MediTest
3 Apr 2019
Author
Norman Yarvin
Title

Campath hijinks

Body

What's been happening with Campath recently:

"From the company’s perspective, the drug was much too cheap. Had Sanofi applied the cancer price to the multiple sclerosis dose, it would have been charging around $6,000 per year when multiple sclerosis drugs had annual prices closer to $60,000. So Sanofi withdrew Campath from commercial sale in late 2012 and re-launched it in 2013 in Europe and in 2014 in the US with a new name, Lemtrada, a new multiple sclerosis indication, and a list price rise of over one thousand – yes, one thousand – percent."

Comments

D W

Nothing's a failure if it makes money. But I do feel that, were the drug effective, Campath results would be trumpeted. Instead, there is an eerie quietness.

D W - [Myalgia and hypertension (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazole. No medication now. Morning BP typically 110/75]

The Cambridge neuros who developed it originally for use as an MS drug didn't think it was a failure: Compston and the reverend Coles thought it was the best MS drug ever.  For a while, a few neuros and some patients thought it was also.  As with Tysabri, there were too many problems, one being one of the possible side effects: death.  Most recently, with Lemtrada, caused by a stroke.

David and Stratton wrote a letter for The Lancet about it, when it was still called Campath, but it was rejected.

I will post it here tomorrow!

They were doing trials for it when I was diagnosed with SPMS.  Since I live in the Cambridge area, I might have been offered a place in the trial.  This was before they knew that people with SPMS showed great improvement at first, then suddenly went much worse than normally expected.

Completed Stratton/Wheldon regime for aggressive secondary progressive MS in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Here is the Campath/Lemtrada letter sent to The Lancet by David and Stratton in 2012.

Since there have been no new posts on the Campath forum on ThisisMS since last October, I think it is proving not to de the Wonderdrug for MS as was originally thought and I am very glad that I didn't take part in that early trial!

 

 

Might Alemtuzumab (Lemtrada) pose risks were Multiple Sclerosis to have an infective input?

 

Charles W Stratton MD Department of Pathology, Vanderbilt University Medical Center, Nashville, TN 37232, USA

 

David B Wheldon MB FRCPath Department of Medical Microbiology, Bedford Hospital, Bedford, MK42 9DJ, UK

 

11th November 2012

The effectiveness of alemtuzumab in reducing the incidence of relapse in the relapsing-remitting form of multiple sclerosis is remarkable. But how will this drug affect the long-term outcome of the disease? Therapy aimed at disabling a component of the immune system presupposes a primary auto-immune aetiology. This may not be the case. Indeed, the inflammation associated with the clearance of damaged myelin may be a secondary ‘housekeeping’ process: the sudden, orderly, local mass-death of oligodendrocytes is the first visible event in the MS relapse.

 

There appear to be two distinct neuropathologies in MS. The more obvious is the sudden destruction of myelin resulting in acute relapse. Less obvious, and more insidious, is the gradual reduction of brain mass. Application of Occam’s Razor to these disparate pathologies suggests a chronic underlying infection periodically but ineffectively targeted by the immune system. Chlamydia (Chlamydophila) pneumoniae is a good candidate. This intracellular pathogen is associated with vasculitic phenomena. Vasculitis was shown to precede neural damage in the 19th century. The organism (which is difficult to grow) was first detected in the CSF of persons with MS in 1999. A prospective study revealed a new respiratory infection with this organism prior to MS relapse. A statistically significant elevation of antibodies to Chl pneumoniae was seen as relapsing-remitting disease became progressive. In a limited pilot study, antimicrobial therapy directed against Chl pneumoniae reduced the loss of brain mass.  We and others have reviewed the evidence for Chl pneumoniae infection in MS.

 

What would be the likely outcome of therapy targeting the immune-system were an underlying infection present? A reduction in visible relapse seems likely. But we would expect the continuation of a more insidious pathology. The barking guard-dogs might have been silenced but the burglars may still be making off with the silver. Alemtuzumab alone may not prevent the onset of progression: it was found ineffective in treating secondary progressive MS despite favourable MRI appearances.

We shall have to await ultimate outcomes.

 

(References omitted)

 

 

Completed Stratton/Wheldon regime for aggressive secondary progressive MS in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.