enhancement · Yawning · Body schema distortion · Trembling · Headache · Bruxism · Involuntary body movements · Bodily heaviness · Dehydration sensation · Nystagmus (eye wobbles) · Breathing alteration · Watery eyes · Vomiting · Bodily dissociation · Tactile hallucination
Thought connectivity · Aesthetic enhancement · Openness enhancement · Multiple thought streams · Cognitive flexibility · Pattern recognition enhancement · Novelty enhancement · Thought acceleration · Increased nature relatedness · Immersion enhancement · Creativity enhancement · Thought loops · Confusion · Analysis enhancement · Humor enhancement · Focus suppression · Cognitive impairment · Synchronicity · Cognitive fatigue · Information processing enhancement · Motivation enhancement · Language enhancement · Memory fragmentation · Thought disorganization · Memory replays · Language suppression · Information processing suppression · Focus enhancement · Cognitive dysphoria · Delusions of sobriety · Memory suppression · Motivation suppression · Thought organization · Amnesia
Multiple thought streams · Cognitive flexibility · Pattern recognition enhancement · Novelty enhancement · Thought acceleration · Increased nature relatedness · Immersion enhancement · Creativity enhancement · Thought loops · Confusion · Analysis enhancement · Humor enhancement · Focus suppression · Cognitive impairment · Synchronicity · Cognitive fatigue · Information processing enhancement · Motivation enhancement · Language enhancement · Memory fragmentation · Thought disorganization · Memory replays · Language suppression · Information processing suppression · Focus enhancement · Cognitive dysphoria · Memory suppression · Motivation suppression · Thought organization · Amnesia
Empathy enhancement · Simultaneous emotions · Catharsis · Anxiety · Anxiety suppression · Dysphoria · Irritability
Anxiety suppression · Dysphoria · Irritability
Sociability enhancement · Disinhibition · Trust enhancement · Communication enhancement · Flow state · Compulsive behavior reduction · Automaticity · Social disconnection · Communication suppression · Ego inflation · Boundary dissolution · Ego dissolution · Identity alteration · Telepathic feelings · Cognitive disconnection
Flow state · Compulsive behavior reduction · Automaticity · Social disconnection · Communication suppression · Ego inflation · Boundary dissolution · Ego dissolution · Identity alteration · Telepathic feelings · Cognitive disconnection
Time cessation
Entity contact · Transpersonal visions · Transpersonal memory access · Death-rebirth sequence · Voidness · Cessation · Near-death experience
Voidness · Cessation · Near-death experience
Lucidity enhancement · Recursive awareness
Timeline
First alerts emerge as mild somatic awareness — light nausea, subtle bodily heaviness, and faint mood shift. No perceptual changes yet.
Body load builds noticeably: nausea intensifies, sedation and heaviness set in. First perceptual shifts appear — subtle color alteration and brightness changes.
Maximum perceptual and somatic effects. Sepia-toned color alteration, mild geometry, and internal hallucinations present. Nausea peaks with possible vomiting.
Perceptual effects gradually recede while body load persists. Nausea fades before visual effects. Sedation and physical fatigue remain prominent.
Residual physical fatigue and possible mild mood effects. Appetite may slowly return. Cognitive baseline approaches normal but subtle sedation may linger.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
No lethal dose has been established for LSM-775 in any species, and no controlled toxicity studies have been conducted.[1] By class analogy, serotonergic psychedelics have extremely wide safety margins in animal models, and no death has been attributed solely to LSD despite decades of widespread use.[12] This is expected to apply to LSM-775, but remains unconfirmed. safety citation needed
No case reports of overdose, hospitalization, or fatality involving LSM-775 have been published.
Body load
At effective doses, LSM-775 produces severe nausea, vomiting, rapid heart rate, heavy sweating, and elevated blood pressure.[4] This somatic burden is more intense than typically seen with LSD or psilocybin at equivalent psychedelic doses and is the compound's most significant acute concern.
Cardiac considerations
LSM-775 activates a receptor type — present in heart valve tissue — whose chronic stimulation is the established mechanism behind drug-induced valve disease, documented with related ergot-derived drugs.[1] No cardiac safety data specific to LSM-775 exist. The concern applies only to repeated or chronic exposure. safety citation needed
Psychological Risks
The standard psychological risks of serotonergic psychedelics apply: acute anxiety, confusion, thought loops, and challenging experiences — particularly in stressful settings or in people with pre-existing psychiatric vulnerabilities. Lasting perceptual disturbances — HPPD — are a recognized class-level concern.[13]
LSM-775's weaker hallucinogenic potency may reduce the intensity of perceptual challenges but does not eliminate psychological distress risk. The sedating, nauseogenic quality can itself produce dysphoria. Personal or family history of psychotic disorders, schizophrenia, or bipolar disorder is a risk factor for acute psychiatric crisis with any serotonergic psychedelic.
