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1Fe-LSD
1-(ferrocenylcarbonyl)-lysergic acid diethylamide
1Fe-LSD (1-ferrocenylcarbonyl-lysergic acid diethylamide) is a synthetic psychedelic of the lysergamide class. It is a designer structural analog of LSD, released to fill a legal niche after its predecessor was banned. In the body it converts to LSD and activates serotonin receptors, producing the visual and cognitive shifts characteristic of classical psychedelics.
1Fe-LSD (1-(ferrocenylcarbonyl)-lysergic acid diethylamide) is an emerging synthetic psychedelic of the lysergamide class. It is an N1-acyl prodrug of LSD, distinguished by an unprecedented iron-containing ferrocene substituent. 1Fe-LSD is a presumed 5-HT₂A receptor agonist, producing its effects through liberation of LSD after metabolic cleavage of its acyl group.[1][2]
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Lizard Labs, a Netherlands-based research chemical company, released 1Fe-LSD on November 26, 2025 — five days after Germany banned its predecessor, 1S-LSD.[1] This continues a deliberate series — each new LSD analog launched within days of its predecessor's prohibition.[2] As of early 2026, it is unscheduled in most jurisdictions and circulates primarily in European research chemical markets.[3]
Subjective effects include geometric visual patterns, emotional intensification, ego dissolution, time alteration, and accelerated thinking. The experience is expected to mirror LSD closely — a slow-building, total alteration of perception and cognition that deepens sharply with dose. Thought loops, anxious fixation, and difficulty sleeping through the extended tail are common unwanted effects.
1Fe-LSD produces no physical dependence, and tolerance builds so quickly that compulsive redosing is self-limiting.[4] The distinctive risk is the ferrocene moiety — an iron-containing group that raised brain iron by up to 50% in animal studies,[5] with unconfirmed computational toxicity signals raising further concern.[6] No peer-reviewed pharmacological data exist; understanding rests on analogy to other LSD prodrugs.[7]
History[edit]
Development
1Fe-LSD was created by Lizard Labs (Synex Synthetics B.V.), a Netherlands-based research chemical company led by British chemist Alexander Stratford.[1] The lab had produced a succession of N1-acyl LSD analogs — 1P-LSD, 1cP-LSD, 1V-LSD, and 1S-LSD — each introduced when its predecessor was scheduled. Patent WO2024028495A1 covers the broader series,[8][9] and 1Fe-LSD appears to be among the lab's final compounds before its closure in December 2024.[1]
Market emergence
1Fe-LSD appeared for sale on November 26, 2025 — five days after Germany prohibited 1S-LSD,[7] following the series' established pattern.[2] It is sold as blotter (200 µg) and micropellets (300 µg).[3] Its distinctive orange color comes from the ferrocene group, not from degradation.[1]
The "Fe" in 1Fe-LSD encodes the chemical symbol for iron (Latin ferrum), naming the compound after its N-1 substituent — consistent with the series' convention (1P = propionyl, 1cP = cyclopropanoyl, 1V = valeroyl). The internal lab designation SYN-L-234 reflects Lizard Labs' systematic catalog. Its orange color — striking and unusual among lysergamides — became an immediate visual identifier on the market and a recurring topic in user forums.[3]
Chemistry[edit]
Structural class
1Fe-LSD belongs to the lysergamide family — synthetic compounds built on the ergoline ring system, the same scaffold as LSD and natural ergot alkaloids. It is an N1-acyl prodrug of LSD: an acyl group at the N-1 position is cleaved in the body to release LSD.[10]
That acyl group is a ferrocenecarbonyl — an organometallic unit with an iron atom sandwiched at its center,[7] making 1Fe-LSD the first lysergamide to contain a transition metal.
Molecular identity
| Molecular formula | C₃₁H₃₃FeN₃O₂ (free base) |
| Molecular weight | 535.45 g/mol (free base) |
| Salt form (commercial) | Hemi-L-tartrate |
At 535.45 g/mol, 1Fe-LSD is substantially heavier than LSD (323.43 g/mol) — the ferrocene group accounts for most of that added mass.[7][3] It is sold as the hemi-L-tartrate salt. The ferrocene unit absorbs blue light, giving blotter and pellet formulations their distinctive orange color.[1]
Pharmacology[edit]
Mechanism of action
1Fe-LSD is a prodrug of LSD: the body breaks down the ferrocenecarbonyl group at N-1 and releases LSD. This mechanism is established for other N1-acyl LSD analogs — 1P-LSD, 1cP-LSD, 1F-LSD, and others convert to LSD in plasma.[10][11][12] One mouse study detected LSD in plasma within 30 minutes of 1Fe-LSD injection and observed head-twitch behavior — a standard marker of psychedelic activity.[7][8]
The ferrocene group is bulkier than any prior N-1 substituent in the series. Bulkier groups reduce conversion efficiency — 1DD-LSD showed 27-fold lower potency due to incomplete hydrolysis.[13] Whether human enzymes cleave the ferrocene group efficiently is unknown.safety citation needed The liberated LSD activates serotonin receptors, driving the psychedelic experience.[14][10]
Pharmacokinetics
No human pharmacokinetic data exist for 1Fe-LSD — the following describes LSD, the presumed active moiety. The liberated LSD reaches peak blood levels around 1.1 hours after ingestion, with a half-life averaging 2.7 hours.[15] Effects last far longer — up to 11 hours at higher doses — because a protein loop closes around LSD inside its receptor, trapping it.[16][17] People with low CYP2D6 enzyme activity experience roughly 75% higher LSD exposure and prolonged effects.[18]
Neuroscience[edit]
No neuroscience data specific to 1Fe-LSD exist. As a presumed LSD prodrug, its brain effects are expected to match LSD once the active compound is released.
