#103

The last post in the thread Mushrooms Magnify Memory is about memory improvement from intake of lion’s mane, after injury.

I thought I posted incorrectly here, so there is the delete and repost. Still trying to find out how to repost a deleted comment.

#104

desertshores, I’ve been experimenting with centrophenoxine for a few weeks at 750 mg daily and have not noticed anything so far. When you use it do you notice any type of effect? Thanks.

#105

If you are in good mental and physical shape, you probably won’t notice any effect of most supplements. I was taking centrophenoxine before I started taking rapamycin and some current senolytics. At the time I thought it definitely cleared up a slight brain fog. Might just be the placebo effect.

#106

May I ask if you are on rapa and if yes, have you noticed any difference in the effect of psilocybin with or without rapamycin?

I plan to take 25-30mg psilocybin also for anxiety and was wondering if I should stop the rapamycin, cause the brain plasticity-increasing effect of psychedelics is apparently mediated through mTOR activation:

#107

You may have seen this already, but worth posting again.

1 Like
#108

Was on weekly rapa. Did not take psilocybin on same day. Did not notice any difference in my own crossovers.

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#109

I take Modafinil when I need to power through a project and really focus. I like it, but can’t imagine taking it everyday. Maybe as a micro-dose…

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#110

Is this a good thing?

I know what LPS is, it’s a sign you have a high microbial burden. How can masking the inflammation help this? I’m hoping somebody smarter than me can explain.

#111

Is anyone still taking Centrophenoxine? I saw @desertshores and maybe @MAC interested or taking it occasionally. Is it worth considering? (I heard about it from a Greg Fahy interview).

#112

I think this old thread is the right place for this. I have been using a bromantane nasal spray from everychem.com for about 5 weeks, and I now feel comfortable recommending it as something to try, since, unlike many things I’ve experimented with, this has actually helped me in a very noticeable way.

Ever since my 2021 ICU stay and a later COVID-19 infection, I’ve had short term memory problems, a general lack of emotion and sometimes motivation, trouble with word recall, trouble focusing, and I believe quite a scary drop in intelligence. I have felt somewhat numb and as if I were always in a haze. The emotional aspect was worsened by a recent experiment with BPC-157, which introduced a sudden, very strong “anhedonia.”

I had very low expectations for it, but the bromantane nasal spray has lifted my symptoms to a surprising degree. I’ve experienced much greater clarity of thought, general alertness without undue stimulation, ability to focus and converse during technical conversations at work, and a significant increase in emotional range, both highs and lows. I’m responding to small sensory cues like smells, things I glance at throughout the day, and music, with old, pleasant memories and feelings. I can once again enjoy small, simple everyday things, and feel much more motivated to pursue interests like I used to. I have a generally higher sense of well being and peace, a reduction in background anxiety. This is borderline shocking to me after 3 years of feeling not fully human.

Bromantane was my choice of experiment because of what I had read about it increasing sensitivity to dopamine in a safe, sustainable way. I believe it has had that effect.

The best writeups I’ve found on bromantane are from the owner of everychem, who was once very active on reddit (yes, he has a conflict of interest, and started everychem as a means of supplying bromantane in bioavailable form). He has summarized the research, and ChatGPT has summarized his posts for me. For links to references, see the reddit posts:

Reddit post number 1
Reddit post number 2

From ChatGPT:
Here’s a combined and comprehensive explanation of Bromantane’s mechanisms, incorporating the role of Medium Spiny Neurons (MSNs) without redundancy:

What are Medium Spiny Neurons (MSNs) and Why Do They Matter?

Medium Spiny Neurons (MSNs) are a key type of neuron located in the brain’s striatum, a region essential for regulating movement and reward processing. These neurons are classified into two main types based on the dopamine receptors they express:

  • Direct-pathway MSNs (D1 receptors): These neurons promote movement, impulsivity, and reward-seeking behavior when activated by dopamine. They are associated with positive motivation, goal-directed action, and optimism.

  • Indirect-pathway MSNs (D2 receptors): These neurons inhibit excessive movement and promote cautious, rational decision-making. They help suppress inappropriate actions, allowing for more measured and controlled behavior.