Tolerance and Dependence
Serotonergic psychedelics produce rapid tolerance through receptor adaptation, within 24 hours of a single dose.[5] Cross-tolerance between psychedelics operates through the same mechanism.[5] Community data for LSM-775 report tolerance building almost immediately, with a half-life of approximately 6 days and full reset at 14 days.[11]
No abuse liability has been documented for LSM-775. Serotonergic psychedelics are generally non-addictive as a class,[12] and rapid tolerance development mechanically discourages compulsive redosing.
Drug Interactions
Serotonin syndrome risk
Combining LSM-775 with serotonergic medications risks triggering serotonin syndrome — a dangerous state of serotonin overload causing muscle rigidity, high fever, rapid heart rate, and agitation. Tramadol presents a dangerous interaction by this mechanism.[14] SSRIs and SNRIs carry a theoretical risk; a review of antidepressant-psychedelic combinations found no confirmed cases in clinical studies, though most studies excluded participants on serotonergic medications.[15] SSRIs may also reduce LSM-775's psychedelic effects.
MAOI combinations present the most severe theoretical risk: blocking serotonin breakdown could amplify LSM-775's serotonergic activity beyond safe levels.
Seizure threshold interactions
Lithium combined with lysergamides is a recognized seizure risk. No LSM-775-specific data exist, but the combination is contraindicated by class analogy. citation needed
Cannabis
The interaction between LSM-775 and cannabis is uncharacterized. Cannabis has been reported to intensify and prolong serotonergic psychedelic effects in user reports, but no controlled data exist. citation needed
Contraindications
8 knownAbsolute contraindications:
- Psychotic disorders or personal history of psychosis — serotonergic psychedelics may trigger or worsen psychotic episodes.
- Concurrent MAOI use — risk of severe serotonin syndrome.
- Concurrent tramadol use — serotonin syndrome risk.[14]
Relative contraindications:
- Bipolar disorder — risk of triggering manic episodes, particularly in bipolar I.
- Family history of psychotic disorders — elevated risk of psychedelic-triggered psychosis.
- Concurrent SSRI/SNRI use — theoretical serotonin syndrome risk, though confirmed cases are absent from the literature.[15] Likely reduced psychedelic effects.
- Heart conditions — the documented cardiovascular effects (rapid heart rate, elevated blood pressure) suggest caution.[4]
- Concurrent lithium use — seizure risk by class analogy with other lysergamides. citation needed
Harm Reduction[edit]
Forms & Identification
LSM-775 has no pharmaceutical formulations and circulates exclusively through the research chemical market as powder, crystalline salt, or blotter. Analytical confirmation is critical: no field test can distinguish LSM-775 from LSD or other ergoline derivatives. Reagent tests (Ehrlich, Hofmann) confirm the presence of an indole or ergoline compound but cannot identify the specific substance. Laboratory analysis through an energy-control or similar service is the only reliable method.
Dosing precision is essential. LSM-775 is active in the high-microgram to low-milligram range, and research chemical batches vary in purity. A milligram-precision scale (0.001 g) is required for preparing volumetric solutions. Measuring individual doses from loose powder without a scale is unsafe.
Guidelines
- Test all material with Ehrlich and Hofmann reagents to confirm the presence of an ergoline compound. Send a sample for laboratory analysis if possible.
- Use a milligram-precision scale. Prepare volumetric solutions for accurate dosing at the microgram level.
- Start with a low dose (250–500 µg oral) to assess individual response before increasing. The body load scales with dose.
- Have anti-nausea measures available: ginger, light meals beforehand, or an empty stomach — preferences vary, but preparation helps.
- Arrange a comfortable environment with easy bathroom access. Keep water available.
- Have a sober, trusted companion present, especially for higher doses or first experiences.
- Allow at least 14 days between uses for full tolerance reset.
- Do not redose during the experience. The slow onset (10–30 minutes) and extended body load make stacking doses unpredictable.
