Chemist4Hire
Bluelighter
- Joined
- Nov 5, 2017
- Messages
- 56
I have a question about Suboxone, specifically the antagonist in it by the name of Naloxone. Now i clearly see the painted picture here on bluelight that it's believed Naloxone has zero effect on the µ receptors. This thread will show what I'm talking about, many users feel Naloxone is inert or inactive and they even go as far to say bupe causes withdrawals and Naloxone does not.
The reasons given for thier belief vary greatly ranging from bupes higher affinity to Naloxone having low BA (bioavailability).
This thread is riddled with misinformation and is viewable to all:
>> Link to thread <<
Obviously iv roa disproves ba being the cause, and quite possibly bupe only being an antagonist to the kappa abd being a partial agonist to the mu.
I'm a former pharmecutical engineer assistant and have a background with organic chemistry, i was under the impression that allthough bupreneorphine has a higher affinity to µ opioid receptors than many full agonists and antagonists like narcan/naloxone still binds to some receptors in the central nervous system and brain. That is showing as a medical certainty, it is yet to be determined what Symptoms are present from the removal of Naloxone caused by the higher affinity of the Partial Agonist. I'm lead to believe this happens to some degree in normal sublingual use, at least Naloxone holds back bupe from attaching when first dosed and later when Naloxone loses grip around 1hour after administration.
All the doctor's and chemistry majors I've asked seem to think 13-30% coverage by Naloxone is present.
Understandably I'm confused with some of the info here.
So if anyone can explain why so many feel symptoms of opiate antagonist present from bupreneorphine alone i would very much like to hear it.
I'm struggling to understand why bupreneorphine/Nor-bupe would pull preexisting bupe/nor-bupreneorphine off the receptors acting like an antagonist which it is not and normally does not behave in such way?
Just to clear up my question:
From what i could identify through my own tests:
(Suboxone Sublingual Films) 8mg Bupreneorphine - 2mg Naloxone, inactive ingredients:
It is my understanding Bupe converts to Nor-Bupreneorphine inside the body before it attaches to µ-receptors. and it has the same affinity to the µ receptors as previous attached bupe as it has a half life of more than 33hours, so dosing multiple times in one day should not account for symptoms of removal?
Many report in double blind studies that users of Suboxone administered subliminally experience the following symptoms believed to be caused by Antagonist removal from receptors by Bupreneorphine:
LINK:
Adverse Events from double blind study:
(?5%)by Body System and Treatment Group in a 4-week study
Symptom>Medication>%experienced
It's entirley possible symptoms are caused by adverse events, but again that's speculative and i have no evidence for that claim, although:
Update: Tuesday, November 14, 2017:
The most common adverse events reported in clinical trials with
Suboxone and Subutex were:
Understanding Adverse Event is the same as Side Effects from medication's or Adverse Reaction's. This is commonly a Blanket term given for explained symptoms and frequently symptoms without identified causes, but notably they where narrowed down to adverse events from both Suboxone and Subutex. So i know these symptoms can occur without Naloxone present. Now I've had over 15 years in pharmaceutical engineering-Bio/Organic chemistry field, but I have not personally worked with anything like Suboxone, I do have quite a bit of familiarity with opiates, opioids and alkaloids/chemicals that mimic opioids attachment to Mu/Kappa, and 3/6 ether's like 9-methoxy-corynantheidine the major alkaloid constituent extracted from Kratom(sometimes called: Ketum) leaves and 7-hydroxymitragynine, a minor constituent of Kratom(Mitragyna speciosa). Most medical professionals i talk with pertaining this matter agree Naloxone is the cause of most of these symptoms listed above excluding: Constipation, nausea, headache and withdrawal syndrome.
My question is if the symptoms are not caused by Naloxone (which my colleges tell me is the case, that is has a lower affinity to the receptors and they get pulled off by the bupe which causes the symptoms of discomfort) what is it caused by if that's not the case, and how and if its not to much to ask what studies and evidence supports this theory?
Note: i know bupreneorphine will cause withdrawals when used when other full agonists are present on receptors but i don't yet understand why opiates of the same affinity to mu opioid receptors would?
I enjoy this forum and don't want to make waves, i simply have questions for presented facts and did not find links of evidence which would have cleared up my understandable confusion.
I am hoping [MENTION]captain heroin[/MENTION] (or one of the many knowledgeable members on here) can answer some of these questions for me.
BTW i thoroughly enjoyed your micron thread, and cudos for educating others on how to use safely, it's a tremendous thing to behold.
Facts:
Web Recordings
July 1, 2015
References and current up to date facts (2017):
https://www.fda.gov/downloads/Drugs/NewsEvents/UCM454748.pdf
https://www.fda.gov/downloads/drugs/drugsafety/postmarketdrugsafetyinformationforpatientsandproviders/ucm191533.pdf
Medical Studies:
https://www.fda.gov/downloads/Drugs/NewsEvents/UCM454748.pdf
The reasons given for thier belief vary greatly ranging from bupes higher affinity to Naloxone having low BA (bioavailability).
This thread is riddled with misinformation and is viewable to all:
>> Link to thread <<
Obviously iv roa disproves ba being the cause, and quite possibly bupe only being an antagonist to the kappa abd being a partial agonist to the mu.
I'm a former pharmecutical engineer assistant and have a background with organic chemistry, i was under the impression that allthough bupreneorphine has a higher affinity to µ opioid receptors than many full agonists and antagonists like narcan/naloxone still binds to some receptors in the central nervous system and brain. That is showing as a medical certainty, it is yet to be determined what Symptoms are present from the removal of Naloxone caused by the higher affinity of the Partial Agonist. I'm lead to believe this happens to some degree in normal sublingual use, at least Naloxone holds back bupe from attaching when first dosed and later when Naloxone loses grip around 1hour after administration.
