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Miscellaneous SAR

Sansert

Bluelighter
Joined
Aug 26, 2026
Messages
132
The history of Structure–Activity Relationship (SAR) research in classic serotonergic psychedelics spans over eight decades, shifting from early transmitter-based paradigms to precise receptor-level pharmacology and structural biology.


Historical Paradigm Shift: Dopamine to Serotonin Hypothesis​


The Early Dopaminergic / Catecholaminergic Era​


In the early to mid-20th century, research into mescaline (a phenethylamine) suggested structural similarities with catecholamine neurotransmitters—dopamine and norepinephrine. Because amphetamines and related catecholaminergic agents produced marked motor, sympathetic, and behavioral changes, early hypotheses posited that psychedelic effects stemmed from dopaminergic overdrive or aberrant catecholamine metabolism (e.g., the "adrenochrome hypothesis" of schizophrenia).


Amphetamine Structure Mescaline (Phenethylamine)
(Dopaminergic) (Psychedelic)
CH₃ OCH₃
/ /
[O]--CH₂--CH--NH₂ H₃CO--[O]--CH₂--CH₂--NH₂
\
OCH₃


Discovery of 5-HT and the Serotonin Hypothesis​


In 1943, Albert Hofmann discovered the profound psychoactivity of Lysergic Acid Diethylamide (LSD). Ten years later, in 1953, Betty Twarog and Irvine Page identified serotonin (5-hydroxytryptamine / 5-HT) in mammal brain tissue. Shortly thereafter, D.W. Woolley and E. Shaw observed that LSD and serotonin shared an indolealkylamine core, leading to the Serotonin Hypothesis of Psychedelic Action:


Serotonin (5-HT) LSD Core (Ergoline)
HO O=C-N(Et)₂
\ |
[Indole]--CH₂--CH₂--NH₂ [Indole Core]--N-CH₃

Subsequent clinical research established that classic psychedelics primarily modulate central serotonergic systems, whereas direct dopamine receptor activation (e.g., D_2 agonism by ergolines) contributes to specific side-effect profiles (stimulant effects, hyperlocomotion) rather than the primary hallucinogenic state.


Evolution of Structure–Activity Relationships (SAR)​


Psychedelic SAR research systematically modifies chemical structures across three core structural classes: Phenethylamines, Tryptamines, and Ergolines.


1. Phenethylamines (Mescaline derivatives)​


Work led by Alexander Shulgin and David Nichols elucidated key rules for phenethylamine potency and 5-HT binding:


  • Core Structure: beta-phenethylamine backbone.
  • Aromatic Ring Substitution: Oxygenation at the 2- and 5-positions (2,5-dimethoxy substitution pattern) is required for high 5 2A affinity (e.g., 2C series).
  • 4-Position Substituents:The lipophilicity and steric bulk at the 4-position determine potency:
    • 4 methoxy (TMA) Moderate activity.
    • 4 halogen (2C-B, 2C-I, DOI) Significantly higher binding affinity and potency.
    • 4 alkylthio (2C-T-7) Prolonged action and unique sensory properties.
  • alpha-Methylation: Adding a methyl group to the side chain converts phenethylamines into amphetamines (e.g., DOB, DOI, DOM), inhibiting monoamine oxidase (MAO) degradation and increasing oral potency and duration.

2. Tryptamines (DMT, Psilocin, 5-MeO-DMT)​


  • Core Structure: Indole-3-ethylamine.
  • N,N-Dialkyl Substitutions: Unsubstituted tryptamine is rapidly degraded by MAO. Adding methyl, ethyl, or propyl groups (N,N-DMT, N,N-DET, DPT) protects against enzymatic degradation, conferring oral or parenteral activity.
  • 4-Position Modifications: A 4-hydroxy group (Psilocin) or 4-phosphoryloxy group (Psilocybin) dramatically increases oral bioavailability and stability. 4-substitution alters the conformation of the ethylamine side chain relative to the indole ring.
  • 5-Position Modifications: A 5-methoxy group (5-MeO-DMT) enhances binding affinity for 5 HT_1A and 5 -HT 2A receptors by orders of magnitude compared to DMT.

3. Ergolines (LSD, ETH-LAD, AL-LAD)​


  • Rigidified Polycyclic Core: Ergolines feature a rigid tetracyclic ring system that incorporates both phenethylamine and tryptamine sub-structures.
  • Amide Substitutions: The N,N-diethylamide group at C-8 is uniquely optimal; converting diethylamide to dimethylamide or monoethylamide drops psychedelic potency by 10 to 100-fold.
  • Position-6 Substitutions: Substituting the N_6-methyl group with ethyl (ETH-LAD) or allyl (AL-LAD) retains or increases potency at 5 HT_2A.