Where it acts
LSD quiets the default mode network — the brain's hub for self-referential thought — while increasing connections between normally separate regions.[19] It also disrupts thalamic filtering, flooding the cortex with unprocessed sensory input, producing intensified perception, synesthesia, and geometric visual phenomena.[19] Blocking serotonin receptors with a drug eliminates all of these effects.[17]
Why it matters
LSD loosens the brain's rigid predictive models, allowing suppressed signals to rise — this may explain why it can revise entrenched thought patterns, and has been proposed as the basis for therapeutic outcomes in depression.[19] LSD also promotes structural brain changes, including new dendritic connections, through serotonin-dependent signaling.[20] These changes persist beyond the experience and may underlie its therapeutic potential.[20]
- Does ferrocene reach the brain intact? 1Fe-LSD's high lipophilicity raises the possibility that the intact prodrug crosses the blood-brain barrier before hydrolysis, delivering iron directly to the central nervous system.[6]
- Does 1Fe-LSD raise brain iron? Ferrocene derivatives increased brain iron by up to 50% in rats, altering dopamine metabolism.[5] Whether this occurs at human recreational doses is unknown.
- Does 1Fe-LSD act before converting? Small acyl groups eliminate direct serotonin receptor activity,[10] but this has not been tested for the ferrocene group.
Subjective Effects[edit]
The experience expected from 1Fe-LSD is that of LSD: a profound, slow-building alteration of perception and thought. Colors and surfaces change character. Time stops behaving normally. The thinking mind is reoriented — toward insight, dissolution, or both. Set and setting shape the outcome as powerfully as the dose.
1Fe-LSD occupies the same experiential territory as 1P-LSD, 1cP-LSD, and 1V-LSD — all described by users as indistinguishable from LSD once active. The critical difference is not felt but structural: the ferrocene moiety introduces unknown risks no other lysergamide carries, and the unknown conversion rate may make onset and intensity less predictable than with well-characterized analogs.
Developed by Lizard Labs in the Netherlands under the broader SYN-L lysergamide patent series,[3] 1Fe-LSD appeared on the European research chemical market on November 26, 2025 — five days after Germany prohibited its predecessor 1S-LSD.[4] It is the latest in a succession of designer lysergamide analogs, each introduced to fill a legal niche vacated by the scheduling of its predecessor. As of early 2026, it is unscheduled in most jurisdictions and circulates primarily in European research chemical markets.[5]
Subjective effects include geometric visual patterns, ego dissolution, emotional intensification, time alteration, and thought acceleration. The experience is expected to mirror LSD once the prodrug converts — a slow-building, encompassing alteration of perception and cognition characteristic of the lysergamide class. Thought loops, anxious fixation, and difficulty sleeping through the extended tail are common unsought effects.
1Fe-LSD produces no physical dependence, and rapid tolerance via 5-HT₂A downregulation makes compulsive redosing self-limiting.[6] The primary risk is unprecedented within the lysergamide class: the ferrocene moiety introduces an iron atom whose derivatives increased brain iron content by up to 50% in animal studies,[7] and computational models flag elevated neurotoxicity probabilities that remain experimentally unvalidated.[8] No peer-reviewed pharmacological data exist for this compound; the current understanding rests on analogy to other N1-acyl LSD prodrugs.[9]
History[edit]
Development
1Fe-LSD was developed by Lizard Labs (Synex Synthetics B.V.), a Netherlands-based research chemical producer led by British chemist Alexander Stratford.[4] The company had introduced a succession of N1-acyl LSD analogs — 1P-LSD, 1cP-LSD, 1V-LSD, and 1S-LSD — each occupying a legal niche vacated by the scheduling of its predecessor. Patent WO2024028495A1, filed in August 2023, covers the broader SYN-L lysergamide prodrug series.[3][10] 1Fe-LSD appears to be among the lab's final compounds before its permanent closure in December 2024.[4]
Market emergence
1Fe-LSD appeared for sale on November 26, 2025 — five days after Germany's Bundesrat voted to prohibit 1S-LSD[9] — following the established pattern where each successor analog launches within days of a new scheduling action.[11] It was sold as a hemi-L-tartrate salt in blotter (200 µg) and micropellet (300 µg) formulations, with a distinctive orange to orange-brown coloration intrinsic to the ferrocene chromophore.[9][5][4]
The "Fe" in 1Fe-LSD references the chemical symbol for iron (Latin ferrum), encoding the ferrocene substituent into the compound name — consistent with the series' convention of naming each analog after its N-1 acyl group (1P = propionyl, 1cP = cyclopropanoyl, 1V = valeroyl). The internal lab designation SYN-L-234 reflects Lizard Labs' systematic cataloguing of its lysergamide prodrug series. The compound's orange coloration — unusual among lysergamide products, which are typically colorless — became an immediate visual identifier on the market and a recurring topic in user forums.[5]
Chemistry[edit]
Structural class
1Fe-LSD belongs to the lysergamide chemical class, built on the tetracyclic ergoline ring system found in ergot alkaloids. It is a member of the N1-acyl LSD prodrug series, in which an acyl group at the indole N-1 position is cleaved in vivo to release LSD.[1]
Prior members of this series — ALD-52, 1P-LSD, 1cP-LSD, 1V-LSD, and 1DD-LSD — bear simple carbon-chain or cycloalkyl acyl groups at N-1. 1Fe-LSD departs from this pattern by incorporating a ferrocenecarbonyl substituent — an organometallic unit in which an iron(II) atom sits sandwiched between two cyclopentadienyl rings.[9] This makes it the first lysergamide designer drug to contain a transition metal atom.
Molecular identity
| Molecular formula | C₃₁H₃₃FeN₃O₂ (free base) |
| Molecular weight | 535.45 g/mol (free base) |
| Salt form (commercial) | Hemi-L-tartrate |
The structure combines the LSD ergoline core — bearing an N,N-diethylcarboxamide at C-8 — with a ferrocenecarbonyl group at N-1.[9] The ferrocene unit adds substantial molecular mass and lipophilicity compared to simple acyl analogs. One source reports a slightly different formula (C₃₁H₃₄N₃O₂Fe, 536.46 g/mol);[5] the discrepancy likely reflects differing protonation state conventions. No independent analytical characterization has been published in peer-reviewed literature.
Stereochemistry
The ergoline scaffold retains the same chirality centers as LSD. The (8β) configuration at C-8 corresponds to the pharmacologically active d-lysergic acid series; the (8α) epimer (iso-LSD) is essentially inactive at serotonin receptors. Whether commercial preparations maintain enantiopurity has not been independently verified. The ferrocene moiety itself is achiral and introduces no additional stereochemical complexity.