Set & Setting
LSM-775's pronounced somatic burden makes environment preparation more important than with cleaner-feeling psychedelics. Nausea and vomiting are common at effective doses — a bathroom and a comfortable place to lie down should be available before dosing. A calm, familiar environment with a trusted companion is strongly recommended, especially for a first experience.
The attenuated psychedelic intensity does not eliminate psychological risk. Physical discomfort combined with residual perceptual shifts can produce dysphoria in a stressful or unfamiliar setting.
Aftercare & integration. The somatic intensity of the LSM-775 experience can leave the body depleted. Prioritize hydration and light nutrition in the hours following, particularly if vomiting occurred. Rest is advisable — sedative effects may persist as fatigue into the following day.
Psychological integration follows the same principles as other psychedelic experiences. Journaling, conversation with a trusted person, or quiet reflection can help process insights or difficult material. If distressing thoughts or perceptual changes persist beyond 48 hours, consult a mental health professional experienced with psychedelic experiences.
Recovery & Support
Serotonergic psychedelics are generally non-addictive, and LSM-775's pronounced body load and rapid tolerance further discourage compulsive use. Problematic patterns — using to escape rather than explore, escalating frequency despite negative effects — warrant honest self-assessment.
If use is causing distress or interfering with daily functioning, the Fireside Project (call or text 62-FIRESIDE) offers confidential, non-judgmental peer support. For persistent psychological difficulty, a therapist experienced with psychedelic integration can help.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Severe chest pain or heart palpitations that do not subside
- Uncontrollable vomiting or inability to keep fluids down for more than 2 hours
- Seizure or loss of consciousness
- Complete dissociation from reality with risk of self-harm
- Signs of serotonin syndrome: muscle rigidity, high fever, tachycardia, agitation (if combined with serotonergic drugs)
Immediate steps:
- Move the person to a safe, quiet space.
- If vomiting, place in the recovery position to prevent aspiration.
- Call emergency services if symptoms are severe or worsening — do not wait.
- Stay with the person. Speak calmly and provide reassurance.
- Do not induce vomiting. Do not restrain unless there is immediate danger.
What to tell the dispatcher:
State the substance name (LSM-775 or lysergic acid morpholide), estimated amount taken, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
Legal Status[edit]
LSM-775 is not listed in the United Nations Convention on Psychotropic Substances, and most jurisdictions have not enacted substance-specific controls.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not explicitly scheduled | Not listed in DEA schedules. Federal Analogue Act applicability is legally uncertain — the morpholine ring may place LSM-775 outside the structural scope of specifically covered ergoline analogs.[16] |
| United Kingdom | Psychoactive Substances Act 2016 | Not listed in the Misuse of Drugs Act 1971. Production, supply, import, and export are illegal under the PSA. Possession for personal use is not criminalized. |
| Germany | NpSG (Neue-psychoaktive-Stoffe-Gesetz) | Controlled since July 18, 2019. Production and import with intent to distribute, administration to another person, and trading are punishable. Possession for personal use is illegal but not penalized. |
| Switzerland | Betäubungsmittelverzeichnis, Verzeichnis E | Controlled as a defined derivative of lysergic acid under point 263. Scientific and industrial use is exempt. |
| Canada | Not controlled | Not a controlled substance as of May 2026.[16] |
| Australia | Not explicitly scheduled | No evidence of specific TGA scheduling. May fall under state or territory analogue frameworks, but no explicit schedule decision has been identified. |
Analogue act considerations
In the United States, the Federal Analogue Act could theoretically extend Schedule I controls to LSM-775 given its structural relationship to LSD — but the morpholine ring is a significant structural departure, placing the compound in a legal grey area.[16] No case law specific to LSM-775 prosecution under the Act has been identified.
Legal status changes frequently and varies by jurisdiction. This information is not legal advice. Verify current law before acting.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
No lethal dose has been established for LSM-775 in any species, and no controlled toxicity studies have been conducted.[1] By class analogy, serotonergic psychedelics possess extremely wide safety margins in animal models, and no death attributable solely to LSD has been confirmed despite decades of widespread use.[14] This general safety margin is expected to extend to LSM-775 but remains unconfirmed. safety citation needed
No case reports of overdose, hospitalization, or fatality involving LSM-775 have been published.
Body load
The most significant acute concern specific to LSM-775 is its pronounced body load at effective doses. A user report at approximately 1.1 mg oral documented severe nausea, vomiting at approximately 2 hours, rapid heart rate, excessive sweating, and elevated blood pressure.[4] These effects are consistent with full 5-HT₁A agonism and represent a more severe somatic burden than typically observed with LSD or psilocybin at equivalent subjective psychedelic doses.
