pharmakos
Bluelighter
Sorry this was my first time coming across such a post in future I go to the forum main page and PM any mod about the post? Cheers
use the report button that's on the top right of every post. looks like this:

Sorry this was my first time coming across such a post in future I go to the forum main page and PM any mod about the post? Cheers
I would guess that cannabinoids cause their brain toxicity by overexcitation of neurons. The reason some people get extreme brain damage is they get so much of the cannabinoid at once that it causes a much higher activity in the body than it does in a normal dose, causing the regular seizing and overheating that leads to kidney failure and brain damage. The easiest way to know which are the most dangerous would probably be ki numbers and IA numbers. I would think a cannabinoid with 100% IA is definitely going to cause toxicity in an "effective" dose.Out of curiosity, if anyone has any idea of which synthetic cannaboid is the least harmful I would like to hear what you have to say [:
I know that generally synthetic cannaboids are nasty on the brain. I was at a rehab once and saw 2 kids that were permanently effed up from "spice"
They were basically retarted.
Here is a list of synthetic cannaboids:
5F-AKB48
5F-PB22
AKB48
AM-2201
AM-2233
EAM-2201
JWH-122
JWH-210
MAM-2201
STS-135
UR-144
XLR-11
Indications
Parkinson's disease
Amantadine is a weak antagonist of the NMDA type glutamate receptor, increases dopamine release, and blocks dopamine reuptake. This makes it a weak therapy for Parkinson's disease. Although, as an antiparkinsonian it can be used as monotherapy; or together with L-DOPA to treat L-DOPA-related motor fluctuations (i.e., shortening of L-DOPA duration of clinical effect, probably related to progressive neuronal loss) and L-DOPA-related dyskinesias (choreiform movements associated with long-term L-DOPA use, probably related to chronic pulsatile stimulation of dopamine receptors).
Despite a 2003 Cochrane review of the scientific literature concluding that there is inadequate evidence to support the use of amantadine for Parkinson's, the drug continues to be prescribed for this indication.[1]
Influenza
Amantadine is no longer recommended for treatment of influenza A infection.
For the 2008/2009 flu season, the United States' Centers for Disease Control and Prevention (CDC) found that 100% of seasonal H3N2 and 2009 pandemic flu samples tested have shown resistance to adamantanes.[6] The CDC issued an alert to doctors to prescribe the neuraminidase inhibitors oseltamivir and zanamivir instead of amantadine and rimantadine for treatment of current circulating flu.[7][8]
Off-label uses
Amantadine is frequently used to treat the chronic fatigue often experienced by patients with multiple sclerosis.[9] Additionally, there have been anecdotal reports[10] and a small number of pilot studies[11][12] that show low-dose amantadine as a potential treatment for ADHD. Limited data has shown that amantadine may help to relieve SSRI-induced sexual dysfunction.[13][14][15]
Adverse effects
Amantadine has been associated with several central nervous system (CNS) side effects, likely due to amantadine's dopaminergic and adrenergic activity, and to a lesser extent, its activity as an anticholinergic. CNS side effects include nervousness, anxiety, agitation, insomnia, difficulty in concentrating, and exacerbations of pre-existing seizure disorders and psychiatric symptoms in patients with schizophrenia or Parkinson's disease. The usefulness of amantadine as an anti-parkinsonian drug is somewhat limited by the need to screen patients for a history of seizures and psychiatric symptoms.
Rare cases of severe skin rashes such as Stevens Johnson Syndrome[16] and suicidal ideation in patients treated with amantadine have also been reported.[17][18]
Livedo reticularis is a possible side effect of amantadine use for Parkinson's disease.[19]
...
Dosage and mechanism of action
A starting dose is often 100 mg once daily. All influenza B strains, many influenza A strains (and virtually all H1N1 "swine flu" strains) are resistant to amantadine, so a failure at this dose is likely due to resistance and not underdosing. For its anti-Parkinsonian effects, a starting dose of 300 mg once daily is normal, but can be increased to a limit of about 400 mg.
- The mechanisms for amantadine's antiviral and antiparkinsonian effects appear to be unrelated.
- The mechanism of Amantadine's antiviral activity involves interference with a viral protein, M2 (an ion channel),[23][24] which is required for the viral particle to become "uncoated" once taken inside a cell by endocytosis.
The mechanism of its antiparkinsonian effect is poorly understood. The drug has many effects in the brain, including release of dopamine and norepinephrine from nerve endings. It appears to be a weak NMDA receptor antagonist[25][26] as well as an anticholinergic, specifically a nicotinic alpha-7 antagonist like the similar pharmaceutical memantine.
Amantadine appears to act through several pharmacological mechanisms, but no dominant mechanism of action has been identified. It is a dopaminergic, noradrenergic and serotonergic substance, blocks monoamine oxidase A and NMDA receptors, and seems to raise beta-endorphin/beta-lipotropin levels.[citation needed]
Research in brain injury
In a 2012 study, 184 patients with severe traumatic brain injury were treated with amantadine or placebo for four weeks. In this study, the drug accelerated functional brain recovery.[27]
Doesn't seem like the worst metabolite in the world.![]()
^^ STS-135
the adamantane group (spiky bit at the top of the image) could potentially cleave off and form the chemical Amantadine:
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from the Wikipedia article on Amantadine:
each 1gram of STS-135 could potentially equal up to 400mg of Amantadine consumed.
2NE1 / AKB-48 / 5F-AKB-48 could all also potentially partially degrade/metabolize into Amantadine.
IDK if this is any better or worse than any of the other potential byproducts from this latest generation of cannabinoids...
there's a lot of cannabinoids on the market today that use this functional group
Out of curiosity, if anyone has any idea of which synthetic cannaboid is the least harmful I would like to hear what you have to say [:
I know that generally synthetic cannaboids are nasty on the brain. I was at a rehab once and saw 2 kids that were permanently effed up from "spice"
They were basically retarted.
Here is a list of synthetic cannaboids:
5F-AKB48
5F-PB22
AKB48
AM-2201
AM-2233
EAM-2201
JWH-122
JWH-210
MAM-2201
STS-135
UR-144
XLR-11
I can only speak for my country (sweden) but here it was 5F-AKB48 during the summer and now in the fall we've had a shift towards AB-FUBINACA. The 5F-AKB48 has been widely reported as causing stomach troubles and hospitalizations after cold-turkey quits (after several grams a week-dosages). AB-FUBINACA hasnt had the same reports of actual "damage" but if youre hooked you will suffer from the good old wake up in the middle of the night with enormous cravings. Both seem to cause physical dependence in some way.What synths are popular currently (haven't stayed with the culture for years) and what's the general consensus on safety and quality compared to the good old JWH series?
I can only speak for my country (sweden) but here it was 5F-AKB48 during the summer and now in the fall we've had a shift towards AB-FUBINACA. The 5F-AKB48 has been widely reported as causing stomach troubles and hospitalizations after cold-turkey quits (after several grams a week-dosages). AB-FUBINACA hasnt had the same reports of actual "damage" but if youre hooked you will suffer from the good old wake up in the middle of the night with enormous cravings. Both seem to cause physical dependence in some cases