Physical properties
The hemi-L-tartrate salt presents as an orange to orange-brown powder, and this coloration persists in blotter and pellet formulations.[5] The color is intrinsic to the ferrocene chromophore, which absorbs in the blue region of the visible spectrum, and is not an indicator of degradation.[4] No data on melting point, solubility, partition coefficient, or thermal stability have been published for 1Fe-LSD.
Pharmacology[edit]
Mechanism of action
1Fe-LSD is presumed to act as a prodrug of LSD. The N-1 ferrocenecarbonyl bond is expected to undergo metabolic hydrolysis, releasing LSD and ferrocenecarboxylic acid (FCA). This prodrug mechanism is well established across the N1-acyl LSD series: ALD-52, 1P-LSD, and 1B-LSD undergo rapid deacylation in rat plasma to yield LSD,[1] and the mechanism has been confirmed for 1cP-LSD in human serum[12] and extended to 1F-LSD and 1T-LSD.[13]
One source reports that LSD was detectable in mouse plasma within 30 minutes of 1Fe-LSD injection, and that the compound induced the head-twitch response — an established marker of 5-HT₂A psychedelic activity.[9] This data is attributed to patent WO2024028495A1,[3] though independent verification is needed. safety citation needed
A critical unknown is the hydrolysis rate of the ferrocenecarbonyl bond. Within the series, bulkier substituents reduce conversion efficiency: 1DD-LSD (with a twelve-carbon acyl chain) shows 27-fold lower potency than LSD, attributed to incomplete hydrolysis.[14] The ferrocene group is substantially bulkier than any prior N-1 substituent, and whether human enzymes cleave it efficiently is unknown.
The liberated LSD acts as a partial agonist at 5-HT₂A receptors — the primary target mediating psychedelic effects — along with 5-HT₂C, 5-HT₁A, and dopamine D₂ receptors.[2][1]
Pharmacokinetics
No human pharmacokinetic data exist for 1Fe-LSD. The parameters below describe LSD, the presumed active moiety.
Oral LSD reaches peak plasma levels at approximately 1.1 hours, with dose-proportional absorption confirmed from 5 to 200 µg.[15][16] The half-life averages 2.7 hours (range 1.5–6.2 hours).[15] Individuals who metabolize CYP2D6 poorly may experience approximately 75% higher LSD exposure and prolonged effects.[17]
A hallmark of LSD pharmacology is the gap between its short plasma half-life (~3 hours) and prolonged subjective effects (up to 11 hours at higher doses).[16] This is explained by a structural feature of receptor binding: a protein loop closes over LSD once it enters the 5-HT₂A binding pocket, trapping the molecule and dramatically slowing its release.[18]
For 1Fe-LSD, all pharmacokinetic parameters depend additionally on the rate of ferrocenecarbonyl hydrolysis — the rate-limiting step that precedes LSD liberation. Slower hydrolysis would delay onset and potentially extend total duration.
Neuroscience[edit]
No neuroscience data specific to 1Fe-LSD exist. As a presumed LSD prodrug, its neural effects are expected to match those of LSD once the active moiety is liberated.
Where it acts
LSD disrupts the default mode network — cortical midline structures supporting self-referential thought and the narrative sense of self — reducing its internal coherence while increasing connectivity between normally segregated brain networks.[19] This elevated neural entropy correlates with ego dissolution.
LSD also disrupts thalamic gating, flooding cortical regions with unfiltered sensory input and producing the intensification of perception, synesthesia, and geometric visual phenomena characteristic of the psychedelic state.[19] At the cellular level, these effects originate at 5-HT₂A receptors on layer V pyramidal neurons of the prefrontal cortex — ketanserin blockade at this receptor completely abolishes all subjective effects.[16]
Why it matters
The REBUS (relaxed beliefs under psychedelics) model proposes that psychedelics flatten the brain's confidence in its existing models of reality, allowing suppressed sensory signals to propagate more freely and creating a window in which rigid belief structures can be revised.[19] This framework has been proposed as the mechanism underlying therapeutic outcomes in depression and addiction.
LSD also promotes structural neuroplasticity — including increased dendritic spine density and enhanced synaptic connectivity — through 5-HT₂A-dependent signaling involving BDNF and mTOR.[20] These changes persist beyond the acute experience and may mediate the therapeutic effects observed in clinical depression trials.[20]
- Does ferrocene reach the brain intact? The high lipophilicity of 1Fe-LSD raises the possibility that the intact prodrug crosses the blood-brain barrier before hydrolysis, delivering the iron-containing moiety directly to the central nervous system.[8]
- Does 1Fe-LSD alter brain iron levels? Ferrocene derivatives increased brain iron content by up to 50% in rats, with consequent changes to dopamine metabolism.[7] Whether this occurs at human recreational doses is unknown.
- Is 1Fe-LSD a true silent prodrug? N1-acyl substitution eliminates direct 5-HT₂A activity for small acyl groups,[1] but this has not been tested for the sterically unusual ferrocene group.
Subjective Effects[edit]
The experiential character of 1Fe-LSD is expected to recapitulate that of LSD — the compound acts exclusively through liberation of LSD after metabolic hydrolysis of its ferrocenecarbonyl bond. If the prodrug model holds, the experience should span the full range of serotonergic psychedelic phenomenology, from gently enhanced perception at lower doses to complete perceptual restructuring and ego dissolution at higher ones. Set and setting sensitivity is pronounced: the same dose can produce experiences ranging from contemplative clarity to overwhelming dissolution depending on psychological state and environment.
1Fe-LSD occupies the same experiential territory as 1P-LSD, 1cP-LSD, and 1V-LSD — all described by users as subjectively indistinguishable from LSD once active. The key distinction is not phenomenological but toxicological: the ferrocene moiety introduces safety unknowns that no prior member of the series carries, and the unknown hydrolysis rate may make onset timing and intensity less predictable than with well-characterized analogs.
Effect Grid
Full psychedelic experience with visible geometry, visual drifting, and pronounced color enhancement. Emotional enhancement is strong — mood becomes highly responsive to set and setting. Conceptual thinking, introspection enhancement, and thought connectivity define the cognitive landscape. Time alteration is prominent. Ego dissolution is possible but not typical at this tier.
Stimulation, body high, and muscle tension are reliable. Pupil dilation is conspicuous. Nausea may occur during onset. Appetite suppression and wakefulness persist throughout.
