(Opiods) does tagament remove oxy/hydro converting to bigger metabolite?

[ColoradoBoy90]

Please move to other drugs as it will not let me post there.

I know many people say tagament boosts pain medication, but I heard it does so by blocking the enzyme, which results in higher peak levels but I believe I heard somewhere that it also doesn't convert any of Vicodin or oxycodone (or very little) to hydromorphone or oxymorphone. Is this true??

I'm not trying to abuse my medications, rather I constantly have pain so wanted to try to make them last longer without going to a higher dosage. But if it blocks conversion over to the "bigger metabolites" that may explain why sometimes for me tagament works (but I get tired and I need to be function. No, I don't care about "a nod" I'm taking these because I have chronic pain and am prescribed them, but need to be able to function). Othertimes if I try tagament it seems to have zero effect.

Like I can take tagament + oxycodone Extended release, figuring I should have enter pain relief either all day or all night depending on when I take the tagament. I've tested it a few times at night. The results? I wake up 5-6 hours later in W/D!!! And that's crazy because I only take 5mg Norco, 4 times daily. So the 10mg oxycodone slow release taken right before bed should stop me waking up in W/D and pain and coughing and restless legs. But it doesn't. How?? The oxycodone is stronger then 5mg Norco and being released over 12 hours so I don't understand how I can wake up in pain and W/D..Is it the tagament possibly? If so my only guess is because it blocks conversion over to the bigger stronger metabolite. I could try to skip tagament at night but I fear I won't get any sleep if I do. Maybe I'll try it on days I don't have to wake up early, but until then wondering if anyone knows the answer.

 

[PotatoMan]

Cd ----> od

 

[Kittycat5]

Oxycodone to oxymorphone and hydrocodone to hydromorphone are both mediated by CYP450 2D6. Tagament can inhibit this enzyme preventing the conversion of the parent compound to its more potent metabolite, so in theory your ideas sound good.

However, there have been quite a few studies that showed that people who are poor metabolizers of CYP2D6 or given stronger, more selective inhibitors of it, had the same outcomes as patients who hadnt. Also Tagamet has primarily been thought to inhibit CYP3A4 more than 2D6, but I need to check exactly how much more. There is data that do indeed show exactly what you are thinking, as well but there is less of it. Perhaps you are just one of those people who would respond.

 

[ColoradoBoy90]

Thanks, that would be good info to know. I believe I could be. Because almost always my instant release pain meds kick in and peak within 20-25 minutes. But then about 45 mins to an 1 hour later it seems I feel it at it's "true peak" for pain relief. My guess was that was the hydromorp or the oxymorph kicking in later, therefore giving more pain relief and lasting longer.

But here's a problem.. I also take Klonopin every night to sleep, and have been for years so I must take or or I won't sleep period. And I read that tagament also boosts Klonopin, but I don't know if tagament also messes with any conversion of Klonopin to other stronger metabolites (I can't recall of the top of my head what they are or if there even is any). But if it doesn't mess with any Klonopin conversion therefore not *possibly* making it weaker then that's good, I could not take tagament and be fine..... But if tagament does heavily boost Klonopin and doesn't mess with any of its metabolites/conversions then I may have a hard time taking the same dose without tagament. Darn