The proper functioning of both pathways is crucial for balancing impulsive behavior with rational restraint. If this balance is disrupted, it can lead to various issues, such as dyskinesia (uncontrolled movement) when direct-pathway MSNs are overactive, or bradykinesia (slowed movement) when indirect-pathway MSNs dominate.

How Bromantane Works:

Bromantane’s mechanism of action can be understood through its ability to modulate both direct and indirect MSNs and enhance dopamine signaling. It bears structural and functional similarities to Amantadine, and much of its theoretical activity can be explained through parallels with this drug, but potentially with stronger dopaminergic effects. Here’s how Bromantane functions:

  1. Neurotrophic Factor Upregulation:
    Bromantane increases the levels of brain-derived neurotrophic factor (BDNF) and possibly glial cell line-derived neurotrophic factor (GDNF), promoting the growth, repair, and maintenance of neurons. These neurotrophic factors help restore and enhance the sensitivity of dopamine receptors by facilitating greater neuronal plasticity and strengthening dopamine pathways over time.

  2. Kir2 Potassium Channel Blockade:
    Like Amantadine, Bromantane may block Inwardly Rectifying Kir2 potassium channels, which indirectly enhances NMDA receptor activity in Medium Spiny Neurons. This leads to improved long-term potentiation (LTP) in indirect MSNs, allowing them to remain active even in the presence of elevated dopamine. This mechanism is crucial for enhancing dopamine receptor sensitivity, particularly in conditions where dopamine signaling might otherwise become unbalanced.

  3. Dopamine Sensitization:
    Bromantane increases dopamine synthesis and release through upregulation of key enzymes in the dopamine production pathway, such as Tyrosine Hydroxylase (TH) and Aromatic L-amino Acid Decarboxylase (AAAD). Over time, this heightened dopamine availability is balanced by enhanced receptor sensitivity, reducing the likelihood of tolerance or withdrawal. By maintaining dopamine receptor responsiveness in both direct and indirect MSNs, Bromantane ensures sustained dopaminergic effects without overstimulation.

  4. Inflammation Reduction:
    Bromantane reduces inflammatory cytokines, which decreases the activity of histone deacetylases. This reduction in inflammation further enhances the expression of neurotrophic factors like BDNF, and may increase C-Fos, a marker commonly associated with dopaminergic activity and stimulant tolerance. This combination helps restore sensitivity to dopamine receptors and prevents the development of tolerance often seen with other stimulants.

Balancing Medium Spiny Neuron Activity:

Bromantane’s unique action on MSNs is what sets it apart as a stimulant that doesn’t produce typical stimulant side effects like dyskinesia, withdrawal, or addiction. The drug appears to balance the activity of direct (D1) and indirect (D2) MSNs, allowing dopamine’s effects to be amplified without causing excessive stimulation. Here’s why this matters:

  • Direct MSNs (D1 receptors): Bromantane’s action increases the activity of direct-pathway neurons, promoting motivation and positive movement, but prevents overstimulation by simultaneously supporting the indirect pathway.

  • Indirect MSNs (D2 receptors): By enhancing neurotrophic factors and NMDA receptor activity in indirect-pathway MSNs, Bromantane ensures that these neurons remain active during periods of elevated dopamine. This prevents the overactivation of direct MSNs, thus mitigating the risk of impulsive behavior, dyskinesia, or other negative side effects.

This balance explains Bromantane’s ability to enhance both cognitive and physical performance without leading to addiction or withdrawal. The neurotrophic upregulation in conjunction with balanced MSN activity allows for heightened mental alertness, improved motor function, and an overall enhanced central nervous system response to stress or stimulation without the risk of dopamine dysregulation.

Other Effects of Bromantane:

  1. Sleep-Wake Cycle and Anxiolytic Properties:
    Despite being stimulating, Bromantane can also normalize sleep patterns. This is due to its ability to increase peripheral serotonin and melatonin synthesis via AAAD upregulation. It also acts as a GABA reuptake inhibitor, increasing GABA levels in the brain and contributing to its calming and anxiolytic effects.

