IL23s, Integrins and MAdCAMs at DDW 2011

Posted by Jeff Berk, BOLT International;  Just to rub it in…  The air temp in AZ is 90, and the pool temp is 93.  There is one cloud.  It’s East of us.  Could be over New Mexico.  Anyway…  Presumably, you’re here to read something about IBD.  DDW (Digestive Disease Week) 2011 is fast approaching.    We could go on and on about this meeting; that itself goes on and on.  And we do in BOLT International’s most recently published Gastroenterology Thought Leader panel.  In this blog we want to touch on a couple of things to look for at the meeting.  These include Merck’s pure anti-IL23 MAb, SCH900222, which we like better for IBD than Stelara (ustekinumab).  We also want to share some color commentary on Takeda/Millennium’s vedolizumab, RG7413 from Genentech, and Pfizer’s (in our humble opinions) overly maligned MAdCAM, PF-00547659.


As the vedolizumab safety data matures, and the IL23 approaches fail to awe, we are picking up greater zeal for vedolizumab.  SCH900222 also intrigues because it may get around the IL12 related infection rate (although maybe not the cardiac toxicity seen with ustekinumab and briakinumab).  And finally PF-00547659 is probably a good pick up for a company whose pipeline isn’t quite as stocked as Pfizer’s.



So here are some thoughts from our panel:


When we polled our Panel last spring, they felt that of all the new classes of biologicals in the late-stage pipeline, most would prefer a new leukocyte trafficking inhibitor.  Improved agents for the prevention of leukocyte trafficking will be slotted at 3rd-line biologicals, behind anti-TNF and behind anti-p40 (IL23), because of a lingering concern over PML (progressive multifocal leukoencephalopathy).


“We have an established alpha-4 pathway that is going to be involved with leukocyte recruitment to the mucosa.  That probably is pretty effective for a number of patients.  We just have very limited access to it the way that drug, natalizumab, got through the FDA pipeline so it is sort of hard for us to go there until things are fairly far along and by then it is too late”.



“The leukocyte trafficking inhibitors being sort of slotted third.  That is just because I think it is going to be hard to completely divorce from the PML issue, even though I am not personally concerned that there is going to be an issue there”.



“Then next I listed the inhibitors of cell trafficking and the closest ones I think are the alpha 4 beta 7 inhibitors like vedolizumab and their other competitors that used to be called MLN-002, but now it is called vedolizumab.  And there are several others and other targets as well but the same overall strategy”.



“Induction and then hopefully maintenance… for the trafficking inhibitors”.



“I think practically speaking probably the inhibitors of cell trafficking are going to be the ones that we end up using the most in the next four or five years”.



SCH900222 (p19 IL-23 selective MAb; Merck / Schering-Plough)


  • Merck (Schering-Plough) has moved a pure anti-IL23 MAb into early clinical development for Crohn’s disease.  The Ph-I program is just underway.  Because there is no inhibition of IL12 with this drug the risks of infection and malignancy are lower.  The expectation is that Merck will be able to push the dose on this agent to a much greater extent than Centocor will be able to do with ustekinumab.


“With Merck I think that you will see there is obviously plans for development.  I think that, if anything, I think that class holds the most promise as long as we don’t see any further significant cardiovascular signals across the class”.


“One of the questions that the RA guys have been trying to deal with is whether not the IL-23 selective monoclonal was originally from Schering Plough but basically Merck’s now, so the question is whether or not that selective molecule is going to be more effective than the 12/23s were. I think obviously that is the hope.  With increased selection, we will get better or more potent efficacy.  I guess I will weigh in on the IL-12/23 as a whole.  I think that the whole class needs to continue to be developed.  I do believe that it is going to work in Crohn’s disease”.


“Don’t know anything about the Merck drug”.



“I don’t know that there is phase II data with the Merck compound yet.  I haven’t seen that.  No, but they said they are taking it forward. Yeah”.



“Merck seems very excited about their IL-23 selective monoclonal. Right. Exactly.  And that is what it may come down to. Briakinumab was an IL-12/23 p40 and maybe it is just that you just need the p35 and that the p40 component is along for the ride and doing something bad or something like that.  It is fascinating but it still sort of eludes us why these tiny little changes in the molecule should make such huge differences at the end of the day in the patient”. 




  • The most likely (but still unproven) mechanism underlying the increase in cardiovascular events seen with briakinumab and ustekinumab is an acute destabilization of plaques.  It’s impossible to predict whether Merck’s molecule is really safer in this regard.


