A year old .....judge your own reality from then till now... MR. WALSH: Dr. Maher, any view on the Celgene product or anything else?
DR. MAHER: No, I think based on the -- I don’t know the study and I only know what was in the abstract from the ERS and again, that data looks interesting and certainly something to dig into in a bit more detail. IPF remains a pretty active field. There are other studies on game with integrin inhibitors, so JSK and Biogen have got Alpha B, Beta 6, different strategies for blocking Alpha B, Beta 6. Galecto, a small Danish biotech presented data at the ATS on the galectin 3 inhibitor.
There’s still the anti-IL 13 approaches, they were still waiting data from Roche and Sanofi on their anti-IL 13 drugs and there are several other companies with sort of very early phase programs looking at a range of very different strategies in IPF. So it remains a very active field of interest for the pharmaceutical industry.
MR. SHRADER: Are you aware of the Prometic program? That’s the question I have.
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DR. MAHER: From a confidential perspective, yes, but nothing I can say out loud. MR. SHRADER: Okay, well, it’s made your radar screen. Adam?
MR. WALSH: Yeah, thanks, Tom. I have a couple more from clients. One of them wants to know your views on the odds of success for FibroGen’s IPF drug reaching the market?
DR. VELPERIO: I think based off of what they’re putting out there, it seems to be right in line with the other drugs and I think, if they do a combination therapy, obviously and we get FDA approved, then combination therapy -- I think a lot of patients will want this drug in combination with the two FDA approved drugs currently. I think unfortunately, this is a pretty open market. There are only two drugs for it. The two drugs are pretty equivocal from my perspective in using them.
So I think anything that gets FDA approved, especially as add-on and then as insurance companies will allow add-on therapy, I think you can really kind of get a niche in this market.
MR. WALSH: Dr. Maher?
DR. MAHER: So, probability of success. Again, not having seen the data, it’s a bit hard to answer robustly on that one. I think one can work out the odds based on its progression down the drug development pipeline and I would just say that it’s mitigated by challenges around manufacturing the drugs and the dosing regimen and the route required, which possibly offsets some of my expectations of success. So if you say it’s 40% on average for a drug that’s (ind), I might go a little bit lower than that.
MR. WALSH: And then I have another one from a client. Dr. Velperio, they specifically want to know your impression of Autotaxin inhibition?
DR. VELPERIO: I think based off of the data that’s out there and previously out there in the animal studies as well as human data, I think Autotaxin has multiple functions be it on inflammatory components, on T-cell components, all IL-13 as well as on fibroblasts. I think it’s very exciting. So I think biologically, it makes sense.
The only problem with that is, the length of the study has been short and I agree, we’ve seen separation of curves early out as 12 weeks. But just based off of other studies where you have these early data, this really makes you worry about more long-term data and I think we’ve pushed the threshold back from 72 weeks to 52 weeks with these trials but I think you’re going to want to see something. You still have to see something at least one year on these drugs.
So I’m a little more skeptical with just 12 weeks as compared to longer-range studies but very hopeful because I think the pathobiology of inhibiting Autotaxin in this pathobiology makes sense.
MR. WALSH: I have another -- Tom, do you have any? Operator, are there any in the queue?
MR. SHRADER: I guess the only question I have is -- and it’s pretty vague. Do you have any sense of whether either mechanism makes more sense in combination with the existing drugs? Is there enough data around to even handicap -- relative to a question like that.
DR. VELPERIO: For me, to me, just more from a basic science view, I love the concept of CTGF. That’s just -- for so many years, it’s been implicated in all these fibrotic processes; liver, kidney, lung and there’s just been an enormous amount of animal molecular data to say its importance. It’s kind of nice to see some of that importance actually come to human trials and make an impact but that’s just from my perspective.
MR. SHRADER: Okay.
MR. WALSH: So another client question real quick; are either of you familiar with the BMS Autotaxin inhibitor? It seems it’s
been out there for a while but not a lot of updates on data. DR. VELPERIO: Yeah, I mean --
DR. MAHER: Yeah, so I have no direct -- sorry, sorry. MR. SHRADER: Okay, no worries.
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DR. VELPERIO: Yeah, they did a trial there and I thought that possibly -- yeah, I don’t know what happened to that trial. I thought that it was stopped but never seen any data from that trial.
DR. MAHER: I’m told that if you dig into the annual reports, you can find that it was stopped for safety, I think, but that’s my only knowledge.
MR. WALSH: That’s right. Okay, good. Operator, any more questions in the queue? OPERATOR: There are no questions in queue.
MR. WALSH: Tom, any questions from you?
MR. SHRADER: I’m good, I’m good. Thank you, everybody, enjoy your Friday afternoon.
MR. WALSH: Yeah, thank you so much for joining both of the doctors, Dr, Maher, Dr. Velperio, really appreciate it. On behalf of Stifel, thanks everyone for joining and I apologize again for the difficulty with the dial-in. Glad we made it through the call, have a great weekend.
DR. VELPERIO: Thank you guys, too. DR. MAHER: All right, thanks all, bye.
OPERATOR: Thank you, ladies and gentlemen, this does conclude today’s conference call. You may disconnect your phone lines at this time and have a wonderful day. Thank you for your participation.
END