  2. Lack of Tolerance or Addiction:
    Bromantane’s balanced effect on MSNs and dopamine pathways ensures that it does not lead to tolerance, dependence, or withdrawal symptoms, which is unusual for a psychostimulant. Long-term use doesn’t appear to result in downregulation of dopamine receptors, likely due to its neurotrophic effects and the prevention of overactivation in any single neuronal pathway.

Summary of Bromantane’s Mechanism:

Bromantane works by:

  • Enhancing dopamine production and sensitivity through neurotrophic factor upregulation.
  • Blocking Kir2 potassium channels to improve NMDA receptor activity and dopamine receptor responsiveness.
  • Balancing the activation of direct (D1) and indirect (D2) Medium Spiny Neurons to avoid overstimulation and prevent side effects like dyskinesia.
  • Reducing inflammatory cytokines to further promote neuroplasticity and prevent tolerance.

This unique combination of effects allows Bromantane to offer mental and physical performance enhancements without the typical stimulant drawbacks, making it a potent yet safe dopamine sensitizer.

In essence, Bromantane enhances dopamine signaling and neuron sensitivity while balancing the brain’s excitatory and inhibitory pathways. By working on Medium Spiny Neurons, it provides powerful yet controlled dopaminergic stimulation, promoting both enhanced cognitive function and physical energy without the negative side effects of conventional stimulants.

4 Likes
#113

More on bromantane as an actoprotector:

Bromantane

Morozov and Ivanova supposed that benzoylaminoadamantanes, adamantane derivatives of para-chlorophenoxyacetic acid, and other structurally close compounds increase the resistance of the human body with respect to extreme environmental factors rather than act as direct stimulants of the physical working capacity under normal conditions. Nonetheless, several compounds, including N-(2-adamantyl)-N-(para-bromophenyl)-amine (bromantane) (Fig. 1B) and N-(2-adamantyl)-N-(para-chlorobenzoyl) amine (ADK-910, chlodantane) (Fig. 6A), can increase physical performance; accordingly, in the literature, they are regarded as actoprotectors (Morozov and Ivanova, 2001).


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Fig. 6.

Chemical structures of three compounds with actoprotector activity, (A) chlodantane (N-(2-adamantyl)-N-(para-chlorobenzoyl) amine); (B) ademol (1-adamantylaethyloxy-3-morpholino-2-propanol hydrochloride); (C) ethomersol (5-ethoxy-2ethylthiobenzimidazole hydrochloride).

Bromantane, upon oral induction, is quickly but not fully absorbed from the gastrointestinal tract into the blood (bioavailability: 42%). It is quickly, and in large quantities, distributed over the tissues and organs, and is slowly eliminated from the body. Bromantane is highly lipophilic, is distributed into the lipids of brain and fat tissue and, finally, is deposited in adipose tissue. The speed of bromantane absorption from the gastrointestinal tract is much higher in women, so the half-life is respectively lower than in men. The time to achievement of the maximum concentration of blood bromantane is 2.75 hours in women, and 4.0 hours in men. The drug is metabolized in the liver, but its elimination occurs mostly through the adrenal gland. Bromantane metabolism is characterized mainly by hydroxylation in the 6th position of the adamantan cycle. All of the determined metabolites can be found in urine, even in two weeks after administration of bromantane (this last fact is important for doping control) (Burnat et al., 1997).

In terms of its pharmacological action, bromantane shows an antiasthenic effect, increases resistance to overheating, and, thereby, contributes to the restoration of working capacity after physical loads. This compound, which possesses combined stimulative and anxiolytic effects, increases physical and intellectual working capacity; inhibits the development of fatigue processes; accelerates restoration under common conditions and conditions complicated by hypoxia and hyperthermia; promotes improvement of mnemic processes (learning); improves the coordination of movements; increases body temperature; has a neuropsychoactivation effect (therefore it is sometimes referred to as a psychomotor stimulator); reveals antagonism to the sedative action of tranquilizers; displays a positive inotropic action without affecting the heart chronotropic function or systemic arterial pressure, and produces immunomodulation activity (Sedov et al., 1999; Morozov et al., 1999).

Whereas bromantane lacks hypno-sedative and neuromuscular relaxant properties, it does not possess any addictive potential. At its application, it does not, unlike typical psychostimulants, develop the phenomena of hyperstimulation.

