#GenzymeSpeak: derisking alemtuzumab; is it too late?
We can make alemtuzumab safer by preventing secondary autoimmunity; why has Genzyme done nothing about it? #GenzymeSpeak #MSBlog #ResearchSpeak
If you read this blog regularly and remember posts from the past some of you may recall that over 2 years ago I posted on derisking alemtuzumab. I discussed derisking infusion reactions and secondary autoimmunity. If I was writing this post today I would include a long section on preventing infections, i.e. herpetic, HPV, PML, TB, nocardiosis, listerioisis, exotic infections, etc.
What gets me is that for over 5-years I have been asking Genzyme to start studies to prevent secondary autoimmunity and nothing has happened. I have put forward two strategies; one was rejected and it looks like tragically the window for doing the second study is rapidly closing.
Once oral cladribine and ocrelizumab are launched most thinking pwMS and neurologists will have a hard time justifying taking the risks of alemtuzumab. Why? You will get similar efficacy from orcelizumab, a maintenance treatment, and if you want to go the PIRT (pulsed immune reconstitution therapy; previously referred to as an induction therapy) route cladribine is much safer than alemtuzumab. With cladribine you get no secondary autoimmunity, no infusion reactions and much fewer infections because cladribine doesn’t take-out innate immunity or deplete T-cells to the same degree as alemtuzumab. Cladribine also has the advantage of being oral and its monitoring requirements will be so much less arduous. The bottom line is would you go into a randomised trial of alemtuzumab vs. alemtuzumab plus a second agent to try and prevent secondary autoimmunity or would you choose ocrelizumab or oral cladribine? I suspect you would choose one of the latter two options. This means we will have lost equipoise and our proposed trial will be unethical.
The immune system has many mechanisms in place to prevent autoimmunity. When you learn how the immune system works it is really quite surprising that autoimmunity is so uncommon. What the immunologists tell us is that there must be a series of underlying biological processes that are causing secondary autoimmunity and if we can work out what these are we can intervene and prevent this complication. This is what the Professor Alasdair Coles, and Dr Joanne Jones, have been trying to do in Cambridge. They think that because the immune system reboots itself from peripheral memory cells it is more likely to result in an aberrant autoimmune responses. They have done a trial to encourage rebooting of the immune system using more naïve cells from the thymus. They have treated MSers after alemtuzumab with a hormone called, Palifermin, that stimulates the thymus to produce more naïve T-cells. The study is called the Cam-Thy study. I would imagine the results from this trial will be presented soon.
We have a different take on what is responsible for the secondary autoimmunity and wanted to test a different strategy; we hypothesised several years ago that it was due to B-cell hyperproliferation. Importantly, when you compare cladribine, another immune system rebooter, with alemtuzumab you can’t help but notice that the B-cell reconstitution profiles are very different. With alemtuzumab they comeback very quickly and overshoot their baseline values. We have hypothesised that if you changed the profile of the B cell reconstitution with a small dose of the B cell depleting antibody rituximab you may be able to prevent this secondary autoimmunity. We are really talking about a very small dose of rituximab, i.e. 50-100mg, just enough to allow to delay B cell reconstitution by 4-6 months. This is the first concept trial that Genzyme rejected several years ago.
Another option is to use alemtuzumab in combination with a small molecule anti-proliferative agent to try and prevent autoimmunity emerging. For example, to start a drug such as methotrexate, azathioprine or teriflunomide after the first course of infusions. The idea would be to prevent naive B-cell proliferation and overshoot, and the subsequent autoimmune B-cell stimulation. My concerns with this strategy is safety; rebooting the immune system in the presence of drugs that are designed to limit T cell proliferation may result in significant immunosuppression. Despite these concerns it is worth trying in the hope we can save alemtuzumab for pwMS. Based on current data I think alemtuzumab has superior efficacy to cladribine and is much safer than HSCT, therefore alemtuzumab should be saved as a treatment option for pwMS. Alemtuzumab, like HSCT, may offer pwMS a potential cure.
Several investigators, including myself, have proposed to Genzyme to bungle alemtuzumab with teriflunomide as a novel way to sequence these two drugs and at the same time derisking alemtuzumab. The problem is may be too late to start and fully recruit such trial. If you work for Genzyme can you please ask why your company is dragging its heels with regard to funding and initiating this trial? Or may be I have misinterpreted your commitment to alemtuzumab and you have written it off.
