Without divulging any obviously NDA-protected information, might i inquire what receptor pathways you're investigating to create the "perfect" painkiller? It's been 70 years of searching by the pharmaceutical industry, and the best opioid receptor-acting drugs seem to be the the classics and then investigational, functionally-selective agonists that don't trigger beta-arrestin recruitment (and even here, despite what seems to be a reduced propensity for tolerance, addiction, and overdose, it's not holy grail: never mind that it hasn't been studied in humans.)
Personally, I believe that different types of pain warrant different treatments, and there will always be a place for opioid drugs in acute, visceral pain. However, when it comes to chronic or neuropathic pain, the efficacy just doesn't seem to be there, and this is where I would be targeting research at what the exact mechanisms here are underpinning the difference in pain propagation and why MOR agonists are poor modulators of it.
In a nut shell, I guess, are you investigating further modulators of the opioid system, or are you looking at other neural systems (e.g. cannabinoid receptors, TOLL receptors)? Thanks for your time!
im_nomit1 karma
Without divulging any obviously NDA-protected information, might i inquire what receptor pathways you're investigating to create the "perfect" painkiller? It's been 70 years of searching by the pharmaceutical industry, and the best opioid receptor-acting drugs seem to be the the classics and then investigational, functionally-selective agonists that don't trigger beta-arrestin recruitment (and even here, despite what seems to be a reduced propensity for tolerance, addiction, and overdose, it's not holy grail: never mind that it hasn't been studied in humans.)
Personally, I believe that different types of pain warrant different treatments, and there will always be a place for opioid drugs in acute, visceral pain. However, when it comes to chronic or neuropathic pain, the efficacy just doesn't seem to be there, and this is where I would be targeting research at what the exact mechanisms here are underpinning the difference in pain propagation and why MOR agonists are poor modulators of it.
In a nut shell, I guess, are you investigating further modulators of the opioid system, or are you looking at other neural systems (e.g. cannabinoid receptors, TOLL receptors)? Thanks for your time!
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