• N&PD Moderators: Skorpio | thegreenhand

Low dose buprenorphine to POTENTIATE opiate agonists

^^

im 99% sure we wouldnt od at reasonable doses and im very confident that at 1-1.5mg sub doses we would get high using opies on top. I just want to get someone to test it first so we kno for sure. ive seen mmany many
anecdotal reports it works fine.
 
Yea same here, id rather have someone else test it first, cuz i took sub sublingual2mg about 4 hours ago and i have FST kratom and the wafer. i just dont wanna waste either you know? but ive heard if you have a tolerance you have more receptors therefore the bupe can be a potentiator
 
If no one else tries by tomorrow ill try taking 1mg of sub and mixing it with like 30 drops of the FST Kratom. usually works well

Id rather try the FST than the full agonist strength of methadone
 
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If no one else tries by tomorrow ill try taking 1mg of sub and mixing it with like 30 drops of the FST Kratom. usually works well

Id rather try the FST than the full agonist strength of methadone

id try the methadone cuz then youd kno for sure whats going to happen for future reference, cant really say with something like kratom.
 
I've taken someone out of a serious OD with suboxone crushed into powder and put in small amounts under his tongue until he awoke, and said it was the highest/best-feeling he had ever been once coming to. I crushed it to use titration so that he didn't go into WD, but I needed to use about half. Came to in 15 seconds after.

Since then, I have had the very unsafe, non-HR idea of putting a suboxone strip under my tongue, and shooting way more than my tolerance, so that I'd get a huge rush, go out in a dangerous way, and be immediately 'brought back' by the slow release of the suboxone with just enough to feel wonderful, and remove the suboxone just as I became again functional. Something along the lines of a "lazarus shot". I don't think I'd try it without extra suboxone on hand and a sitter though.
 
theres no nalaxone in this and im not shooting. Im seeing if this is a possible thing .this ROA is a straight up oral experiment. im gonna try it a lil later today, but ill be sure too tell eveyrthing I took and estimated times and how I felt. Ive just read about it so much and dont have any def proof.so I wanna know for sure.
 
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I ended up just basing this test on the sub i took yesterday (because it shoudl still be partially bound, well the last time i took 2mg of subutex was about 3PM on thursday August 4th. At about 7:03 AM this morning (Friday Aug. 5th) I poured (I think) 27 drops for the Kratom FST into a little tiny medical measuring cup, mixed with water, took the shot, then filled with water again, and made sure to get as much as I could. Starting at about 7:30 AM today I started feel quite a buzz, and now I am just straight up Euphoric. I havent felt like this in so long because I have such a high tolerance for Oxycodone. But this FST is for real, and I am so happy that I am receiving another one for free soon. :) Also I have had a 16oz can of Monster Energy along with the Kratom FST. Dont know if it is at all related, but I wanted to report how 2mg of pure bupe reacted with 27 drops of Kratom FST extract less than even 24 hours after having dose with the bupe. And I feel wonderful.
 
Please remember that bupe is only a partial agonist at the mu opiate receptor but a antagonist at the other opiate receptors. This is important because drugs like oxycodone have a lot less mu activity than say morphine or hydromorphone. For this reason the effects will be different when using different opiates (I've certainly noticed this).
 
Please remember that bupe is only a partial agonist at the mu opiate receptor but a antagonist at the other opiate receptors. This is important because drugs like oxycodone have a lot less mu activity than say morphine or hydromorphone. For this reason the effects will be different when using different opiates (I've certainly noticed this).

agreed. im still feeling the Kratom FST dose though so i must have waited long enough after teh 2mg of bupe to have it potentiate the kratom cuz im still feeling better than the last time i took 75mg of oxycodone. but i have a HIGH tolerance to oxy. cuz now hydrocodone is actually a bettter pain reliever for me than oxy cuz ive had so much oxy over the years
 
agreed. im still feeling the Kratom FST dose though so i must have waited long enough after teh 2mg of bupe to have it potentiate the kratom cuz im still feeling better than the last time i took 75mg of oxycodone. but i have a HIGH tolerance to oxy. cuz now hydrocodone is actually a bettter pain reliever for me than oxy cuz ive had so much oxy over the years

and yet we stilll dont know what normal opiates will do lol..
 
on the 15th I see my pain doctor and will get some real opiates, so i can do some more investigations then, cuz i can always get bupe. What should i get from my doctor to test with?
 
Please remember that bupe is only a partial agonist at the mu opiate receptor but a antagonist at the other opiate receptors.

From my understanding, it was a mixed agonist/antagonist of the same receptors. Not partial of one and antagonist of 'others'
 
Before you read this, I apologize in advance for any repetitiveness. I was writing this entry from memory and doing research at the same time