“The theory is that it should retain all of the activity of ustekinumab but not have the immunosuppression and not have the cardiovascular liability.  The cardiovascular, we do not know the mechanism.   It might well be that if a patient has many plaques, atherosclerotic plaques in other systems, it might well be that the drug acts on the plaques and this is the reason why you have this cardiovascular effect.  Then who knows.  If this is the mechanism, who knows if you give the purely p19 whether you will have more or less.  So far we don’t know.  Yes.



“There was actually some early comments coming out from Schering Plough on their dual p40/p19 monoclonal and they say this thing is a pure anti-IL-23, there is no IL-12 and therefore there is not going to be any of the infection risk.  That is a pretty heady claim. Also if you look at malignant risk, it appears that if you can selectively block IL-23 and not IL-12 you may actually reduce malignancies”. 






vedolizumab (MLN-02 / MLN-0002; Takeda)


  • Without the PML anchor weighing it down, vedolizumab is the drug most likely to displace natalizumab for 2nd line biologic for Crohn’s.  The Ph-III program should complete in early 2012.  The optimistic view is that vedolizumab will probably also get an indication for ulcerative colitis, something Tysabri lacks.


“Vedolizumab.  I really like that drug. I do too. I have been talking it up.  We filled our arms of those trials really quickly and we had some really nice outcomes.  Is this going to displace natalizumab? Yes I think it will.   For both Crohn’s disease and ulcerative colitis. Probably, yeah.  Which one would you hesitate on? Just again, ulcerative colitis because at the end of the day you take somebody’s colon out and you have cured them.  Crohn’s disease, the stakes are so much higher”.



“Is there any reason for Tysabri to still be considered in a GI patient once you have vedolizumab available? Probably not.  Isn’t that amazing?”


“I am holding a lot of hope for vedolizumab, especially in ulcerative colitis.  The trials are now done recruiting, so we will get some good data.  Well the one trial has I think 15 patients to recruit, but essentially they are done.  We are going to get some good high level data and my sense is that we are going to see it work.  I think that they are starting to get out from under the natalizumab PML association slowly but surely.   I think they have done a good job of even premarketing or preapproval or sort of trying to manage that.  Takeda is a very forward thinking company.   I have been impressed with them.  I think that you are going to see them emerge at least with an indication in one, if not both of the diseases.  Then I think that another one of the sort of targeting similar mechanisms I think you will see something else hitting that.  I think as a class they are going to make it.



“Okay, so given that still uncertainty is vedolizumab going to totally displace natalizumab? In the IBD world, yes”.


“Do you see more of a value for vedolizumab in the ulcerative colitis patients or the Crohn’s patients and what is the basis? I would say potentially equal.  The reason is that the mechanism for these agents was first demonstrated in ulcerative colitis before it was demonstrated in Crohn’s disease.  It goes back to the cotton-top tamarin (primate) model.  So I think that it is going to have equal value.  The preliminary data, the animal models, were more suggestive of ulcerative colitis.  But at least with the natalizumab data there was good efficacy at least in maintenance in Crohn’s disease.  But I would see them as equal at the moment until proven otherwise”.


“We need to have something between anti-TNFs and Tysabri.  We will see what happens with vedolizumab.  It might change the paradigm that you kind of don’t respond to an anti-TNF, instead of giving a second go to a different mechanism of action”.



“The bottom line is that vedolizumab has just about completed enrollment, if not completed.  We haven’t seen a speck of data from them yet regarding it.  Yes, I am in the trials, yes I work with them and I am on their ad board and I am on the steering committee of the trial but we haven’t seen any data.  From… Takeda. Yeah.  So I don’t know but it is going to be pretty close.  They are going to be closing things very quickly so I think certainly within six months we will have data.  But I don’t know”.




“When you use natalizumab does that efficacy both on the Crohn’s patients and ulcerative colitis? No, it is only indicated for Crohn’s disease.  You can’t use it in ulcerative colitis.  So why is the vedolizumab trial targeting both groups of patients? Because earlier studies did look at ulcerative colitis and those are studies by Brian Fagan in 2004, 2005 and 2006 and there was as signal there that made them want to move forward.  So that is the bottom line.  Do the trials recruit equal numbers of patients? I don’t know off hand. I don’t remember off hand but I don’t think there was any significant imbalance.  I think they decided to spend a lot of money and try to answer this question.




  • The Ph-III program has evolved over time.  The first part was randomized induction comparing vedolizumab vs. placebo.  The last part of the trial has been open label induction for 8-weeks and then randomization to active therapy versus placebo. The long-term follow up is out a year.