The commercial 200 µg blotter formulation likely falls in or near this range, though LSD-equivalency is unestablished. Set and setting strongly modulate whether the experience trends toward euphoria or anxiety. Sleep is not possible for 8+ hours at this dose.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual breathing · Visual drifting · Holotropic state · Auditory enhancement · Brightness alteration · Environmental patterning · Perspective distortion · Tracers · Visual morphing · Touch enhancement · After-images · Auditory distortion · Auditory misinterpretation · Depth perception distortion · Dreaming suppression · Light sensitivity · Peripheral vision distortion · Proprioceptive distortion · Sound sensitivity · Symmetrical texture repetition · Visual diffraction · Visual haze / noise · Visual melting · Ganzfeld effect · Peripheral misidentification · Spatial disorientation · Synesthesia · Vestibular distortion · Visual acuity enhancement · Visual magnification · Visual processing acceleration · Taste enhancement · Flashbacks · Object activation · Object transformations · Visual recursion · Environmental orbism / cubism · External hallucinations · Internal hallucinations · Perspective hallucinations · Auditory hallucinations · Visual flipping · Visual scenery slicing · Persisting hallucinations
Brightness alteration · Environmental patterning · Perspective distortion · Tracers · Visual morphing · Touch enhancement · After-images · Auditory distortion · Auditory misinterpretation · Depth perception distortion · Dreaming suppression · Light sensitivity · Peripheral vision distortion · Proprioceptive distortion · Sound sensitivity · Symmetrical texture repetition · Visual diffraction · Visual haze / noise · Visual melting · Ganzfeld effect · Peripheral misidentification · Spatial disorientation · Synesthesia · Vestibular distortion · Visual acuity enhancement · Visual magnification · Visual processing acceleration · Taste enhancement · Flashbacks · Object activation · Object transformations · Visual recursion · Environmental orbism / cubism · External hallucinations · Internal hallucinations · Perspective hallucinations · Auditory hallucinations · Visual flipping · Visual scenery slicing · Persisting hallucinations
Insomnia · Appetite suppression · Body high · Spontaneous body sensations · Stimulation · Laughter fits · Muscle tension · Heart rate perception changes · Physical fatigue · Tactile euphoria · Tingling / electric sensations · Vibrations / buzzing · Bodily lightness · Bodily pressures · Body schema distortion · Breathing alteration · Dizziness · Dry mouth · Excessive sweating · Restlessness · Vasoconstriction · Involuntary body movements · Nausea · Nystagmus (eye wobbles) · Abnormal heartbeat · Bodily heaviness · Headache · Sexual arousal enhancement · Trembling · Pain enhancement · Vomiting · Bodily dissociation · Tactile hallucination
Spontaneous body sensations · Stimulation · Laughter fits · Muscle tension · Heart rate perception changes · Physical fatigue · Tactile euphoria · Tingling / electric sensations · Vibrations / buzzing · Bodily lightness · Bodily pressures · Body schema distortion · Breathing alteration · Dizziness · Dry mouth · Excessive sweating · Restlessness · Involuntary body movements · Nausea · Nystagmus (eye wobbles) · Abnormal heartbeat · Bodily heaviness · Headache · Sexual arousal enhancement · Trembling · Pain enhancement · Vomiting · Bodily dissociation · Tactile hallucination
Cognitive flexibility · Conceptual thinking · Introspection enhancement · Multiple thought streams · Openness enhancement · Pattern recognition enhancement · Thought acceleration · Thought connectivity · Cognitive euphoria · Increased nature relatedness · Creativity enhancement · Humor enhancement · Focus suppression · Analysis suppression · Cognitive fatigue · Cognitive impairment · Memory fragmentation · Memory replays · Synchronicity · Thought loops · Analysis enhancement · Confusion · Information processing enhancement · Information processing suppression · Memory suppression · Motivation suppression · Thought disorganization · Focus enhancement · Language enhancement · Motivation enhancement · Cognitive dysphoria · Thought organization · Delusions of sobriety · Thought deceleration · Delusions
Multiple thought streams · Openness enhancement · Pattern recognition enhancement · Thought acceleration · Thought connectivity · Cognitive euphoria · Increased nature relatedness · Creativity enhancement · Humor enhancement · Focus suppression · Analysis suppression · Cognitive fatigue · Cognitive impairment · Memory fragmentation · Memory replays · Synchronicity · Thought loops · Analysis enhancement · Confusion · Information processing enhancement · Information processing suppression · Memory suppression · Motivation suppression · Thought disorganization · Focus enhancement · Language enhancement · Motivation enhancement · Cognitive dysphoria · Thought organization · Thought deceleration · Delusions
Emotional lability · Empathy enhancement · Anxiety · Anxiety suppression · Catharsis · Irritability · Dysphoria
Catharsis · Irritability · Dysphoria
Depersonalization · Disinhibition · Trust enhancement · Automaticity · Communication enhancement · Compulsive behavior reduction · Ego inflation · Flow state · Sociability enhancement · Communication suppression · Sociability suppression · Social disconnection · Boundary dissolution · Identity alteration · Cognitive disconnection · Ego dissolution · Telepathic feelings
Communication enhancement · Compulsive behavior reduction · Ego inflation · Flow state · Sociability enhancement · Communication suppression · Sociability suppression · Social disconnection · Boundary dissolution · Identity alteration · Cognitive disconnection · Ego dissolution · Telepathic feelings
Time cessation
Transpersonal visions · Transpersonal memory access · Death-rebirth sequence · Entity contact
Lucidity enhancement · Mindfulness enhancement · Recursive awareness
Timeline
Gradual emergence of mild stimulation and body awareness. Subtle mood shift and possible mild anxiety. May be slower than LSD or 1P-LSD due to ferrocene hydrolysis kinetics.
Perceptual effects begin building — color enhancement, early geometry, increasing emotional activation. Body high developing with stimulation and possible nausea.
Full spectrum of psychedelic effects — visual geometry, emotional enhancement, conceptual thinking, time alteration. Ego dissolution possible at higher doses.
Gradual reduction of perceptual and cognitive effects. Residual stimulation persists. Mood shifts toward reflective introspection.
