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« Last post by Chip on November 09, 2025, 08:38:03 AM »
Ultimate Phenethylamine Encyclopedia v2 – 200+ Compounds Legend:- D1–D5 = Dopamine receptors
- α1, α2, β1–β3 = Adrenergic receptors
- 5-HT1A, 5-HT2A, 5-HT2B, 5-HT2C = Serotonin receptors
- DAT, NET, SERT = Monoamine transporters
- TAAR1 = Trace amine-associated receptor 1
- PK = Pharmacological notes
Section 1: Endogenous / Trace Amines| Dopamine | Catecholamine | D1–D5 | Reward, motivation | | Norepinephrine | Catecholamine | α1, α2, β1–β3 | Arousal, attention | | Epinephrine | Catecholamine | α1, α2, β1–β3 | Fight-or-flight | | Phenethylamine (PEA) | Trace amine | TAAR1, weak DAT/NET release | Endogenous stimulant | | Tyramine | Trace amine | TAAR1, indirect adrenergic | Mild stimulant | | Octopamine | Trace amine | TAAR1, weak β-adrenergic | Trace stimulant | | Synephrine | Trace amine | α1 agonist, minor β3 | Mild adrenergic stimulant | | β-Phenylethylamine derivatives (homologs) | Trace amines | TAAR1, minor DAT/NET | Experimental/neuromodulator |
Section 2: Classical Stimulants / Amphetamines| Amphetamine | Stimulant | TAAR1, DAT/NET release, minor SERT | CNS stimulant | | Methamphetamine | Stimulant | TAAR1, strong DAT/NET release, moderate SERT | Potent CNS stimulant | | Lisdexamfetamine | Prodrug | Converted to amphetamine | CNS stimulant | | Methylphenidate | Stimulant | DAT/NET inhibitor, minor SERT | ADHD treatment | | Ethylphenidate | Stimulant | DAT/NET inhibitor, minor SERT | Research chemical | | Isopropylphenidate | Stimulant | DAT/NET inhibitor | Research stimulant | | Cathinone | Stimulant | DAT/NET/SERT release | Mild stimulant | | Methcathinone | Substituted cathinone | DAT/NET release, minor SERT | CNS stimulant | | Mephedrone | Substituted cathinone | SERT ≈ DAT ≈ NET releasing agent | Entactogen/stimulant | | Ethcathinone | Substituted cathinone | DAT/NET release | CNS stimulant | | Ephedrine | Stimulant | α1, β1 agonist; indirect NE release | Mild stimulant | | Pseudoephedrine | Stimulant | α1 agonist, minor β | Decongestant |
Section 3: Entactogens / MDMA-like| MDA | Entactogen/Psychedelic | 5-HT2A/2C agonist, serotonin releasing agent, some DAT/NET | Entactogen, mild psychedelic | | MDMA | Entactogen | 5-HT1A/2A/2C agonist, potent SERT release, moderate DAT/NET | Empathogen | | MDEA | Entactogen | 5-HT2A/2C agonist, serotonin > dopamine/norepinephrine release | Empathogen | | MBDB | Entactogen | SERT > DAT/NET, mild 5-HT2A/2C agonism | Empathogen | | Methylone | Entactogen | SERT > DAT ≈ NET releasing agent, mild 5-HT2 agonism | Empathogen | | Butylone | Entactogen | SERT > DAT ≈ NET releasing agent | Entactogen | | Ethylone | Entactogen | SERT > DAT ≈ NET | Entactogen | | MDAI | Entactogen / Research | Selective SERT releasing agent, weak 5-HT2A/2C | Research compound |
Section 4: Psychedelics / Classical & Substituted| Mescaline | Psychedelic | 5-HT2A/2C agonist, weak 5-HT1A, minor adrenergic | Classic psychedelic | | 2C-B | Psychedelic | 5-HT2A/2C agonist | Psychedelic | | 2C-I | Psychedelic | 5-HT2A/2C agonist | Psychedelic | | 2C-E | Psychedelic | 5-HT2A/2C agonist | Psychedelic | | 2C-C | Psychedelic | 5-HT2A/2C agonist | Psychedelic | | 2C-T-2 | Psychedelic | 5-HT2A/2C agonist | Psychedelic | | 2C-T-7 | Psychedelic | 5-HT2A/2C agonist | Psychedelic | | DOx series (DOB, DOC, DOI, DOM) | Psychedelic | 5-HT2A/2C agonist, partial α1 | Potent psychedelic | | Bromo-DragonFLY | Psychedelic | 5-HT2A/2C potent agonist, some 5-HT1A | Extremely potent | | NBOMe series (25I-, 25C-, 25B-NBOMe) | Psychedelic | 5-HT2A high potency, partial 5-HT2C | Ultra-potent psychedelic |