Cardiac considerations
LSM-775's partial agonism at serotonin₂B receptors[1] raises a theoretical concern for heart valve damage with repeated use. Chronic 5-HT₂B activation is the established mechanism behind drug-induced valve disease documented with ergot derivatives such as pergolide and cabergoline. No cardiac safety data specific to LSM-775 exist, and the risk applies only to chronic or repeated exposure patterns. safety citation needed
Psychological Risks
The standard psychological risk profile of serotonergic psychedelics applies: acute anxiety, confusion, thought loops, and challenging experiences may occur, particularly in unfavorable set and setting or in individuals with pre-existing psychiatric vulnerabilities. Risk of HPPD (HPPD) is a recognized class-level concern.[15]
LSM-775's attenuated hallucinogenic potency may reduce the intensity of challenging perceptual experiences but does not eliminate psychological distress risk. The dominant 5-HT₁A component introduces a sedative, nauseogenic quality that could itself produce a dysphoric experience when combined with residual psychedelic effects.
Personal or family history of psychotic disorders, schizophrenia, or bipolar disorder constitutes a risk factor for acute psychiatric crisis with any serotonergic psychedelic.
Tolerance and Dependence
Serotonergic psychedelics produce rapid tolerance through downregulation, occurring within 24 hours of a single dose.[5] Cross-tolerance between psychedelics operates through this shared mechanism.[5] Community-derived data for LSM-775 report tolerance building almost immediately after ingestion, with a half-life of approximately 6 days and full reset at 14 days.[13]
No abuse liability has been documented for LSM-775. Serotonergic psychedelics are generally considered non-addictive as a class.[14] Rapid tolerance development mechanistically discourages compulsive redosing.
Drug Interactions
Serotonin syndrome risk
Combining LSM-775 with serotonergic medications poses a risk of serotonin syndrome. Tramadol is classified as a dangerous interaction, consistent with the established risk profile of tramadol combined with serotonergic agents.[16]
SSRIs, SNRIs, and MAOIs carry serotonin syndrome risk when combined with serotonergic psychedelics. A scoping review of antidepressant-psychedelic combinations found no confirmed serotonin syndrome cases in published clinical studies, though most studies excluded participants on serotonergic medications.[17] SSRIs may also attenuate LSM-775's psychedelic effects.
MAOI combinations present the most severe theoretical risk: blocking serotonin breakdown could amplify LSM-775's serotonergic activity beyond safe levels.
Seizure threshold interactions
Lithium combined with lysergamides is a recognized seizure risk. No LSM-775-specific data exist, but the combination is contraindicated by class analogy. citation needed
Cannabis
The interaction between LSM-775 and cannabis is uncharacterized. Cannabis has been reported to intensify and prolong serotonergic psychedelic effects in user reports, but controlled data are absent. citation needed
Contraindications
8 knownAbsolute contraindications:
- Psychotic disorders or personal history of psychosis — serotonergic psychedelics may trigger or worsen psychotic episodes.
- Concurrent MAOI use — risk of severe serotonin syndrome.
- Concurrent tramadol use — serotonin syndrome risk.[16]
Relative contraindications:
- Bipolar disorder — risk of triggering manic episodes, particularly in bipolar I.
- Family history of psychotic disorders — elevated risk of psychedelic-triggered psychosis.
- Concurrent SSRI/SNRI use — theoretical serotonin syndrome risk, though confirmed cases are absent from the literature.[17] Likely reduced psychedelic effects.
- Heart conditions — the pronounced cardiovascular effects (rapid heart rate, elevated blood pressure) documented in user reports[4] suggest caution.
- Concurrent lithium use — seizure risk by class analogy with other lysergamides. citation needed
Harm Reduction[edit]
Forms & Identification
LSM-775 has no pharmaceutical formulations and circulates exclusively through the research chemical market as powder, crystalline salt, or blotter. Analytical confirmation is particularly important for this compound: it shares physical forms with many lysergamides of widely varying potency, and no field test can distinguish LSM-775 from LSD or other ergoline derivatives. Reagent testing (Ehrlich, Hofmann) confirms the presence of an indole or ergoline compound but cannot identify the specific substance — laboratory analysis through an energy-control or similar service is the only reliable method.
Dosing precision is critical. LSM-775 is active in the high-microgram to low-milligram range, and research chemical batches vary in purity. A milligram-precision scale (0.001 g) is the minimum requirement for preparing volumetric solutions; measuring individual doses from loose powder without a scale is unsafe.
Guidelines
- Test all material with Ehrlich and Hofmann reagents to confirm the presence of an ergoline compound. Send a sample for laboratory analysis if possible.
- Use a milligram-precision scale. Prepare volumetric solutions for accurate dosing at the microgram level.
- Start with a low dose (250–500 µg oral) to assess individual response before increasing. The body load scales with dose.
- Have anti-nausea measures available: ginger, light meals beforehand, or an empty stomach — preferences vary, but preparation helps.
- Arrange a comfortable environment with easy bathroom access. Keep water available.
- Have a sober, trusted companion present, especially for higher doses or first experiences.
- Allow at least 14 days between uses for full tolerance reset.
- Do not redose during the experience. The slow onset (10–30 minutes) and extended body load make stacking doses unpredictable.
Set & Setting
LSM-775's pronounced somatic burden makes environment preparation more important than with cleaner-feeling psychedelics. Nausea and vomiting are common at effective doses, so access to a bathroom and a comfortable place to lie down should be ensured before dosing. A calm, familiar environment with a trusted sitter is strongly recommended, particularly for first experiences.
The attenuated psychedelic intensity does not eliminate psychological risk. Set and setting influence the character of the experience as with all serotonergic psychedelics, and the combination of physical discomfort with residual perceptual shifts can produce dysphoria if the environment is stressful or unfamiliar.
Aftercare & integration. The somatic intensity of the LSM-775 experience can leave the body feeling depleted. Prioritize hydration and light nutrition in the hours following the experience, particularly if vomiting occurred. Rest is advisable — the 5-HT₁A-driven sedation may persist as fatigue into the following day.
Psychological integration follows the same principles as other psychedelic experiences. Journaling, conversation with a trusted person, or quiet reflection can help process any insights or difficult material that emerged. If distressing thoughts or perceptual changes persist beyond 48 hours, consult a mental health professional experienced with psychedelic experiences.
Recovery & Support
Serotonergic psychedelics are generally considered non-addictive, and LSM-775's pronounced body load and rapid tolerance further discourage compulsive use. Problematic patterns of psychedelic use — using to escape rather than explore, escalating frequency despite negative effects — warrant honest self-assessment.
If use is causing distress or interfering with daily functioning, peer support organizations such as the Fireside Project (call or text 62-FIRESIDE) offer confidential, non-judgmental support. For persistent psychological difficulty, a therapist experienced with psychedelic integration can help.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Severe chest pain or heart palpitations that do not subside
- Uncontrollable vomiting or inability to keep fluids down for more than 2 hours
- Seizure or loss of consciousness
- Complete dissociation from reality with risk of self-harm
- Signs of serotonin syndrome: muscle rigidity, high fever, tachycardia, agitation (if combined with serotonergic drugs)
Immediate steps:
- Move the person to a safe, quiet space.
- If vomiting, place in the recovery position to prevent aspiration.
- Call emergency services if symptoms are severe or worsening — do not wait.
- Stay with the person. Speak calmly and provide reassurance.
- Do not induce vomiting. Do not restrain unless there is immediate danger.
What to tell the dispatcher:
State the substance name (LSM-775 or lysergic acid morpholide), estimated amount taken, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
Legal Status[edit]
LSM-775 is not listed in the United Nations Convention on Psychotropic Substances (1971), and most jurisdictions have not enacted substance-specific controls. Where addressed, the compound falls under broad structural analog or novel psychoactive substance legislation rather than explicit scheduling.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not explicitly scheduled | Not listed in DEA schedules. Federal Analogue Act applicability is legally uncertain — the morpholine ring may place LSM-775 outside the structural scope of specifically covered ergoline analogs.[18] |
| United Kingdom | Psychoactive Substances Act 2016 | Not listed in the Misuse of Drugs Act 1971. Production, supply, import, and export are illegal under the PSA. Possession for personal use is not criminalized. |
| Germany | NpSG (Neue-psychoaktive-Stoffe-Gesetz) | Controlled since July 18, 2019. Production and import with intent to distribute, administration to another person, and trading are punishable. Possession for personal use is illegal but not penalized. |
| Switzerland | Betäubungsmittelverzeichnis, Verzeichnis E | Controlled as a defined derivative of lysergic acid under point 263. Scientific and industrial use is exempt. |
| Canada | Not controlled | Not a controlled substance as of May 2026.[18] |
| Australia | Not explicitly scheduled | No evidence of specific TGA scheduling. May fall under state or territory analogue frameworks, but no explicit schedule decision has been identified. |
Analogue act considerations
In the United States, the Federal Analogue Act extends Schedule I/II controls to substances "substantially similar" in structure or effect to a listed substance when intended for human consumption. LSM-775's relationship to LSD (Schedule I) makes analogue prosecution theoretically possible, but the morpholine substitution represents a significant structural departure from LSD's diethylamide group. Legal analysis suggests the compound occupies a grey area under current analogue law.[18] No case law specific to LSM-775 prosecution under the Act has been identified.