All the doctor's and chemistry majors I've asked seem to think 13-30% coverage by Naloxone is present.
Understandably I'm confused with some of the info here.
So if anyone can explain why so many feel symptoms of opiate antagonist present from bupreneorphine alone i would very much like to hear it.
I'm struggling to understand why bupreneorphine/Nor-bupe would pull preexisting bupe/nor-bupreneorphine off the receptors acting like an antagonist which it is not and normally does not behave in such way?
Just to clear up my question:
- why is bupe the only one present on receptors?
- how can we account for symptoms of opioid removal from mu receptors?
- And what evidence do we have from medical studies that show Naloxone is 100% inactive?
From what i could identify through my own tests:
(Suboxone Sublingual Films) 8mg Bupreneorphine - 2mg Naloxone, inactive ingredients:
- acesulfame potassium
- citric acid
- maltitol solution
- hypromellose
- polyethylene oxide
- sodium citrate
- lime flavor
- Sunset Yellow FCF
- white printing ink
It is my understanding Bupe converts to Nor-Bupreneorphine inside the body before it attaches to µ-receptors. and it has the same affinity to the µ receptors as previous attached bupe as it has a half life of more than 33hours, so dosing multiple times in one day should not account for symptoms of removal?
Many report in double blind studies that users of Suboxone administered subliminally experience the following symptoms believed to be caused by Antagonist removal from receptors by Bupreneorphine:
- Headaches
- Persperation
- cold sweats (not common)
- Agitation of skin
- Muscle pain
- neurological pain (mild to moderate)
LINK:
Adverse Events from double blind study:
(?5%)by Body System and Treatment Group in a 4-week study
Symptom>Medication>%experienced
- Headache: Suboxone=36.4% Subutex=29.1%
- Pain: Suboxone=22.4% Subutex=18.4%
- Withdrawal Syndrome: Suboxone=25.2% Subutex=18.4%
- Constipation: Suboxone=12.1% Subutex=7.8%
- Sweating: Suboxone=14.0% Subutex=12.6%
It's entirley possible symptoms are caused by adverse events, but again that's speculative and i have no evidence for that claim, although:
Update: Tuesday, November 14, 2017:
The most common adverse events reported in clinical trials with
Suboxone and Subutex were:
- headache
- withdrawal syndrome,
- pain
- nausea
- insomnia
- sweating
- abdominal pain
- back pain
- constipation
- infection
- asthenia
- rhinitis
- anxiety
- depression
Understanding Adverse Event is the same as Side Effects from medication's or Adverse Reaction's. This is commonly a Blanket term given for explained symptoms and frequently symptoms without identified causes, but notably they where narrowed down to adverse events from both Suboxone and Subutex. So i know these symptoms can occur without Naloxone present. Now I've had over 15 years in pharmaceutical engineering-Bio/Organic chemistry field, but I have not personally worked with anything like Suboxone, I do have quite a bit of familiarity with opiates, opioids and alkaloids/chemicals that mimic opioids attachment to Mu/Kappa, and 3/6 ether's like 9-methoxy-corynantheidine the major alkaloid constituent extracted from Kratom(sometimes called: Ketum) leaves and 7-hydroxymitragynine, a minor constituent of Kratom(Mitragyna speciosa). Most medical professionals i talk with pertaining this matter agree Naloxone is the cause of most of these symptoms listed above excluding: Constipation, nausea, headache and withdrawal syndrome.
My question is if the symptoms are not caused by Naloxone (which my colleges tell me is the case, that is has a lower affinity to the receptors and they get pulled off by the bupe which causes the symptoms of discomfort) what is it caused by if that's not the case, and how and if its not to much to ask what studies and evidence supports this theory?
Note: i know bupreneorphine will cause withdrawals when used when other full agonists are present on receptors but i don't yet understand why opiates of the same affinity to mu opioid receptors would?
I enjoy this forum and don't want to make waves, i simply have questions for presented facts and did not find links of evidence which would have cleared up my understandable confusion.
I am hoping [MENTION]captain heroin[/MENTION] (or one of the many knowledgeable members on here) can answer some of these questions for me.
BTW i thoroughly enjoyed your micron thread, and cudos for educating others on how to use safely, it's a tremendous thing to behold.
Facts:
NSFW:
(FDA.gov): The Food and Drug Administration (FDA), Center for Drug Evaluation and Research (CDER), in collaboration with the National Institutes of Drug Abuse, the Centers for Disease Control and Prevention, the Substance Abuse and Mental Health Services Administration, and the Health Resources and Services Administration, is announcing a scientific workshop to initiate a public discussion about issues surrounding the uptake of naloxone in certain medical settings – such as on ambulances and in association with prescriptions for opioids – as well as outside of conventional medical settings to reduce the incidence of opioid overdose fatalities. Academia, government, industry experts, and patient advocates will discuss which populations are at risk for opioid overdose and how public health groups can work together to use naloxone to reduce the risk of overdose. We will also explore legal, regulatory, logistical and clinical aspects related to making naloxone more widely available. Will show the Web Recording below:
Web Recordings
July 1, 2015
References and current up to date facts (2017):
https://www.fda.gov/downloads/Drugs/NewsEvents/UCM454748.pdf
https://www.fda.gov/downloads/drugs/drugsafety/postmarketdrugsafetyinformationforpatientsandproviders/ucm191533.pdf
Medical Studies:
https://www.fda.gov/downloads/Drugs/NewsEvents/UCM454748.pdf
-I will continue to update as i get more information or as new information presents itself. -
Last edited: