You need to acquire some SR-17018. Its the best and easiest way to lower tolerance and or quit all together. Its essentially a cheat code.
You will experience NO acute withdrawals whatsoever, and PAWS are no more severe than a little aches and pains in your muscles. You reset your opiate tolerance to naive in 2 weeks.
It's not expensive as some people would lead you to believe, in fact it's incredibly cheap at around $50/g. Three grams would be enough to substitute/ stabilize on your current dose of morphine/hydro, and from there you taper down 10-15% every other day until you are taking 25mg. Then at that point you have reset your tolerance and can stop bc the SR will be doing nothing psycho actively speaking, it will just be a mental crutch.
I have no problem with the label "research chemical" itself or many of the substances describable as such in the very modern sense. I'd take any number of them right now.
But SR-17018 is atypical both as an opioid and in some ways as a research chemical.
Concisely, my problems amount to: limited research data let alone any human clinical data whatsoever, and conceptual instability vis a vis the validity and achievability of the G-protein/β-arrestin dichotomy-inspired (lest we end up with a sort of "σ-OR" - or perhaps more "εOR"-like - moment) design.
Perhaps it's the romantic in me, but I don't like the notion of proving a highly proprietary complex molecule basically starting at semi-mass human trials level (after a very limited and inconclusive paltry half-dozen or so non-human trials). Also, I have elementary school nephews who were born before SR-17018 was. For some reason this concerns me.
Perhaps it is all just too wildly hypothetical for me at this point.
So how is SR-17018 supposed to feel? Is it supposed to function as basically superior buprenorphine? In a MAT-esque capacity?
As a highly μOR-specific high-efficacy high-partial agonist opioid ligand with a hypothetical G-protein signalling bias, it would function usefully here... how?
I understand that some draw a conclusion of a possible and markedly less pronounced rate of tolerance to analgesic effect as a primary benefit of SR-17018. And I understand the prospective appeal of a pro G-protein/non β2-arrestin bias in aspiring to a useful but so far dubiously achievable concept for opioid ligands. And doing so at a higher intrinsic activity than buprenorphine can offer. And if it all works as very deliberately intended, that could make for a very clinically-useful opioid analgesic that potently attenuates nociception with an improved safety and side effects profile that includes a delayed or limited development of tolerance. Ok.
So how does any of that plus all the stuff I don't understand about it translate into... SR-17018 being a superior tool in facilitating opioid cessation? In practice or theory?
I'm mostly only getting the sparse lab data and some brief anecdotal takes as I've looked around for info over the past months, and I have this whole thing where probably hell will freeze over before I ever end up on Reddit so I'm at a bit of a loss here presently.
xxxxx
Edit: I guess what I'm saying is, what you're saying doesn't make sense, unless it happens to be that it is amongst the abundance of what we don't know about SR-17018 wherein lies its most miraculous effects that just work out
in vivo in humans.
Also, I don't know if sensational Internet research chemical is aligned with the direction OP is either accustomed to nor attempting to go now.
But mostly just that I don't really know much of anything, and haven't the personal experience. So like with all the drugs, while I can't second your recommendation to anyone, I'd probably try the stuff myself given certain circumstances. For science.
xxxxx
Edit 2:
*Per Kudła et al., "Comparison of an Addictive Potential of μ-Opioid Receptor G-Protein-Biased Agonists SR-14968 and SR-17018 with PZM21 Biomolecules" in 2021:
"We found that SR-14968 and SR-17018 possess addictive characteristics, as they are rewarding and cause withdrawal syndrome. Interestingly, the compounds, especially SR-17018, can slightly delay the development of morphine tolerance and attenuate withdrawal in mice dependent on morphine."
(
https://pmc.ncbi.nlm.nih.gov/articles/PMC8779292/)
*Per Fritzwanker et al., "SR-17018 Stimulates Atypical µ-Opioid Receptor Phosphorylation and Dephosphorylation" in 2023:
"For many years, the biased signaling concept has been reduced to analysis of G-protein signaling versus ß-arrestin 2 recruitment, and the resulting bias factor has been proposed as a predictor of the therapeutic window. SR-17018 is one candidate compound that was developed based on the biased signaling hypothesis [3]. While the initial study reported an extremely high bias factor in different G-protein assays over ß-arrestin 2 recruitment, later work showed no statistically significant bias towards or away from any G-protein activation [4]. Nevertheless, the present study revealed a unique MOP phosphorylation and internalization profile for SR-17018 that does not support the initial report of an extremely high bias factor."
and
"SR-17018 exhibits a peculiar pharmacological profile in preclinical animal models, where it has been shown to prevent opioid withdrawal signs [3,5]. Such activity has previously been observed for buprenorphine but not for any other biased MOP agonist [8,13]. This suggests that opioids with delayed dephosphorylation kinetics may be useful for opioid maintenance therapy."
(
https://www.mdpi.com/1420-3049/26/15/4509)
An opioid... that reduces opioid withdrawal... because it is an opioid that has replaced another opioid? That's a more reasonable starting point. Surely different opioids can have different effects.