_________I have heard different things about buprenorphine's affininty and agonism/antagonism of different opiate receptors. Ive heard its primary method of action is based on the fact that buprenorphine has very high binding affinity for the mu receptor and is a partial agonist (with no mention antagonist properties) at the mu receptors. "Buprenorphine has been shown to act as an epsilon-opioid antagonist.... Buprenorphine is also a kappa opioid receptor antagonist, and partial/full agonist at the recombinant human ORL1 nociceptin receptor". Buprenorphine as been show to be approx. 20 to 40 times more potent than morphine, but due to the fact that it is only a partial agonist, these strong analgesic effects are not felt as they would be for a full mu agonist. Buprenorphine's analgesic effect is thought to be mainly due to it's partial agonist activity at mu opioid receptors: meaning of course, as mentioned, even though buprenorphine has proven to have high analgesic effects than morphine, its full analgesia is not felt.
_________From the research that I have done, it appears to me that buprenorphine is a 'fully' "partial agonist only" on the mu receptors, however on other opiate receptors, buprenorphine appears to be a full competitive antagonist at the epsilon (see link at bottom for information about the epsilon receptor) and Kappa opioid receptors. And from my understanding it appears that mu opioid receptors can mediate changes in neuronal excitability of pre-synaptic release of GABA. "GABA transmission in the ventral tegmental area (VTA) is critical for fine tuning the activity of dopamine neurons in response to opioids. However, the precise mechanism by which GABA input shapes opioid reward is poorly understood."(http://www.jneurosci.org/content/30/42/14029.full). And we know the basics of this because most of us know that benzodiazepines are GABAergic and react with opiates in a synergistic manner.
_________However, for fully agonistic opioids such as morphine and oxycodone, the main analgesic, euphoric, etc effects of these is due to their fully agonistic affinity to the mu and kappa receptors respectively; Side note: This is often a topic of debate because oxycodone (which appears to act mainly on the kappa receptors) in particular produces the anagalgesic effects of other drugs that are primarily mu agonists (i.e. morphine, hydromorphone, diacetylmorphine, the fentanyls, etc). It seems that buprenorphine's main "analgesic and maintenance" effects are based on the fact that buprenorphine has an extremely high binding agonistic affinity for the mu receptors whereas it is a sole competitive antagonist at the Kappa receptors (which we have determined above to be the main receptors for the analgesic, euphoric, etc effects of full agonists such as morphine and oxycodone respectively).
_________So buprenorphine's mechanisms of action are its partial agonist activity at the mu opioid receptor: and its partial or full agonist activity at the "opiate like, but rarely mentioned" ORL1/nociceptin receptors, as well as the delta opioid receptors, (Side note: the Delta receptors to my understanding, mainly mediate opiates' antitussive properties rather than the analgesic properties); however, it has been shown that the opiates that have a higher affinity to delta receptors can cause analgesia to a certain degree, but not to the same degree as mu and kappa receptors. Also, buprenorphine is shown to be a "competitive" antagonist only at the kappa opioid receptors..
_________To summarize, buprenorphine has partial agonistic only effects on the mu receptors and is a "partial or full" agonist of the delta receptors as well as the "opiate like" ORL1/nociceptin receptors. As far as it's antagonist properties go, buprenorphine has proven to be a full antagonist at the epsilon and kappa receptors. (As a reminder; the Kappa receptors are the receptors that oxycodone, in particular, has a high agonistic affinity for and has been shown to be the primary mediator for oxycodone's analgesic, euphoric, etc effects). Side note regarding the existence of 'epsilon receptors': "the existence of the epsilon receptor has been controversial, and this receptor is generally not recognized as a member of the opioid peptide receptor family because it has not been precisely characterized." (see http://www.ncbi.nlm.nih.gov/pubmed/11730972 for more info on the epsilon receptors).
_________In short: Buprenorphine is a known to be a partial mu agonist; a "partial or full" agonist of the 'opiate like' ORL1/nociceptin receptors as well as the delta receptors, and a full antagonist of the Kappa and Epsilon receptors All of these factors (and probably more) are why buprenorphine is considered a partial agonist and anatagonist.
 
First I didn't believe the claim that oxycodone acts mainly on kappa receptors, but then I found this article: http://www.ncbi.nlm.nih.gov/pubmed/9415500 , which seems to confirm it.

How is it possible that oxy causes euphoria at all? Kappa agonists are usually dysphoric. At first I thought that some of oxycodones metabolites would act mainly on mu receptors, but wikipedia says that oxycodones effect is mainly caused by itself and not its metabolites...
 
I know what you mean. I am perplexed by this information which is almost seemingly paradoxical. I actually learned that while writing my last post while researching. I had no idea prior to that that oxycodone is primarily a kappa agonist.
 
^ It reminds me of the "T's and Blues" combination, taking the kappa agonist pentazocine with the antihistamine tripelennamine is reputedly euphoric...

Looks like the opioid mechanism of action isn't as simple as people usually believe.
 
apparently not. like i said, i actually learned a lot of new things while writing that response, and I already thought I had a pretty good idea and handle on things. But now, I have a lot more research to do apparently.
 
Bump...

anything new to report on this subject? I also wonder how much lead time is optimal btw the two doses?
 
An impatient person by nature, I went ahead a did the experiment. ;)
Took 0.5mg suboxone before bed last night. 8 hrs sleep and immediately took another 0.02 mg. Waited 45 min and took only 5 mg hydrocodone with 60 mg codeine (should mention that I'm currently a lightweight; quite this stuff altogether about 2 years ago but gradually been chipping for a few months). Damned good experience. Euphoria was better and longer than normally. More like an energetic oxy experience than the sedation of codeine and/or hydro.

Another tip, this only seemed to work if you give enough time btw the two doses. I just (1 hr ago) tried to do an all at once trial, not feeling anything special.
From this I'm gathering that it will potentate any non-mu-receptor specific opiates. I would avoid if taking oxys.

Overall though, this is a great new tool in the arsenal in the el cheapo toolbox. Also recently tried hydroxyzine, also a great tool. In comparison, they are about equally useful.
And of course taking dxm just to reduce tolerance is a smart choice.
 
ive done it.
at about 9:30 a.m. : i took about .5mgs of suboxone intranasal.
about twelve hours later around. 9:00pm i did about 7mgs of oxymorphone.

the oxymorphone definitely worked but felt a little different. I had been doing .5mgs of sub everyday for about one week prior to this and really did not expect to feel the oxymorphone... I do not think it made it any stronger though, the oxymorphone felt about how it fealt before i got on subs which was nice because I sort of figured that it was gonna be a waste of opana. But maybe since it was a twelve hour difference between the sub and the opana the potential for potentiation was lost. lol.
 
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