I have actually heard someone say that alemtuzumab as a MS DMT has a sell by date on it; the date being the day ocrelizumab gets its license. I am beginning to agree with this comment. I didn’t in the past because I foolishly thought we could derisk alemtuzumab in time. Tragically, we did have the time, but sadly it is running down rapidly.
35 thoughts on “#GenzymeSpeak: derisking alemtuzumab; is it too late?”
Unfortunately I don't think Alemtuzumab offers much durability in maintaining NEDA beyond two years. Where is the long term data? All I have seen is NEDA per individual year over the 5 year extension study. Perhaps it's not worth de-risking for secondary AI diseases if it doesn't deliver long term on its primary goal.
Re: "..So, I'm scheduled for lemtrada infusion at the start of next year. From this I take it I should cancel my appointment?"Can't comment, but in general nothing has changed. Alemtuzumab's risk profile is what it is. Ocrelizumab and oral cladribine are months, and possibly years, away from being available.
Rituxan, the equivalent of ocrelizumab, however, is available now off-label. I was surprised when it was instantly approved for me for the first time by Aetna, my insurance provider in the US this year. In the past, it was denied each time, but approved on appeal. I'd at least ask your doctor about it if you want to avoid the risk profile of alemtuzumab.Aetna updated their CPB in September to consider rituximab "medically necessary" for multiple sclerosis upon failure of natalizumab or other first line drugs (I'm JCV+, so had to switch off of natalizumab). This is great news. http://www.aetna.com/cpb/medical/data/disclaimer/review/200_299/0264_49.html. http://www.aetna.com/cpb/medical/data/200_299/0264.html
Prof G,See Prof coles's website – the camthy trial showed no benefit, so recruitment has stopped.Anon 1.41, time is brain. Lemtrada is a highly effective treatment which for many shuts down the disease (inflammation). The long term resuls are very impressive – I am nine years out from first infusion and disease free NEDA). The side efeects can be picked up by monitoring and are treatable e.g. thyroid side effects. The biggest risk is not the side effects from Lemtrada, but the long term disabilty / unemployment which comes with this disease if not effectively treated. I'd rather take the risk of a thyroid disorder than the risk of losing my functions one by one.Prof G needs to focus on some other MS area rather than highlighting all the potential risks which come with a treatment which is a life-changer for many. I'm not so sure his beloved oral cladribine will be as free from side-effects as he suggests.
Re: " I'm not so sure his beloved oral cladribine will be as free from side-effects as he suggests."I agree; it has its own, but very different, side effect profile. This profile is well-defined and has been discussed many times on this blog.
What about vaccination during therapy with B-cell depleting therapies? I think this will be some problem when you're on Ocrelizumab for several years….
Jules,Anecdotally on an individual level results can be impressive. But the 5 year extension study fails to provide such data and this is needs to be seen by both neurologists and patients to generate confidence.
The blatant and sub conscious pushing of Calbridine on this blog is scary but funny. The drive to come up with the first oral MS medication a few years ago was a valid and potentially profitable one, so I understand. But now, this is purely a pride thing. This drug is no better than the other orals out there, but getting it to market is a cap in the feather for this team/blog. The potential save to the NHS is real but you know that if it gets licence the prices they quote on this blog will raise substantially to the tens of thousands mark, just like what happened with Campath/LemtradaThe risk of alemtuzumab is there, and trying to understand this rebaslining in the results has confused me and no one, not my neuro or this blog can explain to me why rebaslining is a valid thing.Orcelizumab – my neuro is not sure this will get licence, and if it does please bare in mind its 'sister' drug that was about to go off label was going through the process of getting FDA approved for MS, and was pulled to be replaced by Orcelizumab, so again the drug companies will be cashing in. In the OPERA trials it showed 50% NEDA (With rebaslining) so is actually slightly less effective that alemtuzumab if you compare the trial data.It's a shame what can be such a good information source is becoming a marketing tool. Focus on the patients and new/better treatments for MS, not the same/recycling drugs that are all around the same efficiency. What do you think your patients want? Similar efficiency drugs that are tested against interferon (which is now obsolete) or better more effective treatments or even a cure?
Re: "…The potential save to the NHS is real but you know that if it gets licence the prices they quote on this blog will raise substantially to the tens of thousands mark, just like what happened with Campath/Lemtrada."We don't have control of pharmaceutical pricing. But I am sure NICE will do its job and make sure the NHS gets it a cost-effective price.
