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Rimonabant (Marijuana Blocker)

NeoLime

NeoLime

Bluelighter
Joined
Oct 30, 2007
Messages
20
http://en.wikipedia.org/wiki/Rimonabant

I know wikipedia has a less then noble history. However this drug has raised some concerns for me.
Rimoabant blocks the CB1 receptor, the receptor that controls uptake of the drug THC, the main component of Marijuana.
I enjoy my freedom to be high, I do not believe I abuse it or overdo it, except upon occasion. If this drug becomes publicized it could have repercussions not only in the stoner culture, but it may become part of any rehab program.
Its longterm negative side effects (loss of appetite, depression, Rimonabant promotes the development of neurodegenerative diseases of the central nervous system such as Multiple sclerosis, Alzheimer's disease, Amyotrophic lateral sclerosis (ALS), Parkinson's disease, and Huntington's disease in persons who are susceptible.)

As long as marijuana continues to be heavily criminalized, there is high risk of oppression and control of a subculture of the united states.

Thank you for reading,
Neolime
 
Rimonabant promotes the development of neurodegenerative diseases of the central nervous system such as Multiple sclerosis, Alzheimer's disease, Amyotrophic lateral sclerosis (ALS), Parkinson's disease, and Huntington's disease in persons who are susceptible
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No doctor in their right mind is going to force that on a patient because they like getting stoned, esp not in a litigous country like the US - you can just imagine the sort of lecgal actions that woulf lead to.

The fact that it can promote multiple scleroris is, IMO, just another nail in the coffin of the myth of the non-medical status of cannabis. If a CB1 antagonist makes it worse then surely a CB1 agonist will improve it
 
interesting, but like fastandbulbous is kinda saying, the only real way to fight MJ is by creating false pretenses in use and now even "treatment?" . crazy.
 
don't fear rimonabant as a way of forcing people not to use cannabis, because it isn't particularly potent or long lasting.

fear more the development of vaccines against nicotine cocaine morphine and other drugs of abuse. these will appear very soon in the real world as opposed to in trials. they will be siezed upon as tools in the war on drugs. it seems inevitable that such vaccinations will eventually feature in court prescribed substance abuse treatment, In the future it is easy to see how if you get caught with illegal substances you either agree to vaccination or go to jail for a long time.
 
Why would you fear it anyway? If your doctor prescribed it to you and you know the affects would you still put it in your mouth or something??
 
^
my philosophy is....
read the other posts, stop, think, then post.
:\
 
My question was just reinforcement for OP to not be so alarmed. Considering rimonabant isn't long lasting and there is currently no vaccine then he has little to worry about. Taking into context of what may or may not happen in the future is hearsay atm.

Don't be upset cause you felt your post was overlooked. ;)
 
By it's own rights, I find it fascinating that blocking CB1 receptors can lead to such debilitating diseases.
 
It's interesting, it's not blocking the receptors, it's actually an inverse agonist (as opposed to an antagonist), meaning that it is an agonist but it has the reverse pharmacological effect that a regular agonist would have. Correct me if I'm wrong here (I'm no chemist and have no business posting here really =D).

For an example of another inverse agonist, check out R015-4513, which is to benzos what rimonabant is to cannabis.
 
(I'm no chemist and have no business posting here really ).
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A chimist might scratch their head as well as inverse agonists is the realm of pharmacologists! =D
 
I've heard that this rimonabant can cause neurodegeneration in the long term because it's a CB1 antagonist, while pot causes neurogenesis being a CB1 anonist.

I'd be concerned about this drug in that regard. Kinda sickening that they'll market a cb1 antagonist that can cause brain damage in an unscheduled fashion but they won't market a cb1 agonist without controlled status just because it's psychoactive. That's the real reason for controlled drugs, people have a problem with psychoactivity, it's evil in puritanical eyes.
 
resorcinol said:
I've heard that this rimonabant can cause neurodegeneration in the long term because it's a CB1 antagonist, while pot causes neurogenesis being a CB1 anonist.
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I am just wondering what it meant when you say that pot causes neurogenesis.
Neurogenesis occurs as part of pre-natal development. Are you suggesting that pot enhances ability to learn or pick up information? or Allows for more neurons to be produced?

It is a very interesting idea, I am curious where you got the idea or the inspiration for the idea. Is there any research on this?

Thank you,
Neolime
 
NeoLime said:
I am just wondering what it meant when you say that pot causes neurogenesis.
Neurogenesis occurs as part of pre-natal development. Are you suggesting that pot enhances ability to learn or pick up information? or Allows for more neurons to be produced?

It is a very interesting idea, I am curious where you got the idea or the inspiration for the idea. Is there any research on this?