Residual mood elevation or physical fatigue. Enhanced introspection and subtle perceptual sensitivity may persist. Sleep becomes possible.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Moderate
- 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
Ferrocene-specific concerns
1Fe-LSD introduces an organometallic iron moiety unprecedented in the lysergamide class. The safety implications have not been empirically investigated. The concerns below are drawn from published ferrocene toxicology and computational predictions — not from substance-specific data.
Ferrocene derivatives raised brain iron by up to 50% in animal studies, with significant alterations in dopamine metabolism.[5] 1Fe-LSD's high lipophilicity may allow it to cross the blood-brain barrier intact, carrying the iron group directly to the central nervous system. Iron cycles between oxidation states, generating reactive molecules that damage cell components — and because iron acts as a catalyst rather than being consumed, a single atom can produce repeated rounds of harm.[6]
Computer models flag elevated probabilities of neurotoxicity (77%), immune disruption (99%), mitochondrial damage (88%), and liver injury.[6] These are computational predictions, not experimental findings. The metabolic byproduct ferrocenecarboxylic acid is described by vendors as non-mutagenic and of low acute toxicity,[7][3] but no peer-reviewed data confirm this at brain-relevant concentrations. safety citation needed
LSD class acute toxicity
LSD itself has extremely low acute toxicity — deaths directly attributable to LSD alone are exceedingly rare, and the European Union drug agency notes overdose fatalities are "virtually unknown".[21] Most LSD-attributed deaths have involved adulterants, particularly 25I-NBOMe.[22] No case reports or adverse events for 1Fe-LSD have been identified as of May 2026.
Psychological Risks
Acute anxiety, panic, and confusion are dose-dependent, becoming prominent at higher doses.[17] Commercial 1Fe-LSD doses (200–300 µg) may deliver strong-to-very-strong LSD-equivalent doses depending on conversion efficiency, placing users at elevated risk for adverse psychological responses.
Perceptual disturbances from intoxication can persist and recur after the drug wears off — a condition called hallucinogen persisting perception disorder (HPPD).[23] In controlled studies, these episodes were reported by a minority of participants and were usually brief and non-distressing.[24] LSD can also trigger psychosis-like states — paranoia, hallucinations, delusional thinking — in people with predisposing vulnerabilities, particularly personal or family histories of schizophrenia-spectrum disorders.[25]
Tolerance & Dependence
LSD produces rapid tolerance — serotonin receptors downregulate, reducing response within 1–4 days of repeated use.[4] Tolerance resolves after roughly 14 days and cross-tolerates with other serotonergic psychedelics (psilocybin, mescaline) but not with non-psychedelic serotonin activators.[4] LSD produces no physical dependence, no withdrawal, and has minimal abuse liability.
Drug Interactions
MAOIs block serotonin breakdown, dramatically amplifying LSD's effects and raising the risk of dangerous serotonin overload.[26] Lithium combined with LSD has been associated with seizures — an absolute contraindication.safety citation needed Tramadol adds serotonergic load, further elevating serotonin overload risk. The ferrocene moiety's potential interactions with iron-chelating medications or redox-active drugs are unknown.safety citation needed
SSRIs and SNRIs typically reduce LSD's effects through long-term serotonin downregulation; acute co-administration carries low but theoretical serotonin overload risk.[26] CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion, quinidine) slow LSD metabolism and may raise exposure by roughly 75%.[18] Cannabis frequently intensifies and prolongs effects, raising anxiety and paranoia risk. Stimulants (MDMA, amphetamines, cocaine) increase cardiovascular strain and psychological risk. Antipsychotics blunt or stop psychedelic effects and may be used in acute adverse event management.
Contraindications
7 knownPersonal or family history of psychotic disorders is the most significant absolute contraindication — LSD can precipitate acute psychosis and may accelerate onset in predisposed individuals.[25] Current lithium use is an absolute contraindication due to seizure risk.safety citation needed Current MAOI use carries high risk of unpredictable potentiation and serotonin syndrome.[26]
Heart conditions — LSD raises blood pressure and heart rate moderately;[17] uncontrolled cardiovascular disease increases risk. Pregnancy — ergoline compounds have uterotonic properties and no safety data exist.safety citation needed Iron overload conditions (hemochromatosis, thalassemia major, chronic transfusion therapy) — the ferrocene moiety may release iron after hydrolysis, potentially worsening iron accumulation; this contraindication is unique to 1Fe-LSD within the lysergamide class and is based on theoretical reasoning rather than clinical evidence.safety citation needed Severe anxiety disorders or current psychological crisis amplify distress risk.
Harm Reduction[edit]
Forms & Identification
The distinctive orange to orange-brown color of 1Fe-LSD is intrinsic to the ferrocene group — unusual among lysergamide products and a basic visual identifier. Color alone cannot confirm identity or purity.
Standard LSD reagent tests (Ehrlich, Hofmann) are expected to react with the ergoline core. A positive Ehrlich result confirms an indole compound but does not distinguish 1Fe-LSD from LSD or other lysergamides. Quantitative testing (HPLC or mass spectrometry) through a drug checking service is the only reliable way to confirm identity and dose — though given the compound's novelty, some services may not yet carry reference standards.
Guidelines
- Start low. The hydrolysis rate of 1Fe-LSD's ferrocenecarbonyl bond is unknown, making dose-response unpredictable. Begin with the lowest available dose and wait at least 3 hours before assessing whether effects have fully materialized.
- Test the substance. Use Ehrlich reagent as a minimum screen. Send a sample to an analytical testing service if available.
- Arrange a sitter. A sober, trusted companion who can provide reassurance and contact emergency services if needed.
- Prepare the environment. Comfortable temperature, water access, calming music, a private retreat space.
- Do not redose early. Prodrug conversion may delay onset. Premature redosing risks a delayed double dose.
- Avoid mixing substances. The ferrocene moiety introduces unknown interaction risks beyond those of the LSD class.
- Hydrate and eat beforehand. A light meal 2–3 hours before reduces nausea. Keep water accessible throughout.
- Plan for the full duration. Allow 12+ hours with no commitments. Sleep may be difficult for several hours after peak effects subside.
Set & Setting
The experience is powerfully shaped by psychological state and physical environment. A calm, familiar space with access to a private area reduces the likelihood of difficult experiences. The presence of a sober, trusted companion is strongly recommended, particularly for first-time use or higher doses.