Re: "In the OPERA trials it showed 50% NEDA (With rebaslining) so is actually slightly less effective that alemtuzumab if you compare the trial data."Wrong the figure is 80%, not 50%, which is why ocrelizumab looks very good compared to alemtuzumab and the other high-efficacy therapies. Please read my ECTRIMS highlight post on ocrelizumab: http://multiple-sclerosis-research.blogspot.com/2016/09/researchspeak-ectrims-highlight.html
Re: "The blatant and sub conscious pushing of Calbridine on this blog is scary but funny."Not sure it is scary or funny. We have declared our conflicts and it is for the reader to interpret what we say with this in mind. As you know by now I am a proponent of PIRTs and cladribine is simply one of those. Based on the data out there cladribine is in the same efficacy zone as fingolimod and is not as effective as alemtuzumab and HSCT the other PIRTs we have discussed. But you need to be aware average efficacy is not necessarily what happens to individuals. Therefore some pwMS may want to try cladribine with a lower statistical chance of being a responder than alemtuzumab or HSCT. It is all about choice.
Re: "Similar efficiency drugs that are tested against interferon (which is now obsolete) or better more effective treatments or even a cure?"Don't you want to know what has happened to all the pwMS and pwCIS treated with cladribine,long-term? May be a significant proportion are still in long-term remission. I am particularly interested in the CIS cohort. We have started to lobby Merck to do a study to recall these people to see how well they are doing. As you have highlighted the PIRTs are the only drugs that really offer a 'potential cure'. The latter is, however, based on the autoimmune hypothesis of MS that may prove to be wrong.
"Don't you want to know what has happened to all the pwMS and pwCIS treated with cladribine,long-term?"Yes please and thank you for your efforts. My partner has started considering Cladribine/Rituximab in place of Ocrelizumab if she needs future treatment, because for her and with her history of breast cancer, Ocrelizumab just means too many sleepless nights – even if the breast cancers turn out to be a random cluster.Real choices are stuff we dream about.
…. I thought you were business savvy. Don't you know that Sanofi don't want alemtuzumab to be too successful; if it is successful they will have to pay Genzyme's ex-shareholders a shed load of money.
City Boy we had to edit your comment because some of it was not fit for purpose. I am not sure you are correct, but if you are it will be a sad day for pwMS. Alemtuzumab is the most effective treatment we have for pw-active-MS and they should all have the option, where it is available, to be treated with the drug safely.
It is good to note that despite having been over the issues in this post many times before on the blog that repetition can still generate discussion. This post generated a record number of views for a Saturday. Thank you.
Perhaps readers are clicking hoping for something new. Or maybe we just want answers. You continue to ignore the questions on annual rebaselining in the extension study. I'm still hoping to see some raw data from the Lemtrada extension study.
Dear LGOYou are not going to get an answer as Genzyme control the data!, That is unless they publish it, which they probably won't, as it is not going to be good reading. They dump their info in a meeting abstract and hope you won't see it which you wouldn't, but ProfG has a copy. However it is clear that the data shows it is not as good as implied.If in the 2 year trial it was about 40% NEDA or less then it can only be downhill from there.They have not been publishing lots from this trial, some of which, is in my mind…hiding bad news.Although Sanofi has signed to give access to pivotal trial data…the follow-up would not be part of this. I requested access to the raw data from the pivotal trials (via Clinical Study Data) nearly a month ago and am still waiting for a response. I know what the data says already, because I have the trial reports in hand!!!! The raw data will allow us to explore this further
Thanks MD, much appreciated! It's frightening that myself and others have committed to this PIRT, believing that it was far better than it is. I know it's produced outstanding results for some, but statistically they're few and far between.Is Prof G allowed to discuss results from his copy? Can you not discuss anything from the trial reports you have?It's just cruel to withhold such crucial information from those who require it to make an informed and educated commitment. But to deliberately present the data to make it appear better (ie: rebaselining every year) makes me loose all confidence.
While I initially agreed with LGO's questions, I thought this post answered them honestly and comprehensively.I was (when I read this post) and remain very grateful for the time taken and the information provided. I was a little saddened by Prof G's despondency about Sanofi, though not surprised at Sanofi. I'm not sure what else one can demand answers for, unless the demand is to Sanofi execs. We are all pawns in someone else's game.
