Alemtuzumab in a nutshell

A
EpubColes AJ. Alemtuzumab Therapy for Multiple Sclerosis. Neurotherapeutics. 2012 Nov 27. 
Alemtuzumab is a humanized monoclonal antibody that is administered
daily for 5 days, and then no further therapy is required for 12 months.
It causes rapid and prolonged lymphocyte depletion; the consequent
homeostatic reconstitution leads to a radically reformed lymphocyte pool
with a relative increase in regulatory T cells and expansion of
autoreactive T cells. Although previously licensed for the treatment of
B-cell chronic lymphocytic leukemia, it is now been considered for
licensing in the treatment of multiple sclerosis
(MS). From a disappointing experience with alemtuzumab in progressive
MS, Alastair Compston and I argued that immunotherapies should be given
early in the course of the disease. In a unique program of drug
development in MS, alemtuzumab has been compared in 1 phase 2 trial and 2
phase 3 trials with the active comparator interferon beta-1a. In all
trials, alemtuzumab was more effective in suppressing relapses than
interferon beta-1a. In one phase 2 and one phase 3 trial, alemtuzumab
also reduced the risk of accumulating disability compared with
interferon beta-1a. Indeed, alemtuzumab treatment led to an improvement
in disability and a reduction in cerebral atrophy. The safety issues are
infusion-associated reactions largely controlled by methylprednisolone,
antihistamines, and antipyretics; mild-to-moderate infections (with 3
opportunistic infections from the open-label experience: 1 case each of
spirochaetal gingivitis, pyogenic granuloma, and Listeria meningitis);
and autoimmunity. Usually autoimmunity is directed against the thyroid
gland, but causes (1 %) immune thrombocytopenia, and in a few cases
antiglomerular basement membrane syndrome. Alemtuzumab is an effective
therapy for early relapsing-remitting MS, offering disability
improvement at least to 5 years after treatment. Its use requires
careful monitoring so that potentially serious side effects can be
treated early and effectively.




The summary of CAMPATH in a nutshell except he forgot to say that the company producing it are going to whack the price up to extort more cash from MSers. They have been publicly silent after Prof G put done the guantlet because how do they justify it.

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6 comments

  • Dr Coles is my hero. Camppath 1H gave me my life back. Until Team G can get a treatment to market, you will always be in Cambridge's shadow. As grat as research is, patients want real treatments. Will Team G get a neuro-protective to market? Hopefully, Charcot Project will be your Campath 1H.

    • I agree about Campath, but it is not there yet. I worked on cladribine for over 10 years and it was felled at the last hurdle by the regulators. We assume things will be different with Alemtuzumab, but the EMA are a bit of a black-box. The other worry is that will restrict access of the drug to a small subgroup of MSers who have failed previous treatments. As you know from reading this blog time is everything; if you delay your treatment and leave MS active you never catch-up.

    • I forgot to mention that I have massive conflicts of interest in relation to both Alemtuzumab/Campath and Cladribine.

  • About the price of Alemtuzumab : for your information dimethyl fumarate (Fumaderm in germany) is 2.8 € /120 mg. What will be the price of BG-12 if approved?

    • Can I suggest we stop second guessing the price of the new DMTs? Untile the are licensed we will not know the price. We have to accept that drug development programmes and the commitment to post-marketing programmes (safety, etc.) are substantial (billions of dollars), therefore all new drugs will be expensive. At present there is no alternative. We also have to have a profitable and thriving Pharma industry as they are the only show in town and we need as much future innovation as possible to treat emerging diseases of ageing and progressive disease. If you have a solution to expensive drugs please sign up to BPA and share them with us.

    • Thank you for answering to my post which was not made to start guessing on future prices. I agree with you that if a very efficient product comes on the market with a low price, it will probably kill further research on MS. I just wanted to widen the discussion which was only targeting Alemtuzumab.
      Of course, we need the right price for the right product. Considering the three IFN, I am afraid we have not reached this point yet. I sent you on October 8th a mail on my publication about IFN, attrition bias and need for raw data (may be swallowed by your spam box anyway). I could have concluded the publication on the waste of money induced by bad evaluation of trials. Making raw data of clinical trial publicly available could help to diminish waste of money. The link to my publication can be found in a response to F Godlee editorial in BMJ about Clinical trial data for all drugs in current use.

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