Avoid use during periods of emotional distress, unresolved conflict, or significant life stress. Clear the schedule for the full duration including the extended tail, and ensure there are no obligations requiring driving, operating machinery, or making important decisions.
Aftercare & integration. The 24–48 hours following a psychedelic experience are a sensitive period. Sleep, hydration, and light nutrition support physical recovery. Avoid major life decisions in the days immediately following.
Journaling or talking through the experience with a trusted person can help process difficult or meaningful content. If the experience surfaced distressing material, professional psychedelic integration therapy is available through directories maintained by organizations such as MAPS and the Psychedelic Support Network. Persistent perceptual changes (visual haze / noise, halos, trailing) lasting more than a few days warrant consultation with a healthcare provider familiar with HPPD.
Recovery & Support
LSD-class compounds carry minimal physical dependence risk, but patterns of repeated use to avoid difficult emotions can develop. Peer support groups and psychedelic harm reduction organizations offer non-judgmental guidance.
For broader substance use concerns, SAMHSA's National Helpline (1-800-662-4357) offers free, confidential support. The Fireside Project (62-FIRESIDE / 623-473-7433) provides peer support specifically for psychedelic experiences.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency
Most difficult psychedelic experiences are uncomfortable but not medically dangerous. Seek immediate help if any of the following occur:
- Self-harm behavior or expressed intent to harm oneself or others
- Complete loss of contact with reality — the person does not recognize where they are or who is present
- Seizures
- Severe chest pain or difficulty breathing
- Loss of consciousness
Immediate steps
- 1. Move the person to a calm, quiet space with minimal stimulation.
- 2. Speak in a calm, reassuring tone. Simple, grounding statements: "You are safe. You took a substance. This will pass."
- 3. Do not physically restrain unless there is immediate danger of self-harm.
- 4. If the situation escalates beyond what a sitter can manage, call emergency services.
- 5. Place an unconscious person in the recovery position and monitor breathing.
What to tell the dispatcher
Provide: the substance taken (1Fe-LSD, a lysergamide psychedelic), the approximate dose, when it was taken, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
Legal Status[edit]
As of early 2026, 1Fe-LSD is not explicitly scheduled in most major jurisdictions.[3][2] Its organometallic ferrocene group falls outside the structural definitions in most lysergamide-targeting laws. LSD — the presumed active compound — is Schedule I under the UN 1971 Convention on Psychotropic Substances.
| Jurisdiction | Status (early 2026) | Key provisions |
|---|---|---|
| Germany | Not controlled | Does not fall within structural classes prohibited under the NpSG, BtMG, or AMG. Market introduction timed after 1S-LSD prohibition (November 2025)[3] |
| United Kingdom | Not controlled (personal use) | Not listed under Misuse of Drugs Act 1971. Psychoactive Substances Act 2016 prohibits supply but exempts personal possession[2] |
| United States | Not explicitly scheduled | Not listed in Controlled Substances Act. Federal Analogue Act (21 U.S.C. § 813) may apply if intended for human consumption and deemed substantially similar to Schedule I LSD[2] |
| Canada | Not explicitly listed | Not scheduled under the Controlled Drugs and Substances Act as of early 2026[7] |
| Australia / New Zealand | Unconfirmed | Not specifically researched. Likely subject to analogue provisionscitation needed |
| International (UN) | Not scheduled | Not listed under the 1971 Convention on Psychotropic Substances. LSD (active moiety) is Schedule I under that convention |
Analog act considerations
In jurisdictions with structural analog legislation (United States, Australia, New Zealand), 1Fe-LSD's legal status depends on whether it is deemed structurally and pharmacologically similar to LSD.[2] The ferrocene group is unlike any substituent previously assessed under analogue laws, complicating this determination. No prosecution under any analogue act has occurred as of May 2026.
Legal status changes frequently. The information above reflects available sources as of early 2026 and is not legal advice. Verify current law in the relevant jurisdiction before acting on this information.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Moderate
- 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
Ferrocene-specific concerns
1Fe-LSD introduces an organometallic iron moiety unprecedented in the lysergamide class. The safety implications have not been empirically investigated. The concerns below are drawn from published ferrocene toxicology and computational predictions — not from substance-specific data.
Ferrocene derivatives administered to rats produced up to 50% increases in iron content in the substantia nigra, cerebellum, and cerebral cortex, with significant alterations in dopamine metabolism.[7] The concern for 1Fe-LSD is that its high lipophilicity may allow it to cross the blood-brain barrier intact, delivering the ferrocene moiety directly to the central nervous system.
Iron cycling between oxidation states generates hydroxyl radicals capable of damaging lipids and proteins — a process known as the Fenton reaction. Because iron acts as a catalyst rather than being consumed, a single atom can generate multiple rounds of oxidative damage. Chronic brain iron accumulation is an established mechanism in neurodegenerative disease.[8]
Computational models (ProTox-3.0, ADMETlab 2.0) report elevated probabilities of neurotoxicity (77%), immunotoxicity (99%), mitochondrial disruption (88%), and drug-induced liver injury (score 0.808).[8] These are in silico outputs, not experimental findings — computational platforms overpredict positive signals for structurally unusual compounds and have not been validated for organometallic scaffolds. They establish a prior concern, not clinical evidence.
Vendor sources describe the metabolic product ferrocenecarboxylic acid (FCA) as non-mutagenic and of low acute toxicity.[9][5] No peer-reviewed data confirm FCA safety at brain-relevant concentrations, and whether ferrocene-to-FCA conversion occurs in the periphery or also within the brain is unresolved. safety citation needed
LSD class acute toxicity
LSD itself has extremely low acute toxicity. Deaths directly attributable to LSD alone are exceedingly rare; most fatalities attributed to LSD have involved adulterants, particularly 25I-NBOMe.[21] The European Union Drugs Agency notes that overdose deaths from LSD are "virtually unknown".[22]
For N1-acyl LSD analogs, in silico toxicity analysis of five compounds yielded predicted rat LD₅₀ values of 49–85 mg/kg.[23] No LD₅₀ data exist for 1Fe-LSD. The ferrocene moiety introduces a toxicological variable — potential organ-specific iron loading — not captured by LSD class literature.
