The Effect of Neutrinos on EDSS Scores in patients with Multiple Sclerosis

Posted by Jeff Berk; BOLT International


In the interest of investigative reporting, I snuck into the Women’s restroom in one of the trendy Snottsdale bars last night, just to get a handle on any differences in what a woman could get from her vending machine compared to what I could get from the Men-ding machine on my more typical side.  The only major difference I can report is that the Women-ding machines sell Medic’s Choice Tear Gland Refills.



So we’ve come to learn that neutrinos in 2011 can go faster than the speed of light.  This is clearly a change from the mid-‘70’s, when my South Korean (or was he North Korean?) teaching assistant gave me a “D” in Physics 101 because I couldn’t solve the prevailing statement of reality as it existed back then; E=MC2.  See, he “said” that “nothing can go faster than the speed of light” and argued that the logical conclusion of the “yes it could” drivel that I put on my test suggested otherwise.


Now, I’m not saying that the kid was wrong and I was right.  Just because he couldn’t speak a lick of English (yeah, call me old-fashioned, but I really do expect teaching assistants in US-based schools to teach in English), doesn’t mean that back then, neutrinos weren’t slower than they are today.  Maybe they were.  But I do have half an itch to climb on board the neutrino train, go back in time, learn some Korean, and give that boy a piece of my mind (as if I could afford to part with any brain cells anymore).  Which brings me, in a roundabout way, to the subject of today’s blog…


I WAS WRONG.  I’m going to admit it, and make my amends, here and now (before ECTRIMS in Amsterdam, this October, when Teva does it for me).


So here goes…


Okay, so this is hard to say…


Okay.  Some blogs back I think that I said that laquinimod is a dog.  I recant.  Now I’m saying “Laquinimod is a good drug and is going to be a big winner”.  If, that is, Teva / Active Biotech bite the bullet and run a Ph-III program that doesn’t look anything like BRAVO.   Come to think of it, this isn’t my fault after all.  Teva’s the one who should take the fall for me having to apologize for their lousy inflammation-presupposed trial design.  Here’s why:


“Back in the day”, showing an improvement in relapse rate was not only a good thing, it was possible.  That’s because patients on placebo relapsed at a rate that was at least measurable.  When compared to historical controls, trials run today may or may not show a meaningful difference relapse in placebo arm patients.  So showing a benefit on this dimension is a crapshoot. And really, the key point is: does the MS world need ANOTHER antiinflammatory?



BOLT just completed a series of seven thought leader interviews.  One of the questions that we asked was “why is BG-12 so good, and why does laquinimod suck so badly?”.  It turns out that, we are probably pretty off-base with the second part of our loaded question.  Both drugs, in fact, have neuroprotective properties, and laquinimod appears to be the better of the two on this dimension.  If you want the mechanistic “why”, you’re going to have to cough up for the report (email me, or check the BOLT Buy Now page on Sept 30).  But the punchline is that laquinimod only sucks if you try to view the drug as having antiinflammatory properties.  Clearly what we learned from BRAVO is that a drug with mad antiinflammatory skills is going to decrease relapse rate, and in the comparison with Interferon β-1a (Avonex®) and with placebo, laquinimod looks more like the latter than the former.


So what if laquinimod isn’t an antiinflammatory.  Not to fear.  At ECTRIMS 2011, Teva is going to present EDSS and mechanism of action data that shows that laquinimod is really a good neuroprotective agent.  The monoclonal therefore should be studied in a protocol which combines it with any antiinflammatory in patients with EDSS scores at baseline in the 3.5 – 5.5 range.  And there’s already scuttlebutt from some of our Panelists that you can see significant improvement in the disability index in patients treated with an antiinflammatory + laquinimod combination.


BG-12 has a lot of different modes of activity, and one of them is a neuroprotective effect.  Since BG-12’s antiinflammatory effect is only moderate, ultimately it too will be combined with a “real” antiinflammatory.  So these two orals are probably going to be used the same way, and ultimately the choice of which neuroprotectant to use in which patient will be side effect driven.





A final, cryptic comment on orals: teriflunomide has a lot more intriguing activity than a lot of people are expecting.  Sanofi-Aventis just doesn’t blab on publicly like “some” Taxachussets-based companies do.

Categories: IMMUNOLOGY, Multiple Sclerosis, multiple sclerosis, Neurology
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