Thank you,
Neolime
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I made a wrong choice of words. I meant that pot is neuroprotective, and by antagonizing the cb1 receptors, you're removing the ability for both endogenos and exogenous (eg pot) ligands from acting out their neuroprotective action.

Which makes rimonabant possibly not good for the brain.
 
CB1 agonists do promote neurogenesis, they stimulate release of neurotrophic factors like BDNF, NGF etc which stimulate growth and differentation of new neurons, as do various other drugs such as SSRIs and 5HT2A agonists. I believe THC also has seperate neuroprotective actions through a different mechanism.

This doesn't mean that CB1 antagonists will necessarily be neurotoxic however. Most of the really addictive drugs (nicotine, amphetamines, opioids) inhibit neurogenesis by reducing production of BDNF (as do chronic stress and depression), but this does not cause neurotoxicity directly (although it does tend to reduce survival of newly formed brain cells it doesn't kill existing ones)

CB1 antagonists are interesting but I haven't seen anything yet that would make me want to take them, although the research suggesting CB1 antagonists as general purpose anti-addictive drugs suggests they might have some potential (which is lucky as rimonabant isn't that great as a weight loss drug!)
 
I thought Rimonabant was an inverse agonist, not just an antagonist?
 
NeoLime said:
I am just wondering what it meant when you say that pot causes neurogenesis.
Neurogenesis occurs as part of pre-natal development. Are you suggesting that pot enhances ability to learn or pick up information? or Allows for more neurons to be produced?

It is a very interesting idea, I am curious where you got the idea or the inspiration for the idea. Is there any research on this?

Thank you,
Neolime
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IANAD, but I think this is about adult neurogenesis (which happens naturally).

More neurogenesis doesn't automatically mean cognitive improvement; cognition is a higher-level phenomenon. If anyone knows what these new neurons are used for, please tell :)

Research: http://scholar.google.com/scholar?hl=en&lr=&safe=off&c2coff=1&q=cannabinoid neurogenesis&btnG=Search

mad_scientist: Would you happen to know the effect of both an SSRI and nicotine? I hope the SSRI is stronger ;)
 
fastandbulbous said:
A chimist might scratch their head as well as inverse agonists is the realm of pharmacologists! =D
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Then you can clearly see how much I know! :D

Anyway, I find pharmacology (as well as chemistry) fascinating, even if I don't understand it all right away. I see something like "inverse agonist" and I go "COOL! exciting!" Gotta start somewhere I suppose. I guess excitement is the first step towards really getting the hang of something.
 
MattPsy said:
I thought Rimonabant was an inverse agonist, not just an antagonist?
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That is quite correct. Also please know for you cannabis users it may be a good drug for you to take in low doses as needed.

Behav Pharmacol. 2007 Dec;18(8):767-76. Links
Cannabinoid-induced tolerance is associated with a CB1 receptor G protein coupling switch that is prevented by ultra-low dose rimonabant.

Paquette JJ, Wang HY, Bakshi K, Olmstead MC. Department of Psychology, Queen's University, Kingston, Ontario, Canada.

The analgesic effect of opioids is enhanced, and tolerance is attenuated, by ultra-low doses (nanomolar to picomolar) of an opioid antagonist, an effect that is mediated by preventing the receptor from coupling to Gs proteins. Recently, we demonstrated a cannabinoid-opioid interaction at the ultra-low dose level, suggesting that the effect might not be specific to opioid receptors. The purpose of this study was to examine, both behaviorally and mechanistically, whether the cannabinoid CB1 receptor was also sensitive to ultra-low dose effects. Antinociception was tested in rats after an injection of either vehicle, the CB1 receptor agonist WIN 55 212-2 (WIN), an ultra-low dose of the CB1 receptor antagonist rimonabant (SR 141716), or a combination of WIN and the ultra-low-dose rimonabant. In the acute experiment, tail-flick latencies were recorded at 10-min intervals for 90 min; in the chronic experiment, tail-flick latencies were recorded 10 min after a daily injection over 7 days. Ultra-low dose rimonabant extended the duration of WIN-induced antinociception. WIN produced maximal tolerance by day 7, whereas WIN+ultra-low dose rimonabant continued to produce strong antinociception, demonstrating that ultra-low dose rimonabant prevented the development of WIN-induced tolerance. Animals chronically treated with WIN alone had CB1 receptors predominantly coupling to Gs receptors in the striatum, whereas the vehicle, ultra-low dose rimonabant, and WIN+ultra-low dose rimonabant groups had CB1 receptors predominantly coupling to Gi receptors. Cannabinoid-induced tolerance is thus associated with a G protein coupling switch from the inhibitory Gi protein to the excitatory Gs protein, an effect which is prevented by the ultra-low dose rimonabant.
 
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