Regarding ocrelizumabs ( and its sister drug Rituximab):We all know there is probably a higher incidence of cancer for patients using ocrelizumab (Ocrevus). Referring especially to the ORATORIO trial with 2.3% Malignancies in Ocrelizimab arm versus vs 0.8% in placebo. And 6 cases of breast cancer with Ocrelizumab vs 0 cases in control arm (Opera I+II plus Oratatorio)But what is more worrying, is the silence of the fact that Ocrelizumab was halted in Lupus and artriris due to Opportunistic infections of which several were fatal.I quote news from Reuters from mars 2010:"ZURICH, March 8 Swiss drugmaker Roche Holding AG ROG.VX and U.S. biotechnology company Biogen Idec (BIIB.O) are suspending experimental rheumatoid arthritis and lupus treatment ocrelizumab after deaths following its use, casting doubt over its future".http://www.reuters.com/article/roche-idUSLDE62705720100308Now, also Ocrelizumabs sister drug, Rituximab, had also several fatal cases of Opportunistic infections in Lupus and was halted due to that. I wonder: WHY are there no discussions about the safety risks connected to Ocrelizumab and its sister drug Rituximab ? How can anyone imagine that you can live without your B-cells in the long-term … (?) Larry
Hi LarryLarry Steinman I presume. Yes, I agree with Anon 6:45pm; we are not saying they are safe, simply safer than alemtuzumab in the short-term. I hope you are well. Gavin
Its no secret people can have relapses after alemtuzumab, even after HSCT (not if you go with Dr. Freeman protocol), i cant understand why theres no offer to have your indultion, pulse werever you wana call it, and then have a maintenance treatment…. pharma would probably love to have people on this meds for life, and patients having fewer relapses would pay happily, does this work? we dont know, needs to go on trial, but in my mind it makes sense. They letting alemtuzumab die because its too cheap, you have it once and then theres no more profit, thats the cinic in me talking.
Unfortunately I don't think Alemtuzumab offers much durability in maintaining NEDA beyond two years. Where is the long term data? All I have seen is NEDA per individual year over the 5 year extension study. Perhaps it's not worth de-risking for secondary AI diseases if it doesn't deliver long term on its primary goal.
This is MS we're talking about. If anything produced NEDA over long term it would be nothing short of revolutionary.
So, I'm scheduled for lemtrada infusion at the start of next year. From this I take it I should cancel my appointment?
Re: "..So, I'm scheduled for lemtrada infusion at the start of next year. From this I take it I should cancel my appointment?"Can't comment, but in general nothing has changed. Alemtuzumab's risk profile is what it is. Ocrelizumab and oral cladribine are months, and possibly years, away from being available.
Rituxan, the equivalent of ocrelizumab, however, is available now off-label. I was surprised when it was instantly approved for me for the first time by Aetna, my insurance provider in the US this year. In the past, it was denied each time, but approved on appeal. I'd at least ask your doctor about it if you want to avoid the risk profile of alemtuzumab.Aetna updated their CPB in September to consider rituximab "medically necessary" for multiple sclerosis upon failure of natalizumab or other first line drugs (I'm JCV+, so had to switch off of natalizumab). This is great news. http://www.aetna.com/cpb/medical/data/disclaimer/review/200_299/0264_49.html. http://www.aetna.com/cpb/medical/data/200_299/0264.html
Prof G,See Prof coles's website – the camthy trial showed no benefit, so recruitment has stopped.Anon 1.41, time is brain. Lemtrada is a highly effective treatment which for many shuts down the disease (inflammation). The long term resuls are very impressive – I am nine years out from first infusion and disease free NEDA). The side efeects can be picked up by monitoring and are treatable e.g. thyroid side effects. The biggest risk is not the side effects from Lemtrada, but the long term disabilty / unemployment which comes with this disease if not effectively treated. I'd rather take the risk of a thyroid disorder than the risk of losing my functions one by one.Prof G needs to focus on some other MS area rather than highlighting all the potential risks which come with a treatment which is a life-changer for many. I'm not so sure his beloved oral cladribine will be as free from side-effects as he suggests.
Re: " I'm not so sure his beloved oral cladribine will be as free from side-effects as he suggests."I agree; it has its own, but very different, side effect profile. This profile is well-defined and has been discussed many times on this blog.
What about vaccination during therapy with B-cell depleting therapies? I think this will be some problem when you're on Ocrelizumab for several years….
Jules,Anecdotally on an individual level results can be impressive. But the 5 year extension study fails to provide such data and this is needs to be seen by both neurologists and patients to generate confidence.