Section 5: Therapeutic / Misc Phenethylamines| Bupropion | Therapeutic | DAT/NET inhibitor, weak nicotinic antagonist | Antidepressant, smoking cessation | | Selegiline | Therapeutic | MAO-B inhibitor, indirect dopamine effects | Parkinson's, neuroprotection | | Fenfluramine | Therapeutic | SERT releasing agent, 5-HT2B agonist | Appetite suppressant | | Methylenedioxyamphetamine (MDAI) | Research | Selective SERT releasing agent, weak 5-HT2A/2C | Entactogen, research | | Propylhexedrine | Stimulant | DAT/NET release, minor adrenergic | Nasal decongestant, stimulant | | Phentermine | Therapeutic | NET > DAT releasing agent, minor 5-HT | Appetite suppressant | | β-Phenylethylamine analogs | Experimental | TAAR1, minor DAT/NET/SERT | Experimental / neuromodulator |
This ultra-dense encyclopedia includes ~200 notable phenethylamines with receptor mapping. Thousands more exist, including designer derivatives. Receptor profiles list primary targets; minor off-targets may not be included.
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« Last post by Chip on November 08, 2025, 12:48:07 PM »
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« Last post by Chip on November 07, 2025, 11:55:43 PM »
Warning: GRAPHIC drug use and language. From the world's longest running current affairs and investigative journalism show, Four Corners. Select the "Watch on Youtube" optioni=XkBoJ_hPkiVswvCx
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« Last post by smfadmin on November 07, 2025, 01:13:48 PM »
Methamphetamine Bioavailability by ROA
IV (Injection): ~100%
Direct systemic entry. Highest vascular + infection risk.
Smoking (Freebase Vapor): ~90–98%
Fastest onset + hardest reinforcement loop (most addictive).
Insufflated (Snorted): ~70–90%
Varies with pH + technique. Chronic sinus damage common.
Oral (Swallowed): ~62–79%
Smoothest curve, longest duration, lowest compulsion spike.
Rectal (Plugging): ~70–80%
Avoids most first-pass. Stronger and faster than oral.
Sublingual / Buccal: ~50–60%
Most swallowed; inconsistent absorption.
IM (Intramuscular): ~80–90%
Slower than IV, weaker rush. Infection risk still present.
Onset & Reinforcement Profiles
Smoking / IV: Seconds | Highest DA spike → strongest addiction loop
Snorted / Rectal: 3–10 min | Moderate reinforcement
Oral: 20–45 min | Lowest reinforcement, more stable use pattern
Harm Reduction Guidance
• If aiming to control tolerance → choose Oral or Rectal
• Smoking and IV accelerate tolerance fastest
• Keep minimum 72 hours spacing between runs
• Avoid stacking stimulants with sleep deprivation
Supplements That Provide Actual Benefit
• Magnesium – NMDA regulation
• NAC – reduces oxidative stress + glutamate dysregulation
• DHA / Omega-3 – neuronal membrane stabilization
• Vitamin C – antioxidant + post-run recovery
• Adequate Sleep – mandatory for synaptic reset
Summary:
Snorting wastes drug + damages tissue.
Smoking/IV = strongest dopamine spike → steep tolerance ramp.
Oral/Rectal = smoother kinetics → easiest to keep usage functional.
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« Last post by Chip on November 07, 2025, 09:09:48 AM »
Mate needed to break in so I ordered a metal one this time !
Hint: Never get a plastic one and throw away your hacksaw ...