Common Mechanism of Action: The 5-HT_2A Axis​


Primary Target​


Despite structural variations, all classic psychedelics share a primary mechanism: partial agonism at cortical 5HT_2A receptors.


Psychedelic Binding to 5-HT₂A
│
▼
Activation of Layer V Pyramidal Neurons
│
▼
G_q/11 & β-Arrestin-2 Signaling Pathways
│
▼
Increased Intracellular Ca²⁺ & Glutamate Release
│
▼
Disruption of Thalamocortical Gating & Default Mode Network (DMN)

  1. Receptor Activation: Ligands bind deep inside the orthosteric binding pocket of the 5HT_2A G-protein coupled receptor (GPCR).
  2. Functional Selectivity (Biased Agonism): Psychedelics differentially engage downstream signal transduction pathways—specifically favoring the G_{q/11} path (activating phospholipase C and releasing intracellular calcium) and beta-arrestin signaling over standard endogenously mediated pathways.
  3. Cortical Microcircuitry: 5-HT_2A receptors are densely expressed on the apical dendrites of Layer V pyramidal neurons in the prefrontal cortex. Receptor stimulation causes localized glutamate release, driving desynchronization of alpha rhythms and disrupting the integrity of top-down brain networks such as the Default Mode Network (DMN).

Cross-Tolerance and Receptor Downregulation​


One of the defining pharmacological features validating the unified 5HT 2A mechanism is cross-tolerance.


Repeated 5-HT₂A Activation (e.g., LSD, DOI)
│
▼
Rapid Receptor Phosphorylation & Internalization
│
▼
Downregulation of Cell-Surface 5-HT₂A Density
│
▼
Tachyphylaxis / Cross-Tolerance to other 5-HT₂A Agonists (e.g., Psilocybin)

Mechanism of Tolerance (Tachyphylaxis)​


  • Rapid Onset: Daily administration of LSD, psilocybin, or phenethylamines (like DOI) causes a profound decrease in physiological and subjective sensitivity within 24–72 hours.
  • Receptor Internalization: Repeated exposure triggers phosphorylation of the 5-HT_2A receptor, leading to endocytosis and cell-surface downregulation.
  • Empirical Cross-Tolerance: A subject tolerant to LSD displays immediate cross-tolerance to psilocybin and mescaline, confirming that these distinct structural classes act through the same target receptor population.
  • Selectivity: Non-psychedelic 5-HT_2A agonists (such as lisuride) or non-serotonergic hallucinogens (such as ketamine, an NMDA receptor antagonist) do not induce cross-tolerance with classic psychedelics.
 
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this terminology for tolerance is great, I had been saying that the receptor becomes non-functional and has to be replaced
Receptor Internalization: Repeated exposure triggers phosphorylation of the 5-HT_2A receptor, leading to endocytosis and cell-surface downregulation.
here it describes that the receptor is consumed by the neuron (and presumably replaced over the next few days - It may be re-instated after breakdown or after repair, but most likely breakdown)
 
this terminology for tolerance is great, I had been saying that the receptor becomes non-functional and has to be replaced

here it describes that the receptor is consumed by the neuron (and presumably replaced over the next few days - It may be re-instated after breakdown or after repair, but most likely breakdown)
From a historical standpoint from how it came about, they noticed the molecules had different structure, yet produced comparable effects. Cross tolerance indicated a common mechanism of action, which defined the drug class, LSD type drugs, given the label psychedelics, which is then a noun for the name of the class, instead of the adjective psychedelic, which is different.
HALLUCINOGEN
subclass anticholinergics
Subclass dissociative anaesthetics
Subclass psychedelics
You wouldnt claim a subclass anticholinergic is synonymous with dissociatives?
 
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this terminology for tolerance is great, I had been saying that the receptor becomes non-functional and has to be replaced

here it describes that the receptor is consumed by the neuron (and presumably replaced over the next few days - It may be re-instated after breakdown or after repair, but most likely breakdown)
The science term is down regulate
Reduce number of those type cells
So affect on the reduced count may diminish
As is reported
 
I think this interpretation of the effect is inaccurate:
Disruption of Thalamocortical Gating & Default Mode Network (DMN)
Instead - at the location of 5HT receptors (non-thalamic) the action potential is reduced enabling lower signal strength activation which extends thalamo-cortical feedback - thus Cortical neural activation is extended in duration, and the psychedelic effect is persistence and overlapping of sequential signals. ---> trails etc.

Normal thalamo-cortical feedback (6hz theta waves) fades after 3 cycles - increased sensitivity can enable up to 30 cycles before white-out or blackout.

Some Gating is managed at the thalamus via hypothalamic gabaergic neurons which can be articulated by frontal and prefrontal efferents. this enables suppression of thalamic traffic to various parts of the cortex.

Among the 6 layer cortical columns high speed short axon neurons suppress patterns (from thalamo-cortical activation) that are unchanging and that assures that our awareness follows what is changing in our sensory and cognitive contexts.