“Why would vedolizumab…if they just finished recruiting how long does it take for that last patient to make it through the trial? The trial has evolved over time.  The last part of the trial has been open label induction and then randomization to active therapy versus placebo.  So the open label induction is like eight weeks or something.  And then the long-term study is up to a year and it is not longer than that.  They will have preliminary data but then it depends on whether they are going to go for induction only or induction and maintenance.  I would imagine they are at least two years away if not longer in terms of the process of getting FDA approval.  So everybody is on drug for eight weeks? There were different parts of the study.  Some part of the study was just a randomized induction and then once they reached a certain number – both of our patients were blinded but then they got to the point where there were some people who were open induction and then randomized to placebo versus continued therapy.  I think there are like 600 patients in each arm.  So it is a big trial”.





“There is always a potential, but it is not theoretically valid because this is a gut-specific compound that should not cross the blood brain barrier.  So I am thinking it is safer.  I guess the only way to know if it is safer is to give it to people in clinical trials and see if they get PML.  That is a bad way to do it but that is kind of the only way I think to do it.  If this drug does what it is supposed to do and stays out of the brain I think we could feel pretty comfortable that people aren’t going to get PML.  What can I say?  You are right, it is theoretically possible but hopefully very, very, very unlikely and while you worry about it you don’t have to worry about it that much.  I am excited about this drug because I know that Tysabri works.  The people I have on Tysabri are very happy.  And they are on it for a long time and they can’t get them off of Tysabri because they are so happy.  They have never been this happy.  Tysabri is like the perfect drug if it weren’t for PML, therefore, I am expecting vedolizumab to be “the perfect drug” with an excellent response, a durable response and no serious side effects.  What could we ask for more than that?  While yes there is a theoretical PML risk, I think the company has done its best to minimize it and I am very bullish on that”.




“So we would like something with a different mechanism of action (than another anti-TNF) that would have a durable effect that is safe and effective.  It looks like vedolizumab will be one of those drugs.  I am very excited to see what the clinical trials show that that it is as safe as it is supposed to be”.




  • Vedolizumab inhibits leukocyte trafficking without passing through the blood-brain barrier. It has the highest steroid sparing effect seen for a leukocyte trafficking inhibitor.  The one piece of data that our Panelists do know for sure is that there have been no cases of PML in the trials.   There don’t appear to be any significant safety signals emerging at this point.  While they are still blinded to the specific regimens each patient is on, Panelists report that they think that they can pick out (some of the) patients on vedolizumab because they have obvious symptomatic improvement.


“Do you know any patients that were on drug that responded or is it still all blinded? Let’s put it this way, they do get better.  Part of the trial is blinded but then at some point you can go on open label.  People know that they were on drug because they feel so much better and they know when they are not on drug and when they get open label.  It is obvious that it works”.


“So we go under the premise that vedolizumab is not going to have any cases of PML in its trials. That I know.  But that doesn’t tell you what it is going to look like once it is in mass production. Absolutely”.


“Number three, I think is vedolizumab, so it would be MLN-002, obviously being developed both in ulcerative colitis and Crohn’s disease.  The advantage is this is a class where there is a proven track record on mechanism of action being important and having succeeded in at least Crohn’s disease with natalizumab without carrying the potential for PML.  Speaking to that with this class leukocyte trafficking inhibitors it has demonstrated the highest steroid sparing results we have ever seen”.


“Do you have any toxicity issues with vedolizumab? Not that I am aware of.  There is a lot of noise obviously with these agents because they are given just as we have seen with the other biologics they are given on top of other therapies and often the side effects from the combinations come out, particularly infections. But it doesn’t appear to be high and at least my knowledge of the general safety to date has not been an issue.  There haven’t been any major issues that I am aware of”. 


“That is the MLN…yeah, theoretically you shouldn’t have any PML because it doesn’t cross the blood-brain barrier.  It is gut specific.  So that is good.  I am glad they didn’t find anything in the clinical trial.  Have you had any personal experience yet? Yeah, we were in the clinical trials”.


“So they basically are escaping from the PML?  In other words, you don’t think that will taint them? I think they are going to be able to explain to people how they are different.  They are anti-integrin but they are not the same molecule, so it is sort of like comparing a mini cooper to the newest Cadillac.  They are both cars but they are different.  Maybe that is to dramatic of an example, but the point is that they are not the same”.