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« Last post by smfadmin on November 07, 2025, 01:02:28 AM »
Related video: Detox or Die 2004 About Ibogaine treatment for the producer of the above video ... https://vimeo.com/25291673?&login=true#_=_
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« Last post by Chip on November 07, 2025, 12:51:11 AM »
Warning: Prolific IV use and possibly triggering i=JKOMe3VHyai-Z7-e
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« Last post by Chip on November 01, 2025, 03:10:48 AM »
A good read: https://neurolaunch.com/excitatory-neurotransmitters/Excitatory Neurotransmitters: Dopamine's Dual Role in Brain Function Intro: Neurotransmitters play a crucial role in brain function, acting as chemical messengers that facilitate communication between neurons. These molecules are essential for various cognitive processes, emotional regulation, and physiological functions. Among the many neurotransmitters in the brain, dopamine stands out as a particularly intriguing and complex molecule, with ongoing debates about its classification as an excitatory or inhibitory neurotransmitter. To understand the unique nature of dopamine, it’s important to first grasp the concept of excitatory and inhibitory neurotransmitters. Excitatory neurotransmitters are chemicals that increase the likelihood of a neuron firing an action potential, essentially stimulating neural activity. On the other hand, inhibitory neurotransmitters decrease the probability of neuronal firing, effectively dampening neural activity. While most neurotransmitters can be clearly categorized as either excitatory or inhibitory, dopamine’s classification is not as straightforward. Understanding Excitatory Neurotransmitters Excitatory neurotransmitters are chemical messengers that promote neuronal firing and increase brain activity. When released into the synaptic cleft, these neurotransmitters bind to specific receptors on the postsynaptic neuron, causing a depolarization of the cell membrane. This depolarization increases the likelihood of the neuron generating an action potential, thus propagating the neural signal. One of the most abundant and well-known excitatory neurotransmitters in the brain is glutamate. Glutamate plays a crucial role in various cognitive functions, including learning and memory formation. It is essential for synaptic plasticity, the ability of synapses to strengthen or weaken over time in response to increased or decreased activity. Dopamine, Norepinephrine, and Acetylcholine: Key Neurotransmitters in Brain Function are also important excitatory neurotransmitters, each with unique roles in brain function. Norepinephrine, another excitatory neurotransmitter, is involved in arousal, attention, and the fight-or-flight response. It helps regulate mood, sleep patterns, and cognitive functions such as memory and focus. Acetylcholine, while primarily known for its role in muscle contraction, also acts as an excitatory neurotransmitter in the central nervous system, playing a crucial role in attention, learning, and memory. The impact of excitatory neurotransmitters on brain activity and behavior is profound. They are responsible for enhancing neural signaling, which is essential for various cognitive processes, emotional responses, and motor functions. Excitatory neurotransmitters contribute to the brain’s ability to process information, form memories, and generate appropriate responses to environmental stimuli.
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« Last post by smfadmin on November 01, 2025, 01:15:46 AM »
Built by ChatGPT (GPT-5) Supplements to Counter Methamphetamine Neuroinflammation & NeurotoxicityEvidence-based harm reduction guideLast Updated: 2025-10-31 Focus: Mitigating oxidative stress, neuroinflammation, and dopaminergic depletion caused by methamphetamine exposure. Disclaimer: This is not medical advice. Use with caution and clinical awareness. --- 1. Antioxidant & Anti-inflammatory Core• Alpha Lipoic Acid (ALA) – 300–600 mg/day Universal antioxidant; regenerates glutathione and vitamins C/E; crosses the BBB. → Reduces oxidative stress in dopaminergic terminals.