Revimmune and Campath differences

[patientx]

Could someone point me to some references that highlight the differences between Campath and HiCy? I know both drugs target destruction of parts of the immune system, but I'm curious to know how each is supposed to work.

[NHE]

Could someone point me to some references that highlight the differences between Campath and HiCy? I know both drugs target destruction of parts of the immune system, but I'm curious to know how each is supposed to work.

Revimmune kills off everything but your stem cells in the marrow. Campath just takes down the b-cells.

NHE

[Lyon]

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[patientx]

That's what I thought - that Campath wiped out both B and T cells, which had the CD52 receptor

[Lyon]

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[patientx]

Hi Bob,

I didn't mention (or maybe I did in a post on the general section), that I've been recently diagnosed. From what the neuros told me, I'm in the very early stages of the disease. Hence, my interest in Campath. I've read about the problems with ITP and autoimmune thyroid, but it seems like they've gotten very careful about tracking patients for platelet counts and thyroid problems. But, I live in close proximity to Hopkins, so I am also trying to gather information on HDC.

Mike

[Lyon]

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[NHE]

Revimmune kills off everything but your stem cells in the marrow. Campath just takes down the b-cells.

Are you sure you aren't thinking of rituximab/rituxan NHE?

You're right, Campath targets T-cells.

http://www.mult-sclerosis.org/Campath1H.html

Campath-1H is something called a humanised anti-CD52 monoclonal antibody. I will try to explain what this means.

Because antibodies are so specific, researchers have looked at engineering antibodies to disable specific cells in the human body. These are known as monoclonal antibodies and have been called "magic bullets". Campath-1H is just such a monoclonal antibody. It is designed to latch onto cells expressing a protein called CD52 thereby killing them.

CD52 is a type of protein known as a leukocyte antigen. It is expressed on the surface of several types of white blood cells (leukocytes) including lymphocytes (which include T cells), macrophages, monocytes and thymocytes (immature lymphocytes). Campath-1H has been shown to be very effective at destroying T-cells, the cells responsible for initiating the damage in multiple sclerosis. CD52 is also expressed on the cells lining the male reproductive tract. I am unaware whether Campath-1H has any implications for male fertility.

After the initial infusion with Campath, the body's T cell population takes many years fully to regenerate. To make up for the lost immune function, reconstituted lymphocytes of a kind that weren't associated with the disease process in MS were given to the trial volunteers (Th2 cells).

It is thought that because the Campath-1H treatment moves the body's immune response away from a Th1 type of response, one third of the volunteers developed antibodies to a protein found in the thyroid organ (the thyrotropin receptor) and thus developed autoimmune thyroid disease.

NHE

[Lyon]

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[patientx]

NHE:

Thanks good link.

Bob:

That's exactly my question. I guess I have some more research to do, but I've read so much the last few days, my head is spinning.

[Loobie]

One thing that sort of gives Campath's mechanism of action away is the last three letters of the drugs chemical name. The whole family of Tysabri, Rituxan and Campath all end in MAB. That denotes that they are a monoclonal antibody. Now what the hell a monoclonal antibody does, I'm not sure. I only know that Tysabri's mech. is to keep things from crossing the blood brain barrier, but I know there are some major differences between the three. Sorry I couldn't be more specific. I hope that helps, but after reading the links and answers, I think you already have better answers than that!

[RedPenguins]

I think the more recently you've been diagnosed - the more likely something like HiCy will be most beneficial to you! (I don't know much about Campath, other than reading some people's accounts that were kinda icky, so I can't speak for it.)

Anyhow, I was at JH, in the hospital on day 2 of the HiCy, on the 6 month "anniversary" of my diagnosis. (I hadn't been sick before diagnosis.) However, in that 6 months I declined rapidly. The docs there told me that I was an ideal candidate for the treatment. And I hope I continue to prove them right!

I go back for my 3 month follow-up at the end of October. Will be more like 4 months, but that's fine with me. I just hope to get positive validation that I am continuing to head in the RIGHT direction and not into a wheelchair! ha ha.

I think the less damage you have - or rather the less time that your brain/spine has been attacked, the better you might respond to treatment. I think this is the rationale behind approving some of the current meds for treatment of CIS, in hopes of stopping things from progressing into MS.

PatientX - I say: Research, research, ask questions, and then ask some more!

Good luck to you on this somewhat miserable journey.

~Keri

[Jamie]

Bob as ever raises a great point ref MS experience, what a wonderful conversation to even have though.