  • Making it to 1st-line is going to be considerably harder for vedolizumab.  It is an IV like Remicade, so it is going to cost the same (drug + administration) to the payer.  Its efficacy is not likely to be greater than Remicade, and any assumptions regarding lower immunogenicity are premature.


“So what is the hurdle to keep Takeda or Millennium from pushing vedolizumab actually into first line?  What would they have to show? That is a good question.  They wouldn’t have to do much.  They have to show that it works and it is safe.  We know that TNFs work, but they are not terribly safe.  So if you can show there is an advantage over TNFs it might be first line, it might be given over TNFs.  If you wanted to rig the trial to give yourself the best chance to demonstrate vedolizumab was better than a TNF, which TNF would you put into that head-to-head?  Do you run it against Humira? This is given IV.  I think you would go against Remicade.  Really?  Yeah, because Remicade has the most infusion reactions, about 10 percent, and it is another IV medication.  We know all about Remicade and if you can take Remicade’s spot you will take everybody’s spot”.



  • NCT00619489 is a Ph-II long-term safety trial, just concluding, looking at vedolizumab in 80 pts with Crohn’s or UC.



  • NCT00783718 is a Ph-III protocol in 826 pts with moderate/severe ulcerative colitis. This study is set to report August 2012. NCT00783692 is the Ph-III protocol in 1052 pts with moderate / severe Crohn’s.  This trial is set to report December 2012. Unlike the Tysabri trials, Millennium is including in the Ph-III protocol patients who are anti-TNF naive as well as anti-TNF experienced.  Most Panelists say that there is more of an unmet need in Crohn’s, but given that adalimumab has failed in UC, Millennium is going to make the case that there is only infliximab, and thus it is “almost” an orphan indication.


“What is going on with vedolizumab? We are involved in that clinical trial.  We entered two patients; one in Crohn’s and one in ulcerative colitis.  I think it is in the public domain that the study is going to be closed in the next couple of weeks.  So they have successfully enrolled and will be waiting for the initial analyses”.


“What is the protocol and what will patients have already been treated with before they can come onto vedolizumab? They are allowed to have been on biologic but they have to be off of it, of course, for a period of time.  I think it is a very inclusive protocol as long as you are not currently on a biologic”.


“The good thing about the Millennium drug is that it is already shown to work.  Like I said, they did reformulate it because of immunogenicity but it is nice to know the earlier trials that did show some efficacy and now they are in phase III trials.  So the best drugs are the ones that work in the patients.  So they still have to obviously clear the hurdle and get out so they can get approval.  And do you think it will target Crohn’s disease, ulcerative colitis or both? I know that some of the earlier Millennium stuff was more in ulcerative colitis but they had smaller Crohn’s trials.  I wouldn’t know if they would be pushing more towards one or the other.  I think as a company it would be interesting if you are saying, well, if for ulcerative colitis you only have infliximab, the adalimumab data doesn’t look too good, that might be more of an opportunity and also even pushing to the FDA saying, hey, for ulcerative colitis we only have one approved, for minor to severe ulcerative colitis there is only one approved drug right now so it is next to an orphan.  It is not in orphan status but nearly so.  There is a real need and the fact that the other anti-TNF really didn’t work that well suggests that we do need another pathway.  You could argue that more strongly”.


“Number three and I am probably not doing them in order of preference, would be a pathway that is proven but giving a different pathway option would be something in the anti-adhesion molecule, so Tysabri is on the market.  You are probably well aware of Millennium’s drug. Vedolizumab. Right.  Vedolizumab, which had early data in IBD but then they reformulated.  The original one was MLN-02 and now it is MLN-0002 and made it much less immunogenic.  That was the problem with the initial one.  So that is going through trials and again while it is not a requirement many of us are using it in trials right now for patients who didn’t do well with the TNFs.  And in Tysabri, unfortunately, even though this wasn’t a requirement in the trial, at least in Crohn’s disease, Tysabri, you have to have either have been on a TNF and have failed or been allergic to it before you can get to Tysabri”.



“I think it is an unmet need that will be helpful in both ulcerative colitis and Crohn’s disease.  I think vedolizumab is just further along.  Any sense of when vedolizumab will be approved? I think if they have the data maybe late this year or early next year, but I didn’t hear anything new about it at ECCO”.