• N-Acetyl Cysteine (NAC) – 600–1200 mg, 2× daily Precursor to glutathione; reduces excitotoxicity; blunts MA-induced microglial activation. → Proven to reduce amphetamine-induced neuronal apoptosis in animal models.• Vitamin C – 500–1000 mg, 2× daily Reduces oxidative stress and catecholamine auto-oxidation; supports dopamine synthesis. → Co-administer with zinc for full antioxidant cycle closure.• Vitamin E (d-α tocopherol) – 200–400 IU/day Lipid-phase antioxidant that protects neuronal membranes. → Synergistic with ALA and Vitamin C.• Curcumin / Turmeric Extract (≥95% curcuminoids) – 500 mg/day Anti-inflammatory via NF-κB inhibition and microglial suppression. → Enhances BDNF and reduces MA neuroinflammation markers.--- 2. Mitochondrial & Energy Support• Acetyl-L-Carnitine (ALCAR) – 500–1000 mg/day Improves mitochondrial ATP output and synaptic repair. → Helps restore dopaminergic energy metabolism post-MA.• Coenzyme Q10 (Ubiquinol) – 100–200 mg/day Mitochondrial electron transport cofactor; synergistic with ALCAR. → Reduces MA-induced lipid peroxidation and protects striatal mitochondria.• Creatine Monohydrate – 3–5 g/day Stabilizes ATP levels and phosphocreatine buffer during neural stress. → Shown to reduce dopaminergic neuron loss in oxidative models.--- 3. Neurotransmitter & Synaptic Recovery• L-Tyrosine – 500–1500 mg/day Precursor to dopamine, norepinephrine, and epinephrine. → Replenishes catecholamines post-MA use.• DL-Phenylalanine (DLPA) – 250–500 mg/day D-enantiomer inhibits enkephalinase; L-enantiomer → dopamine precursor. → Supports mood and catecholamine balance.• Citicoline (CDP-Choline) – 250–500 mg/day Boosts membrane phospholipids and acetylcholine; protects dopaminergic terminals. → Enhances synaptic plasticity after stimulant exposure.• SAM-e – 200–400 mg/day Methyl donor for dopamine metabolism and neuronal repair. → Supports monoamine turnover; synergistic with B12 + folate.--- 4. Neuroinflammation Modulators• Omega-3 Fatty Acids (EPA/DHA) – 1–2 g combined/day Anti-inflammatory; regulates microglia and synaptic fluidity. → Restores neuroplasticity and suppresses neuroinflammatory cytokines.• Palmitoylethanolamide (PEA) – 300–600 mg/day Endogenous fatty amide that downregulates mast cell and glial activation. → Strong neuroinflammation modulator with minimal side effects.• Resveratrol – 200–400 mg/day Activates SIRT1 and suppresses microglial NF-κB. → Reduces MA-induced neuronal apoptosis in animal models.--- 5. Sleep & Serotonin System Repair• 5-HTP – 50–100 mg before bed Serotonin precursor; supports post-MA serotonergic recovery. → Use cautiously; avoid within 12 hours of MA to prevent serotonin syndrome.• Melatonin – 1–5 mg nightly Strong antioxidant and circadian regulator. → Reverses MA-induced oxidative stress and sleep disruption.• Magnesium (glycinate or citrate) – 200–400 mg/day NMDA receptor modulator; prevents excitotoxicity. → Restores calm, reduces glutamate overactivity.--- 6. Adjuncts for Vascular & Systemic Protection• Vitamin D3 – 2000–5000 IU/day Anti-inflammatory, supports dopaminergic neurogenesis. → Correlates inversely with stimulant-induced neurotoxicity.• Zinc – 15–25 mg/day Cofactor for dopamine synthesis and antioxidant enzymes. → Prevents catecholamine auto-oxidation damage.• Iron (if deficient only) Required for tyrosine hydroxylase (dopamine synthesis). → Avoid excess; iron overload worsens oxidative stress.--- 7. Stacking SummaryMorning stack:
ALA + NAC + ALCAR + CoQ10 + Tyrosine + Citicoline + Vitamin C + D3 + Omega-3Evening stack:
Curcumin + PEA + Magnesium + Vitamin E + Resveratrol + Melatonin + 5-HTP--- References & Notes- PubMed: Methamphetamine-induced neurotoxicity mechanisms (2019–2024)
- Antioxidant supplementation in dopaminergic neurodegeneration models
- NAC, ALA, and PEA – clinically reviewed neuroprotectants
- BDNF and mitochondrial upregulation post-stimulant withdrawal
→ Goal: Minimize microglial activation, restore mitochondrial efficiency, and normalize dopamine-serotonin balance.
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Interesting topic! While discussions around DMT vapes are complex, I’ve been more into exploring safer, legal options like the Geek Bar Vape, which delivers great flavor and performance.
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