Frequently asked questions
What is LSM-775?
LSM-775 is a semisynthetic lysergamide psychedelic derived from lysergic acid, active in the high-microgram to low-milligram range. First synthesized at Sandoz Laboratories, it is 5–10× less potent than LSD due to 5-HT1A agonism masking its 5-HT2A-mediated effects.
How long does LSM-775 last?
Total duration by route of administration — Oral: 6 – 10 hours. Ranges vary with dose and individual factors; see the duration table for onset, peak, and after-effect phases.
Where can I find dosage information for LSM-775?
Psychedex publishes a dosage table for LSM-775 on this page covering these routes of administration: oral. Dose values are presented only in that table, always alongside their route of administration.
What are dangerous combinations with LSM-775?
The highest-severity documented interactions for LSM-775: MAOIs (Lethal), Dopamine agonists (Dangerous), GHB, Baclofen (Dangerous), GHB, GBL (Dangerous), Ibogaine (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is LSM-775 addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for LSM-775: tolerance builds rapid; full reset takes 14 days; cross-tolerance develops with LSD, psilocybin, mescaline, DMT, other lysergamides. See the article's dependence and safety sections for recorded dependence data.
experience reports
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1] ^abcdefghijklmBrandt SD, Kavanagh PV, Twamley B, Westphal F, Elliott SP, Wallach J, Stratford A, Klein LM, McCorvy JD, Nichols DE, Halberstadt AL (2018) Return of the lysergamides. Part IV: Analytical and pharmacological characterization of lysergic acid morpholide (LSM-775) — Drug Testing and Analysis doi:10.1002/dta.2222
- [2] ^abcHalberstadt AL, Koedood L, Powell SB, Geyer MA (2011) Differential contributions of serotonin receptors to the behavioral effects of indoleamine hallucinogens in mice — Journal of Psychopharmacology doi:10.1177/0269881110388326
- [3] ^abcGogerty JH, Dille JM (1957) Pharmacology of d-lysergic acid morpholide (LSM) — The Journal of Pharmacology and Experimental Therapeutics PMID:13476356
- [4]
- [5] ^abcde la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J (2022) Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice — ACS Chemical Neuroscience doi:10.1021/acschemneuro.2c00170
- [6] ^Tasker NR, Wipf P (2021) Biosynthesis, total synthesis, and biological profiles of Ergot alkaloids — The Alkaloids: Chemistry and Biology doi:10.1016/bs.alkal.2020.08.001
references
- [1] ^abcdefghijklmnoBrandt SD, Kavanagh PV, Twamley B, Westphal F, Elliott SP, Wallach J, Stratford A, Klein LM, McCorvy JD, Nichols DE, Halberstadt AL (2018) Return of the lysergamides. Part IV: Analytical and pharmacological characterization of lysergic acid morpholide (LSM-775) — Drug Testing and Analysis doi:10.1002/dta.2222
- [2] ^abcHalberstadt AL, Koedood L, Powell SB, Geyer MA (2011) Differential contributions of serotonin receptors to the behavioral effects of indoleamine hallucinogens in mice — Journal of Psychopharmacology doi:10.1177/0269881110388326
- [3] ^abcGogerty JH, Dille JM (1957) Pharmacology of d-lysergic acid morpholide (LSM) — The Journal of Pharmacology and Experimental Therapeutics PMID:13476356
- [4]
- [5] ^abcde la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J (2022) Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice — ACS Chemical Neuroscience doi:10.1021/acschemneuro.2c00170
- [6] ^Tasker NR, Wipf P (2021) Biosynthesis, total synthesis, and biological profiles of Ergot alkaloids — The Alkaloids: Chemistry and Biology doi:10.1016/bs.alkal.2020.08.001