“Is this both for ulcerative colitis and Crohn’s?  No, just Crohn’s.  Why is it less effective?  And is the same thing held for Tysabri?  Is Tysabri limited to Crohn’s?  Yes.  I don’t know about ulcerative colitis.  We have terrific medicines.  We have 5ASA for ulcerative colitis.  It is not great for everybody.  It is really a good long-term safe medicine.  So the need for a new drug for ulcerative colitis is not that great and that is not on my wish list.  I don’t think I would wish for a better drug for ulcerative colitis because I am pretty happy with what we have.  But Crohn’s we need better drugs and so vedolizumab is very interesting to me”.



  • The theoretical risk of PML is low for vedolizumab because, unlike natalizumab, it doesn’t cross the blood brain barrier.  FDA will require Millennium to include class labeling for PML.  It will take the community a while to get comfortable with vedolizumab because it does carry PML baggage; as JC virus, present systemically, could theoretically be activated outside the cerebrospinal fluid and then penetrate the blood brain barrier.  A biomarker would enhance the benefit / risk ratio, but none is yet available.


“The disadvantage of it is even though the mechanism because of it is specificity should not lead to cases of PML, I still think that the community may be sensitized to PML.  If they are successful in their development programs in both ulcerative colitis and Crohn’s disease it will take the community a little while to get comfortable with the drug.  I think that it is going to be successful, but it does carry that PML baggage, which I think is going to harm its marketing”.



“Is there any biomarker that is going to suggest response to vedolizumab?  Not that I know if yet”.



“So let’s say things go fine for vedolizumab, I can’t really imagine the FDA giving them a different requirement than Tysabri.  They are the same drug class.  That was just something someone made up because of the rare risk of the PML.  The theory is that you won’t have PML in the brain from the Millennium drug because it doesn’t affect transit of little white cells into the CNS.  The JC virus can be seen in other organs.  Most of us have it in our body, so whether the JC virus would cause problems in the gut if you don’t have transit of white cells into there that remains to be seen.  I have never heard that speculation before. There are studies that show that they isolate JC virus in the lymph nodes and elsewhere.  It is excreted in the urine”.




RG7413; rhuMAb-b7 (Genentech)


  • Genentech’s RG7413 (rhuMAb-b7) is a couple of years behind vedolizumab.  The drug is about 1-year away from beginning Ph-III trials.  Genentech was very slow to recruit its Ph-II ulcerative colitis trials; notably much longer than it took Takeda to recruit for vedolizumab.  There are positive signals, particularly in the Ph-II ulcerative colitis program.  Genentech appears confident that, lacking any a4 activity, rhuMAb-b7 is mechanistically superior to vedolizumab.   While vedolizumab can still theoretically cause PML (note: no cases of PML have been observed with the drug), because not all EJD virus is within the cerebrospinal fluid, selectivity for b7 integrin subunit should preclude any possibility of developing PML.


“The Genentech approach, remember we are early days.  They are sort of phase IIa trials, they have had trouble recruiting into their ulcerative colitis protocol.  The Genentech product has a lot of potential upsides because it blocks something that the other molecules in the class don’t.  But for whatever reason they haven’t been able to operationalize their clinical trials as well as some of their competitors.  I really don’t know where they are faltering on that because Genentech should be able to pull this off.  That is an interesting choice of words “operationalize”.  What does that mean? For example, when they were doing the trial in ulcerative colitis they just couldn’t get centers to recruit into their trial.  And it was very, very, very slow as compared to some other ones.  I don’t want to comment on the trial management team, but that is the only way I can explain it.  Why is it taking you so long to do this where your competitors have flown through this process?  It is more of a company question I think than a drug question”.



“So the rhuMAb I didn’t class it together, but rhuMAb beta 7 is a little further away but sort of was number four on my list here.  And the reason is that it has some unique properties that may differentiate it from other leukocyte trafficking inhibitors.  There is some preliminary data, again, some stuff that is not in the public domain, but out of the drugs that are available there I am pretty confident even though they are a couple years from going into phase III, or I should say at least a year from going into phase III.  There are a lot of positive signals with that molecule right now that at least in ulcerative colitis would make us enthusiastic. So Genentech focused at least in the last presentation they focused on the purity, the selectivity for beta 7 integrin for that sub unit.  The premise I took was that okay, in some way that is going to not interfere with lymphocyte trafficking in the CNS.  But at the same time my premise also is that vedolizumab doesn’t penetrate the blood brain barrier either.  So do we simply have two alternative ways to getting to the same benefit? You do.  There is something addition about the rhuMAb beta 7 molecule that differentiates it from vedolizumab.  The mechanism of action, and I just can’t…it is something that is just relatively new that has just been discovered by the scientists at Genentech so that is not in the public domain yet”.




