RE:RE:RE:RE:RE:RE:RE:RE:JD AnniversaryWow! That's scientific mumbo jumbo and historical revisionism if I've ever read it. That post is completely irresponsible, poof. You are attempting to discredit me more than you wish to address the IL-1Ra question.
Most everything crosses the BBB, poof, in some small amount. The delivery of anakinra across the BBB almost assuredly depends on a leaky BBB damaged by the inflammation processes of MS. It's the same thing with Bioagen's anducanumab. Dosing will need to be high to be effective. This could cause unforeseen interruptions to the normal functions of IL-1 alpha and IL-1 beta.
And then, you unwittingly argue against your own argument about the potential success of the anakinra clinical trial by pointing out that IL-1 has other functions than to promote destructive inflammation, including excess neuroinflammation.
And, of course, you purposefully "forgot" that a characteristic of xB3 is that it allows extremely broad dosing flexibility, and because it gets so much of its payload into the brain, doses to the brain can be far more precisely controlled with xB3 and with very low doses to the periphery. I discuss that stuff in my xB3-004 article. It's why I discussed the reasons for using MS as a target in clinical trials.
And of course, you forgot that xB3 drugs don't require a leaky BBB like aducanumab and anakinra require. In fact, early diagnoses of neuro-disorders could allow treatment with xB3 drugs before there is very much, if any, damage to the BBB caused by the disease. Non-xB3 won't compete with that. Large molecule drugs like xB3 drugs will be able to cross a healthy blood-brain barrier and allow the lowest and most precise dosing levels in both the CNS and periphery.
Your post is irresponsible, prophet, and displays hate rather than objective thinking. Shameful!
But the fact you blew up your own argument is, at least, a bit humourous. Reminds me of
Butterfingers Irving who gunned himself down.
jd