Generic minocyline has been tested in Clinically Isolated Syndrome to see if it effects conversion to clinically definte MS. It was found that minocylcine reduces the risk of developing MS by 27.4% and relative risk by
44.6%. What will happen next...will they have to do another trial? Pharma would have to and so can the rules be bent.
However, what you want to know is what happens in the PPMSers trial treated with anti-CD20
People in the trial were younger people below 55 (mean 44 years) as was suggested from the rituximab trial. They were also only a mean of 3 years from diagnosis and so they loaded the trial with potential responders are waiting for this news.
A differnece from placebo was noted within 12 weeks of the beginning of the trial and the rate of progression was reduced by about 25%. The brain volume loss, when rebaselined to allow for pseudo atrophy, was also reduced.
The were a few infections but of note there were a number of cancers in group treated with the treated group and remembering what happened in the cladribine trial as the data does not look that disimilar, Will the regulators ask for another trial as they did with claribine. If they do that will delay things.
But as to the question we all really want to know is does this work for all PPMSers or just those with gadolinium enhancement...The issue was dodged and MRI was not really talked about...Why?. I
It was evident that over 25% had gadolinium lesions which is more than the average PPMSer and so and when asked they said they havn't done the analysis. Of course this would be the first thing you would do!!!. The trial was loaded with gadolinium enhancing people and therefore you have the conditions for a positive trial . That they did not properly address this makes me very cautious and therefore I withdrawn my apologies.
When the results were announced on the news I said I was wrong because I had predicted the trial would fail, with the previso that relapsing, gadolinium PPMSers would respond, so until I see the data I am going to stick to this opinion.
The company will not want get a sublicence and so will not want to release data that only the active PPMSers responded.
So it is a start remember when interferons arrived we have the 30% level of efficacy and now we are up to 70-80% effective. It is a start but not enough to make me get my p45 yet and we still need to get neuroprotective drugs in addition to immune modulatory DMT
Conflixts None relevant however ProfG and DrK were involved in the trial design and undertaking the trial and they may want to say more, or may not be allowed to.
Next up is Anti-Lingo1 and its effect on visually evoked potential in optic neuritis. You shine a light in the eye and measure electrical response from the visual cortex of the brain. In the presentation there was a significant (P=0.05) improvement in the latency (a measure of improvement in myelination. The original press release was something like p=0.054 = non-significant:-) in the eye with optic neuritis. Now they looked in the other eye, without optic neurtis and there was loss in amplitude of the VEP. This is evidence of nerve loss and anti-LINGO-1 slowed this down. was it remyelinating subclinical demyelination or was it promoting neurogenesis and synaptic plasticity because remember the original function of LINGO-1 is an inhibitor of nerve growth. Block LINGO-1 and nerves may grow.
Conflicts: None ... ProfG multiple
Finally high dose biotin continued to show some benefit in Secondary Progressive MS, there is insufficient evidence to say it is of any benefit in PPMS
Conflicts: None ... ProfG multiple