“Genentech had their beta 7 selective integrin, rhuMAb beta 7.  Their argument is that by not having the alpha 4 component they are also going to avoid PML.  Right.  Is that credible? Theoretically, the Millennium drug shouldn’t be a PML thing because it is alpha 4 beta 7 and I guess their studies had shown that is not involved in trafficking of white cells into the CNS.  Is there anything else that would differentiate the Genentech from the Millennium drug?  I wouldn’t really know.  There are a lot of things on paper and theory but then there is actually practice”.



“So how does Genentech RhuMAb beta 7 differ from vedolizumab? I think that you have less of the antibody molecule itself.  Isn’t a fragment?  I think it has none of the alpha 4 activity? Right.  Sorry.  So it is just the beta 7 and not the alpha 4.  Again, why the alpha 4 component just like with the IL-23 receptor that you have the p35 and the p40 subunits and you take one of them away or you have both of them how it makes it different if you have the alpha 4 versus the beta 7 versus both of them together why that makes such a huge difference in safety.  Who knows?  We don’t understand the human immune system at all I don’t think.  We pretend to”. 





PF-00547659 (Pfizer)


  • Last Spring the “consensus” of our Panel was that Pfizer’s MadCAM inhibitor, PF-00547659 reportedly lacks the efficacy to be commercialized for IBD.  True, Pfizer is shopping this drug and, instead, focusing on their JAK3 inhibitor, CP-690550.  But one Panelist who we think should know says that the drug definitely had an efficacy signal in the Ph-Ib study, and appears to be very safe.  So while Pfizer has too many other opportunities to warrant developing PF-00547659, it may be a good in-licensing candidate for somebody else.



“There is also a Pfizer drug which you shouldn’t overlook.  There is a MAdCAM I antagonist from Pfizer which is quite interesting as well.  I want to do all of those.  The reason I didn’t mention MAdCAM was because, once again, panelists have said to me they really felt it lacked the efficacy to be commercialized for IBD.  If you disagree with that, I absolutely want to understand why you are excited about it. If we look at the MAdCAM antagonist, for example, this antagonist has a very clear signal in the phase Ib and it is very unusual that you get a signal in the phase Ib.  And the Genentech molecule also has a kind of a signal in the phase Ib.  So this is very unusual to see that drugs that early deliver efficacy signals.  The last one we have seen is anti-TNF.  My feeling is that this points to the potential as a drug.  The second potential point of this drug class is that it was almost side effect free by way of immunosuppression.  No clear immunosuppression.  It is not completely side effect free, natalizumab, I think is the first one running down there, had viral diseases that came up more frequently.  I think this is probably something you will see.  But I think with more selective antagonists, the viral disease of the brain, the PML, which really switched out the lights for natalizumab, will not happen with the others.  I think the chances are not that high.  And then you have very effective drugs that may not act as forceful as anti-TNFs, but could be side effect free without the immunosuppression and the occasional dead patient you have with pneumonia.  So I think this is a tremendous advantage and that is the reason why so many people are excited about it.  I think nobody has ever put the result of natalizumab into doubt that there is efficacy behind it and that the efficacy is strong in the tough patient population.  But come back to the… If you think of the commercialization of MAdCAM antagonist of Pfizer why it has been put up for sale.  As you may know, it has been advertised all over the place brought to other companies. The reason was that Pfizer merged with Wyeth and Wyeth has a tremendous pipeline obviously.  So the drugs which I had described earlier, as you know the Pfizer drugs like the JAK inhibitor and so on, all drugs that came in through the Wyeth side.  Wyeth has new anti-TNFs and I don’t know what.  There is an IL-6 with Pfizer.  I think Pfizer has too many arrows up their sleeve”.


“One compound that did not make your list was Pfizer’s MAdCAM inhibitor.  Is that simply because you already chose two anti-integrins to be on your list?  That is part of the reason, but not the complete reason.  Is there something else in the public domain so you can speak to?  It’s not in the public domain, but so you can think about that.  And you guys have probably done your homework, but remember that molecule was also being shopped around, right?   And part of that reason, which is in the public domain, is because they have other things in the pipeline like their JAK inhibitor and small molecules that they believe will give them a foothold or a stronghold in the field.  But there is some more recent data, again, that will be available in the next two or three months where the story that was told at DDW last year was not a complete.  It didn’t tell the whole story as far as efficacy is concerned”.


Categories: Crohn's disease, gastroenterology, inflammatory bowel disease, ulcerative colitis
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