The blatant and sub conscious pushing of Calbridine on this blog is scary but funny. The drive to come up with the first oral MS medication a few years ago was a valid and potentially profitable one, so I understand. But now, this is purely a pride thing. This drug is no better than the other orals out there, but getting it to market is a cap in the feather for this team/blog. The potential save to the NHS is real but you know that if it gets licence the prices they quote on this blog will raise substantially to the tens of thousands mark, just like what happened with Campath/LemtradaThe risk of alemtuzumab is there, and trying to understand this rebaslining in the results has confused me and no one, not my neuro or this blog can explain to me why rebaslining is a valid thing.Orcelizumab – my neuro is not sure this will get licence, and if it does please bare in mind its 'sister' drug that was about to go off label was going through the process of getting FDA approved for MS, and was pulled to be replaced by Orcelizumab, so again the drug companies will be cashing in. In the OPERA trials it showed 50% NEDA (With rebaslining) so is actually slightly less effective that alemtuzumab if you compare the trial data.It's a shame what can be such a good information source is becoming a marketing tool. Focus on the patients and new/better treatments for MS, not the same/recycling drugs that are all around the same efficiency. What do you think your patients want? Similar efficiency drugs that are tested against interferon (which is now obsolete) or better more effective treatments or even a cure?
Re: "…The potential save to the NHS is real but you know that if it gets licence the prices they quote on this blog will raise substantially to the tens of thousands mark, just like what happened with Campath/Lemtrada."We don't have control of pharmaceutical pricing. But I am sure NICE will do its job and make sure the NHS gets it a cost-effective price.
Re: "In the OPERA trials it showed 50% NEDA (With rebaslining) so is actually slightly less effective that alemtuzumab if you compare the trial data."Wrong the figure is 80%, not 50%, which is why ocrelizumab looks very good compared to alemtuzumab and the other high-efficacy therapies. Please read my ECTRIMS highlight post on ocrelizumab: http://multiple-sclerosis-research.blogspot.com/2016/09/researchspeak-ectrims-highlight.html
Re: "The blatant and sub conscious pushing of Calbridine on this blog is scary but funny."Not sure it is scary or funny. We have declared our conflicts and it is for the reader to interpret what we say with this in mind. As you know by now I am a proponent of PIRTs and cladribine is simply one of those. Based on the data out there cladribine is in the same efficacy zone as fingolimod and is not as effective as alemtuzumab and HSCT the other PIRTs we have discussed. But you need to be aware average efficacy is not necessarily what happens to individuals. Therefore some pwMS may want to try cladribine with a lower statistical chance of being a responder than alemtuzumab or HSCT. It is all about choice.
Re: "Similar efficiency drugs that are tested against interferon (which is now obsolete) or better more effective treatments or even a cure?"Don't you want to know what has happened to all the pwMS and pwCIS treated with cladribine,long-term? May be a significant proportion are still in long-term remission. I am particularly interested in the CIS cohort. We have started to lobby Merck to do a study to recall these people to see how well they are doing. As you have highlighted the PIRTs are the only drugs that really offer a 'potential cure'. The latter is, however, based on the autoimmune hypothesis of MS that may prove to be wrong.
"Don't you want to know what has happened to all the pwMS and pwCIS treated with cladribine,long-term?"Yes please and thank you for your efforts. My partner has started considering Cladribine/Rituximab in place of Ocrelizumab if she needs future treatment, because for her and with her history of breast cancer, Ocrelizumab just means too many sleepless nights – even if the breast cancers turn out to be a random cluster.Real choices are stuff we dream about.
…. I thought you were business savvy. Don't you know that Sanofi don't want alemtuzumab to be too successful; if it is successful they will have to pay Genzyme's ex-shareholders a shed load of money.
City Boy we had to edit your comment because some of it was not fit for purpose. I am not sure you are correct, but if you are it will be a sad day for pwMS. Alemtuzumab is the most effective treatment we have for pw-active-MS and they should all have the option, where it is available, to be treated with the drug safely.
It is good to note that despite having been over the issues in this post many times before on the blog that repetition can still generate discussion. This post generated a record number of views for a Saturday. Thank you.
Perhaps readers are clicking hoping for something new. Or maybe we just want answers. You continue to ignore the questions on annual rebaselining in the extension study. I'm still hoping to see some raw data from the Lemtrada extension study.
I have commented on this before with the poster. I will repost if you want. Repetition won't hurt anyone.
Apologies if I've failed to see it. What was the NEDA percentage at 5 years *without* rebaselining after 2 years?
