- Jan 2019
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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inverse agonist activity was not required for mu-opioid receptor up-regulation and supersensitivity.
The question, then, is whether the opioid receptors are involved at all in this upregulation. For example, it could be mediated by TLR4 or filamin A.
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- Nov 2018
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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The full text describes how ultra-low-dose naloxone and naltrexone enhance opioids at very slim dose margins. A mere two fold difference on naltrexone dose can determine efficacy: 2 micrograms is effective whereas 4 is not. What's more, this optimal dose changes with sex, mouse strain, opioid agonist used, etc.; this making precise dosing challenging. The mechanism suggested is that filamin A has two binding sites, where only 1 has the desired effect.
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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We measure the binding affinity of NLX or naltrexone to FLNA in cell membranes as 4 picomolar, i.e. approximately 200-fold higher than their binding affinity for MOR
This sentence appears to indicate equal potency between the two drugs.
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Naloxone binding to A7 cells was displaced by naltrexone but not by morphine, indicating a target distinct from opioid receptors and perhaps unique to naloxone and its analogs.
So, naloxone has a 200 times higher potency at Filamin A compared to opioid receptors, but I need clarification on whether naltrexone achieves similar potency.
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