No case reports, emergency presentations, or adverse event reports for 1Fe-LSD have been identified as of May 2026. The substance has been commercially available for fewer than six months.
Psychological Risks
No psychological adverse event data specific to 1Fe-LSD exist. The following risks are inferred from the LSD class.
Acute anxiety, panic, and confusion are dose-dependent, becoming prominent at higher doses.[16] The commercial formulation doses (200–300 µg) may deliver strong-to-very-strong LSD-equivalent doses depending on hydrolysis efficiency, placing users at increased risk for adverse psychological responses.
Hallucinogen persisting perception disorder (HPPD) — recurrent, involuntary re-experiencing of perceptual disturbances from intoxication — is a recognized risk of LSD use.[24] In controlled studies, flashback-like phenomena were reported by a minority of participants, with most episodes being brief and non-distressing.[25]
LSD can trigger psychosis-like states in individuals with predisposing vulnerabilities, particularly those with personal or family histories of schizophrenia-spectrum disorders.[26] Suicidal ideation is rare and typically occurs in the context of difficult experiences or pre-existing conditions.
Tolerance & Dependence
No tolerance or dependence data specific to 1Fe-LSD exist.
LSD produces rapid tolerance mediated by 5-HT₂A downregulation.[6] Tolerance develops within 1–4 days of repeated use and resolves over approximately 14 days of abstinence. Cross-tolerance develops between LSD and other serotonergic psychedelics (psilocybin, mescaline) but not with non-psychedelic 5-HT₂A agonists such as lisuride.[6]
LSD does not produce physical dependence or withdrawal. Psychological compulsion to redose is uncommon given rapid tolerance development and the self-limiting nature of the psychedelic experience. The LSD class has minimal abuse liability.
Drug Interactions
No interaction studies specific to 1Fe-LSD exist. All data below are inferred from the LSD class.
Monoamine oxidase inhibitors (MAOIs) may intensify and prolong effects by inhibiting serotonin breakdown. Serotonin syndrome is theoretically possible but rare with LSD under MAOI co-administration.[27] Combined use is high-risk.
SSRIs and SNRIs typically reduce LSD's subjective effects through chronic 5-HT₂A downregulation. Acute co-administration carries a theoretical serotonin syndrome risk, generally considered low for the LSD class.[27]
CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion, quinidine) may substantially increase LSD exposure after hydrolysis, as CYP2D6 is the primary enzyme metabolizing LSD.[17] Poor metabolizers and those taking strong CYP2D6 inhibitors may experience approximately 75% higher LSD exposure and prolonged effects.
Lithium — combination with LSD has been associated with seizures. This is an absolute contraindication. safety citation needed
Antipsychotics — 5-HT₂A antagonists (risperidone, quetiapine, olanzapine) attenuate or abort psychedelic effects and may be used in acute adverse event management.
Stimulants — co-administration with amphetamines, MDMA, or cocaine increases cardiovascular risk and may intensify adverse psychological effects.
Cannabis — frequently reported to intensify and prolong psychedelic effects; may increase risk of anxiety and paranoia.
Tramadol — serotonergic activity combined with a serotonergic psychedelic elevates serotonin syndrome risk.
The ferrocene moiety's potential interactions with iron-chelating medications, redox-active drugs, or liver metabolism pathways are unknown. safety citation needed
Contraindications
7 knownNo substance-specific contraindication data exist for 1Fe-LSD. The following are inferred from the LSD class.
Personal or family history of psychotic disorders — the most significant absolute contraindication. LSD can precipitate acute psychosis and may accelerate onset in prodromal schizophrenia-spectrum conditions.[26]
Current lithium use — associated with seizures when combined with LSD. Absolute contraindication. safety citation needed
Current MAOI use — risk of unpredictable potentiation and serotonin toxicity.[27]
Heart conditions — LSD produces moderate increases in blood pressure and heart rate.[16] Individuals with uncontrolled blood pressure, irregular heartbeat, or significant cardiovascular disease face elevated risk.
Pregnancy — no safety data exist. Ergoline compounds have uterotonic properties. Contraindicated. safety citation needed
Severe anxiety disorders or current psychological crisis — amplification of distress can produce sustained adverse psychological outcomes.
Iron overload conditions (hemochromatosis, thalassemia major, chronic transfusion therapy) — the ferrocene moiety may release iron following hydrolysis. In individuals with pre-existing iron overload, even small additional iron contributions could be clinically significant. This contraindication is unique to 1Fe-LSD within the lysergamide class and is based on theoretical reasoning rather than clinical evidence. safety citation needed
Harm Reduction[edit]
Forms & Identification
1Fe-LSD's distinctive orange to orange-brown coloration — intrinsic to the ferrocene chromophore — is unusual among lysergamide products and serves as a basic visual identifier. Color alone cannot confirm identity or purity. Standard LSD reagent tests (Ehrlich, Hofmann) are expected to react with the ergoline core, but no validated reagent testing protocol specific to 1Fe-LSD has been published. A positive Ehrlich result confirms the presence of an indole compound but does not distinguish 1Fe-LSD from LSD or other lysergamides.
Quantitative testing through a drug checking service (HPLC or mass spectrometry) is the only reliable way to confirm identity and dose. Given the compound's novelty, even analytical services may not yet carry reference standards for 1Fe-LSD in their databases.
Guidelines
- Start low. The hydrolysis rate of 1Fe-LSD's ferrocenecarbonyl bond is unknown, making dose-response unpredictable. Begin with the lowest available dose and wait at least 3 hours before considering whether effects have fully materialized.
- Test your substance. Use Ehrlich reagent as a minimum screen. Send a sample to an analytical testing service if available.
- Arrange a sitter. A sober, trusted companion who can provide reassurance and contact emergency services if needed.
- Prepare the environment. Comfortable temperature, access to water, calming music, a private space to retreat to.
- Do not redose early. Prodrug conversion may delay onset compared to LSD. Premature redosing risks a delayed double dose.
- Avoid mixing substances. The ferrocene moiety introduces unknown interaction risks beyond those of the LSD class.
- Hydrate and eat beforehand. A light meal 2–3 hours before reduces nausea. Keep water accessible throughout.