Dear LGOYou are not going to get an answer as Genzyme control the data!, That is unless they publish it, which they probably won't, as it is not going to be good reading. They dump their info in a meeting abstract and hope you won't see it which you wouldn't, but ProfG has a copy. However it is clear that the data shows it is not as good as implied.If in the 2 year trial it was about 40% NEDA or less then it can only be downhill from there.They have not been publishing lots from this trial, some of which, is in my mind…hiding bad news.Although Sanofi has signed to give access to pivotal trial data…the follow-up would not be part of this. I requested access to the raw data from the pivotal trials (via Clinical Study Data) nearly a month ago and am still waiting for a response. I know what the data says already, because I have the trial reports in hand!!!! The raw data will allow us to explore this further
Thanks MD, much appreciated! It's frightening that myself and others have committed to this PIRT, believing that it was far better than it is. I know it's produced outstanding results for some, but statistically they're few and far between.Is Prof G allowed to discuss results from his copy? Can you not discuss anything from the trial reports you have?It's just cruel to withhold such crucial information from those who require it to make an informed and educated commitment. But to deliberately present the data to make it appear better (ie: rebaselining every year) makes me loose all confidence.
I am not sure why, but MD is becoming my favourite thing on planet earth!Keep go Prof. B and merry christmas everyone.Tony F.
We commit to drugs that are available today but the grass is often greener round the corner, but as time is brain, one can wait and wait and wait for something better but you can wait until it is too late.ProfG will post the poster, the important thing is to monitor yourself if you have activity consider another dose.In this respect make sure you deplete. The information you need is published you just need to know where to look.Make sure your neuro reads. http://www.ema.europa.eu/docs/en_GB/document_library/EPAR_-_Public_assessment_report/human/003718/WC500150522.pdfI believe page 34 is of relevance for people needing multiple doses if NEDA is not achieved.As to the trial reports they suggested a few things to us and the ideas are been reported.http://www.ema.europa.eu/docs/en_GB/document_library/EPAR_-_Public_assessment_report/human/003718/WC500150522.pdf
While I initially agreed with LGO's questions, I thought this post answered them honestly and comprehensively.I was (when I read this post) and remain very grateful for the time taken and the information provided. I was a little saddened by Prof G's despondency about Sanofi, though not surprised at Sanofi. I'm not sure what else one can demand answers for, unless the demand is to Sanofi execs. We are all pawns in someone else's game.
Another example of Pharma greed, which has thakfully been stomped on. Phenytoin was used in Prog G's optic neuritis trial.https://www.theguardian.com/business/2016/dec/07/pfizer-fined-nhs-anti-epilepsy-drug-cma
Prof coles's website – the camthy trial showed no benefit, so recruitment has stopped.Thanks for this info, just as I predicted.
Actually I predicted it would make things worse.
Maybe that is why it was stopped
Right again MD. Wonder what happened?
Regarding ocrelizumabs ( and its sister drug Rituximab):We all know there is probably a higher incidence of cancer for patients using ocrelizumab (Ocrevus). Referring especially to the ORATORIO trial with 2.3% Malignancies in Ocrelizimab arm versus vs 0.8% in placebo. And 6 cases of breast cancer with Ocrelizumab vs 0 cases in control arm (Opera I+II plus Oratatorio)But what is more worrying, is the silence of the fact that Ocrelizumab was halted in Lupus and artriris due to Opportunistic infections of which several were fatal.I quote news from Reuters from mars 2010:"ZURICH, March 8 Swiss drugmaker Roche Holding AG ROG.VX and U.S. biotechnology company Biogen Idec (BIIB.O) are suspending experimental rheumatoid arthritis and lupus treatment ocrelizumab after deaths following its use, casting doubt over its future".http://www.reuters.com/article/roche-idUSLDE62705720100308Now, also Ocrelizumabs sister drug, Rituximab, had also several fatal cases of Opportunistic infections in Lupus and was halted due to that. I wonder: WHY are there no discussions about the safety risks connected to Ocrelizumab and its sister drug Rituximab ? How can anyone imagine that you can live without your B-cells in the long-term … (?) Larry
I am not sure anyone is saying B-cell depleting antibodies are safe.
Hi LarryLarry Steinman I presume. Yes, I agree with Anon 6:45pm; we are not saying they are safe, simply safer than alemtuzumab in the short-term. I hope you are well. Gavin
Its no secret people can have relapses after alemtuzumab, even after HSCT (not if you go with Dr. Freeman protocol), i cant understand why theres no offer to have your indultion, pulse werever you wana call it, and then have a maintenance treatment…. pharma would probably love to have people on this meds for life, and patients having fewer relapses would pay happily, does this work? we dont know, needs to go on trial, but in my mind it makes sense. They letting alemtuzumab die because its too cheap, you have it once and then theres no more profit, thats the cinic in me talking.