It was determined that bromantane has a positive influence on the indices of psychophysiological conditions: range and stability of attention, complex sensomotor reaction, and the parameters of successful operator activity (Viatleva et al., 2000).

The mechanism of bromantane action is based on the facility to increase the activity of the lower centers of the central nervous system (the hypothalamus nuclei, the reticular nuclei of the operculum, the hippocampus). It does not exert any expressed action on noradrenergic mediators, but implements the activation properties through the dopaminergic system. Bromantane strengthens GABA-ergic mediation, reducing gene expression, supervising synthesis of GABA-transporters, and functioning as a return capture mediator. A potentiality for central serotonin holding effects is also assumed.

A definite role in the implementation of the bromantane pharmacological effect is played by its antiradical and membrane protective properties: bromantane increases immunity even after a single dose (increases the level of B-cells and circulating immune complex in the blood-stream), and it is more powerful than another synthetic adaptogen, levamizol, in terms of its effect on immunity (Morozov et al., 1999).

Bromantane stimulates synthesis of cytochrome P-450 and thus facilitates detoxifying liver functions and reduces the hypnotic action of thiopental sodium (but at the same time, does not weaken the anxiolytic effect of benzodiazepines).

Bromantane administration in therapeutic doses is characterized by the almost full absence of side effects including manifestations of withdrawal syndrome and hyperstimulation (Morozov et al., 1999). In animal experiments, toxic reactions were observed only after high doses of bromantane administration (>600 mg/kg). Lower doses (30-300 mg/kg) stimulated, and higher doses (600-9,600 mg/kg) suppressed behavioral activity. Spontaneous motor activity was increased after single treatment of bromantane in doses of 30-300 mg/kg, was not changed after treatment in doses of 600 mg/kg, but was inhibited after treatment in doses above 600 mg/kg. The drug reduced the pain sensitivity threshold in doses of 300-600 mg/kg, and elevated it, along with tactile sensitivity and reaction to knock, in doses above 600 mg/kg (Iezhitsa et al., 2002).

Additional and more detailed information on the pharmacological properties of bromantane is available in a foundational book, some review articles (Morozov et al., 1999; Morozov and Ivanova, 2001), and numerous clinical and experimental studies first and foremost from the laboratories of I.S. Morozov and S.B. Seredenin.

1 Like
#114

Piracetam, an approved drug, is a powerful nootropic, I use it occasionally

2 Likes
#115

What dosing protocol are you using?

#116

2 sprays per morning when I wake up. Each spray delivers 9mg, which the everychem owner says is equivalent to a larger oral dose. The spray bottle lasts 90 days. The effect built up over about 2 weeks.

5 Likes
#117

I have problems judging Russian literature. Surely there’s some legit stuff there, but they also have a reputation for, uhm, overly creative research practices.

Is there any non-Russian evidence that Bromantane behaves as claimed?

2 Likes
#118

Yep, much of the research on many ‘nootropics’ is entirely based on poor quality Russian research. With exceptions for things like phenibut where the pharmacology largely overlaps with Western drugs like pregabalin and gabapentin.

I’ve taken bromantane quite a lot though (favorite dose is about 20mg sublingual), and it definitely does something. Increased body temp, small increase in motivation, sometimes increased sociability. Slight boost in the gym. Minimal sympathomimetic activity. But the effect size isn’t profound so I’ve never ran it daily for long periods of time. I have combined it with many other substances with no issues, and at least acutely it seems non-toxic.

4 Likes
#119

Psilocybin therapy for mood dysfunction in Parkinson’s disease: an open-label pilot trial 2025