- Plan for the full duration. Allow 12+ hours with no commitments. Sleep may be difficult for several hours after peak effects subside.
Set & Setting
As with all serotonergic psychedelics, the 1Fe-LSD experience is powerfully shaped by psychological state (set) and physical environment (setting). A calm, familiar, and safe environment with access to a private space reduces the likelihood of difficult experiences. The presence of a sober, trusted companion is strongly recommended, particularly for first-time use or higher doses.
Avoid use during periods of emotional distress, unresolved psychological conflict, or significant life stress. Clear the schedule for the full duration — including the extended tail — and ensure there are no obligations requiring driving, operating machinery, or making important decisions.
Aftercare & integration. The 24–48 hours following a psychedelic experience are a sensitive period. Sleep, hydration, and light nutrition support physical recovery. Avoid making major life decisions in the days immediately following.
Journaling or talking through the experience with a trusted person can help process difficult or meaningful content. If the experience surfaced distressing material, professional psychedelic integration therapy is available through directories maintained by organizations such as MAPS and the Psychedelic Support Network. Persistent perceptual changes (visual haze / noise, halos, trailing) lasting more than a few days warrant consultation with a healthcare provider familiar with HPPD.
Recovery & Support
While LSD-class compounds carry minimal physical dependence risk, patterns of repeated use to avoid difficult emotions or escape psychological distress can develop. If use is becoming a coping mechanism rather than an occasional experience, peer support groups and psychedelic harm reduction organizations offer non-judgmental guidance.
For broader substance use concerns, SAMHSA's National Helpline (1-800-662-4357) offers free, confidential support. The Fireside Project (62-FIRESIDE / 623-473-7433) provides peer support specifically for psychedelic experiences.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency
Most difficult psychedelic experiences are uncomfortable but not medically dangerous. Seek immediate help if any of the following occur:
- Self-harm behavior or expressed intent to harm oneself or others
- Complete loss of contact with reality — the person does not recognize where they are or who is present
- Seizures
- Severe chest pain or difficulty breathing
- Loss of consciousness
Immediate steps
- 1. Move the person to a calm, quiet space with minimal stimulation.
- 2. Speak in a calm, reassuring tone. Simple, grounding statements: "You are safe. You took a substance. This will pass."
- 3. Do not physically restrain unless there is immediate danger of self-harm.
- 4. If the situation escalates beyond what a sitter can manage, call emergency services.
- 5. Place an unconscious person in the recovery position and monitor breathing.
What to tell the dispatcher
Provide: the substance taken (1Fe-LSD, a lysergamide psychedelic), the approximate dose, when it was taken, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
Legal Status[edit]
As of early 2026, 1Fe-LSD is not explicitly scheduled under the drug control laws of most major jurisdictions. Its ferrocene moiety — an organometallic group outside the structural definitions in existing lysergamide-targeting legislation — has allowed it to occupy a legal position exploited for the European research chemical market.[5][11] LSD, the presumed active moiety, is Schedule I under the United Nations 1971 Convention on Psychotropic Substances.
| Jurisdiction | Status (early 2026) | Key provisions |
|---|---|---|
| Germany | Not controlled | Does not fall within structural classes prohibited under the NpSG, BtMG, or AMG. Market introduction timed after 1S-LSD prohibition (November 2025)[5] |
| United Kingdom | Not controlled (personal use) | Not listed under Misuse of Drugs Act 1971. Psychoactive Substances Act 2016 prohibits supply but exempts personal possession[11] |
| United States | Not explicitly scheduled | Not listed in Controlled Substances Act. Federal Analogue Act (21 U.S.C. § 813) may apply if intended for human consumption and deemed substantially similar to Schedule I LSD[11] |
| Canada | Not explicitly listed | Not scheduled under the Controlled Drugs and Substances Act as of early 2026[9] |
| Australia / New Zealand | Unconfirmed | Not specifically researched. Likely subject to analogue provisionscitation needed |
| International (UN) | Not scheduled | Not listed under the 1971 Convention on Psychotropic Substances. LSD (active moiety) is Schedule I under that convention |
Analog act considerations
In jurisdictions with structural analog legislation (United States, Australia, New Zealand), 1Fe-LSD's legal status depends on whether it is deemed "substantially similar" in structure and effect to LSD. The ferrocene group represents a structural departure from conventional organic chemistry that may complicate traditional structure-activity reasoning in legal proceedings — while 1Fe-LSD shares the LSD core and is presumed to produce identical effects via prodrug activation, the organometallic moiety is unlike any substituent previously assessed under analogue laws. No prosecution under any analogue act has occurred for 1Fe-LSD as of May 2026.
Frequently asked questions
What is 1Fe-LSD?
1Fe-LSD is a synthetic lysergamide presumed to act as a prodrug of LSD, bearing an organometallic ferrocene moiety at the indole N-1 position. It appeared on European research-chemical markets in November 2025 and has no peer-reviewed pharmacological characterization.
How long does 1Fe-LSD last?
Total duration by route of administration — Oral: 8 – 12 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 1Fe-LSD?
Psychedex publishes a dosage table for 1Fe-LSD 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 1Fe-LSD?
The highest-severity documented interactions for 1Fe-LSD: MAOIs (Lethal), Buspirone (Dangerous), Dopamine agonists (Dangerous), GHB, Baclofen (Dangerous), GHB, GBL (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is 1Fe-LSD addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 1Fe-LSD: tolerance builds rapid; full reset takes 14 days; cross-tolerance develops with LSD, psilocybin, mescaline, DMT, 1P-LSD, 1cP-LSD, 1V-LSD, other 5-HT2A agonist psychedelics. 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]
- [2]
- [3]
- [4] ^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
- [5] ^abcWard RJ, Dexter D, Florence A, Aouad F, Hider R, Jenner P, Crichton RR (1995) Brain iron in the ferrocene-loaded rat: its chelation and influence on dopamine metabolism — Biochemical Pharmacology PMID:7598744
- [6]
references
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- [2] ^abCummins BR, Billac GB, Nichols DE, Nichols CD (2025) 5-HT2A receptors: Pharmacology and functional selectivity — Pharmacological Reviews doi:10.1016/j.pharmr.2025.100059
- [3]
- [4]
- [5]
- [6] ^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