The DMN is not actually a network, it is an artifact of brain activity that reveals where oxygen was used recently. the information in fNMR is a smear over time although it looks like a wiring diagram.
 
The science term is down regulate
Reduce number of those type cells
So affect on the reduced count may diminish
As is reported
right the cell consumes the receptor and instantiates new receptors as a matter of course.
 
I think this interpretation of the effect is inaccurate:

Instead - at the location of 5HT receptors (non-thalamic) the action potential is reduced enabling lower signal strength activation which extends thalamo-cortical feedback - thus Cortical neural activation is extended in duration, and the psychedelic effect is persistence and overlapping of sequential signals. ---> trails etc.

Normal thalamo-cortical feedback (6hz theta waves) fades after 3 cycles - increased sensitivity can enable up to 30 cycles before white-out or blackout.

Some Gating is managed at the thalamus via hypothalamic gabaergic neurons which can be articulated by frontal and prefrontal efferents. this enables suppression of thalamic traffic to various parts of the cortex.

Among the 6 layer cortical columns high speed short axon neurons suppress patterns (from thalamo-cortical activation) that are unchanging and that assures that our awareness follows what is changing in our sensory and cognitive contexts.

The DMN is not actually a network, it is an artifact of brain activity that reveals where oxygen was used recently. the information in fNMR is a smear over time although it looks like a wiring diagram.
Had the ai help on it, those seem to make occasional errors. Feel free to chip in to tidy!
 
Like a self defense mechanism
Keeps people from abusing it like some sort of addicted junkies druggies
I would not assume that each neuron has "intent" or "reasonaing" capacity, hahaha.
This neural behavior is similar to the effect of emotional activation, and adaptively we had to be able to recover from emotion as well.

Brains operate as systems in which memory and perceptive reflexes occur... many neurons firing at the same time.... what fires together wires together (6 times per second) and really everything subtends from that. (and what fires together (based upon the high speed logic of cortical columns) is what is changing in context (the rest is suppressed from awareness)).

(check familiar and strange link in my sig. illustrating how what fires together wires together and how a small sample of the original pattern can evoke a reflex that brings back the whole pattern to a lesser or greater extent)
 
I would not assume that each neuron has "intent" or "reasonaing" capacity, hahaha.
This neural behavior is similar to the effect of emotional activation, and adaptively we had to be able to recover from emotion as well.

Brains operate as systems in which memory and perceptive reflexes occur... many neurons firing at the same time.... what fires together wires together (6 times per second) and really everything subtends from that. (and what fires together (based upon the high speed logic of cortical columns) is what is changing in context (the rest is suppressed from awareness)).

(check familiar and strange link in my sig. illustrating how what fires together wires together and how a small sample of the original pattern can evoke a reflex that brings back the whole pattern to a lesser or greater extent)
Wasnt trying to imply such, more of a natural selection, severe selection pressure evolutionary arms race.
 
From a historical standpoint from how it came about, they noticed the molecules had different structure, yet produced comparable effects. Cross tolerance indicated a common mechanism of action, which defined the drug class, LSD type drugs, given the label psychedelics, which is then a noun for the name of the class, instead of the adjective psychedelic, which is different.
HALLUCINOGEN
subclass anticholinergics
Subclass dissociative anaesthetics
Subclass psychedelics
You wouldnt claim a subclass anticholinergic is synonymous with dissociatives?
 
Interestingly Salvia Divinorum is not anaesthetic and it's binding is unrelated to any other psychotropic drug, and yet it also can generate persisting cortico-thalamic feedback, and layered experiencing of both temporal and sensory impressions. I suppose the Kappa opioid receptor has some parallel behaviors to the 5HT group. People have argued if it is psychedelic or dissociative. I think it is psychedelic in it's results (similar to DMT when smoked as a fast acting psychedelic) but unlike those that compete at 5HT sites.
 
Interestingly Salvia Divinorum is not anaesthetic and it's binding is unrelated to any other psychotropic drug, and yet it also can generate persisting cortico-thalamic feedback, and layered experiencing of both temporal and sensory impressions. I suppose the Kappa opioid receptor has some parallel behaviors to the 5HT group. People have argued if it is psychedelic or dissociative. I think it is psychedelic in it's results (similar to DMT when smoked as a fast acting psychedelic) but unlike those that compete at 5HT sites.
 
<5 year old dexer accent>
Sally D has similar letters, and might be similar to this other 3 letter thing.
</5 year old dexer accent>
And there the similarity ends.
<5 year old dexer accent>
No, dxm has 3 letters too
</5 year old dexer accent>
How astute and observant of you to be keenly aware of that. We might have almost missed that similarity if you weren't there to point that out. Wait til i tell the whole world about it, think of how much the news will make them overjoyed to know that fact!
 
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