© Website designed by Alasdair Coles, 2012
The University of Cambridge has made a video on the history of alemtuzumab.
The beginnings of alemtuzumab
Early use in progressive MS
Treating relapsing-remitting MS
Licensing of alemtuzumab
The beginnings of Alemtuzumab
Campath-1H (now called alemtuzumab) was originally synthesized by Herman
Waldmann at the Department of Pathology in Cambridge University (hence Cam-
Path). He has written the early history of Campath (pdf). Geoff Hale has written
something similar here.
Campath was licensed to Burroughs Wellcome via British Technology Group (BTG).
The original intention was to use alemtuzumab to treat leukaemia. But in the
1980s, Martin Lockwood explored its efficacy in vasculitis and autoimmune
disease. In 1990, Alastair Compston and Herman Waldmann began discussions
over the use of alemtuzumab in multiple sclerosis.
Burroughs Wellcome conducted discontinued development because of
disappointing results in phase II rheumatoid arthritis trials.
Early use in progressive multiple sclerosis
In 1991 the first patient with multiple sclerosis (secondary progressive) was
treated with one cycle of Campath-1H. Between 1992-1993, 6 more patients (5
with secondary progressive, 1 with primary progressive) were treated with one
cycle of Campath-1H (Moreau 1994). Between 1994-1997, 29 patients with
secondary progressive were treated with one cycle of Campath-1H combined with
anti-CD4 or corticosteroids (Coles 1999).
The main lesson from this experience was that, in order to maximise the benefit
from alemtuzumab, we needed to treat early in the course of relapsing-remitting
In 1997 Leukosite licensed rights to Campath-1H from BTG and went into joint
venture with ILEX Oncology. In 1999 Millennium purchased Leukosite and co-
developed Campath-1H with ILEX Oncology. In 2001, Campath-1H licensed, as
MabCampath, for the treatment of CLL
Treating relapsing-remitting multiple sclerosis
From 1999 to2002, 22 patients with relapsing-remitting multiple sclerosis treated
using two cycles of Campath-1H (Coles 2006).
Dec 2002-Sep 2007: the CAMMS223 trial.
In 2004 Genzyme acquired ILEX from Millennium. In June 2005 the death of a
patient on the CAMMS223 trial led to suspension of dosing of Campath-1H.
From Aug 2005 to 2009, we treated 20 people with Campath-1H and a non-
binding variant of Campath-1H called SM3.,designed to reduce immunogenicity. It
proved effective (Somerfield 2010).
Sep 2007-Apr 2011: the CARE-MS1 trial
Oct 2007-Sep 2011: the CARE-MS2 trial
In 2009 Genzyme and Bayer (previously Schering AG) agreed that Genzyme would
take sole responsibility for further development of Campath-1H. In Feb 2011,
Sanofi aquired Genzyme.
1999- March 2011 45 people treated at Cambridge with relapsing-remitting
multiple sclerosis, outside of Genzyme-sponsored studies, NOT including 20 on
SM3 trial and 22 reported in Coles J Neurol 2006. A summary on the long-term
follow-up of these 87 patients is currently being written up.
Licensing of alemtuzumab
On 17 September 2013, alemtuzumab was licensed as a treatment of “adult
patients with relapsing remitting multiple sclerosis with active disease defined by
clinical or imaging feature” in Europe, including the UK. Licensing followed in
Canada, Australia, Brazil and Mexico. On 5 April 2014 NICE, the UK body which
determines cost-effectiveness of drugs, approved alemtuzumab for “active
relapsing remitting multiple sclerosis” (see here).
However, on 30 December 2013, the FDA announced that alemtuzumab should not
be approved in the United States (see here), because of concerns around blinding
in the phase 3 trials. Public details of the FDA meetings can be found here, (under
the November 13th meeting). There was a public and professional protests from
US and European neurologists. On 7 April 2014, after discussions with the FDA,
Genzyme resubmited its application and dropped its appeal (see here).
The efficacy of alemtuzumab is high, but so too are concerns over its safety
profile. We aim to reduce the risks associated with alemtuzumab by identifying
those in advance who would be at low risk of autoimmunity after alemtuzumab;
and we are conducting a trial in which we test whether boosting the thymus gland
reduces autoimmunity after alemtuzumab (see here).
History of alemtuzumab