Mood dysfunction is highly prevalent in Parkinson’s disease (PD), a main predictor of functional decline, and difficult to treat—novel interventions are critically needed. Psilocybin shows early promise for treating depression and anxiety, but its potential in PD is unknown, as safety concerns have excluded people with neurodegenerative disease from previous trials. In this open-label pilot (NCT04932434), we examined the feasibility of psilocybin therapy among people with mild to moderate stage PD plus depression and/or anxiety. 12 participants (mean age 63.2 ± 8.2 years, 5 women) received psilocybin (one 10 mg followed by one 25 mg dose) with psychotherapy. There were no serious adverse events, no medical interventions required to manage effects of psilocybin, and no exacerbation of psychosis. Ten participants experienced treatment-emergent adverse events; the most frequent were anxiety, nausea, and increased blood pressure. We observed no worsening of PD symptomology measured by the Movement Disorder Society Unified Parkinson’s Disease Rating Scale (MDS-UPDRS). On the contrary, non-motor (MDS-UPDRS Part I: –13.8 ± 1.3, p < 0.001, Hedges’ g = 3.0) and motor symptoms (Part II: –7.5 ± 0.9, p < 0.001, g = 1.2; Part III: –4.6 ± 1.3, p = 0.001; g = 0.3) as well as performance in select cognitive domains (Paired Associates Learning [-0.44 ± 0.14, p = .003, g = 0.4], Spatial Working Memory [–0.52 ± 0.17, p = 0.003, g = 0.7], and Probabilistic Reversal Learning [2.9 ± 0.9, p = 0.003, g = 1.3]) improved post-treatment, and improvements were sustained until the final safety assessment one month following drug exposure. Baseline Montgomery-Asberg Depression Rating Scale (MADRS) and Hamilton Anxiety Rating Scale (HAM-A) scores were 21.0 ± 8.7 and 17.0 ± 3.7, respectively. Both improved to a clinically meaningful degree post-treatment; these improvements persisted to the final assessment three months following drug exposure (MADRS: -9.3 ± 2.7, p = .001, g = 1.0; HAM-A: –3.8 ± 1.7; p = 0.031, g = 0.7). This study provides the first data on psilocybin’s effects in any neurodegenerative disease. Results suggest that psilocybin therapy in PD warrants further investigation.

#120

Why did you choose the nasal spray version?

#121

Better bioavailability. Oral is bad, sublingual takes 30 minutes, nasal requires a lower dose and works well.

From the Everychem owner:
https://www.reddit.com/r/NooTopics/s/MTRHqztQnQ


Meta

This is a continuation to my exploration of the dopamine upregulator Bromantane. If you want a quick summary on Bromantane nasal spray, feel free to watch this youtube video I created on the subject: https://www.youtube.com/watch?v=UA1D-LeiA_0.

Caprylic acid: Recently I have developed the Bromantane nasal spray, an invention that utilizes a high concentration Bromantane with Caprylic acid, a medium-chain fatty acid that, unlike long-chain fatty acids, does not pose a threat for Lipoid Pnemonia. This allows it to be used as a solvent for intranasal use. Additionally, it is anti-bacterial, anti-fungal and anti-viral, so rest assured it is sterile.

Since Caprylic acid is lubricating, it won’t dry your nose out, therefore it’s better than snorting the powder and there’s less risk for nasal membrane damage, which could still be an issue despite Bromantane’s non-toxic nature.

Bromantane’s bioavailability: Bromantane has never been used intranasally in studies, but we can reference other things. There is a study on actoprotectors claiming its oral bioavailability is 42% but after thorough investigation, I have found there is no evidence to back this up. Anecdotally, we see that oral always fails and sublingual takes up to 30 minutes. This means another route of administration is more desirable.

Amantadine, Bromantane predecessor, has been investigated for intranasal use in previous studies: Development and Evaluation of a Novel Intranasal Spray for the Delivery of Amantadine - PubMed

Furthermore, our results have indicated the potential for nose-to-brain delivery of Amantadine, yielding a potentially novel avenue therapeutics delivery route to avoid the blood brain barrier.

Caprylic acid, referenced here as Octanoic acid, is perfectly absorbed intranasally, where there is then a direct route to the brain through the nasal cavity: Source. Since it is a small fatty acid, and Bromantane is lipophilic in nature, this perfects the absorption of Bromantane and allows it easy transport to the brain, where there is then far greater effect.

Essentially, Bromantane is perfect for intranasal use, and this explains why it works so well intranasally.

I know this is straight from the horse’s mouth, but it has been working great for me and I truly believe in it.

Edit: now available on https://bromantane.co/.

1 Like
#123

What do you take Tryptophan for? I took it for some time for better sleep but didn’t notice any changes. Wondering how it works.