Ok Thank you – the last presentation was by Christopher Misling?, CEO and president ofAnavexLife Sciences.

The next presentation is Resverlogix Corp, and Don McCaffrey president and CEO will be presenting. Thank you.

Thank you very much.It’s a pleasure to be here today. I’ve got an interesting update, we’ve had quite a turbulent summer with this particular company, but I think we came out the winners in the last week or so here, and I’ll explain that as we go.

So today we’re going to go through the ASSURE trial, That’s the recent trial we did with Intravascular ultrasound led by the Cleveland clinic, and the safety data review from that trial.We’ll talk about IP and an indication review, and then we’ll do a summary,

But we do want to remind you that we’ll be using forward looking statements, so we do have a safe harbor posting up there.

I talked about a turbulent summer.On June 27th we announced the top line data from the ASSURE trial, and unfortunately it missed the end point of .06 by just .2 of one percent, and it was deemed a problem. It was very negative on the stock price, so you definitely have a buying opportunity during the summer.

So for us the key findings of this trial were quite obvious.We went in and looked at the secondary data, the primary data, we did no ad-hoc, we didn’t cherry pick and I’ll explain that as we go here, we’ve got some very solid learnings from this exploratory trial.

So basically the baseline in this trial was 39 mg/DL. We found that a little high, considering 80% of the patients were male, and the male rating was below 40 mg/DL to be in this trial. We already knew that the drug itself works exceptionally well in low HDL, but as it’s an HDL-raising drug, people with high HDL have no benefit from this drug and they probably don’t need it.So we’ve been looking at our market, which is low HDL.

Rosuvastatin ended up being the savior for us.All patients, because of standard of care, we had on either rosuvastatin or atorvastatin, the reason we did that was because going forward we believe those will be the two generics out there that will be the most prominent, and we wanted to look at possibilities of co-medications and work it from that angle. And we certainly did learn a lot of news from that.So we learned that the PAV, percent atheroma volume regression, in the patients was a quarter of the time and a quarter of the dose from rosuvastatin in their own ASTROID trial, so that’s pretty phenomenal findings. We’re pretty pleased with that.

And let’s jump right in to some of that data here.So before we get there though, I do want to touch on this, that sixty patients in this trial ended up not meeting the trial requirement of being low HDL. We left all sixty of those in this analysis we’re going to show you, so it gets even better if we did cherry pick and take those out.Also on top of that, we had PK assessments done of all patients. So 17 patients in this trial out of 280 some treated didn’t even take the drug.There was no trace of the drug in them at all.We left those patients in, even though one of them actually had a progression of five percent plaque.Also beyond that, we had additional patients who were very poor in compliance, but we left everybody in. And as we go through this, please remember, our trial was designed vs. baseline, but even vs. placebo although it was underpowered, we did very well. And it would have had to have been six hundred forty patients instead of three hundred twenty four in order to be properly powered for placebo.And as this is a trial with a double invasive procedure of two intravascular ultrasounds, that size just didn’t seem prudent.

So looking at this chart, it’s a very busy chart, I don’t expect you to take it all in, but the key areas here are, these are the PAV values the five of them across the top in the yellow bars.Now everything below that was statistically significant in this trial, including many of them at .0001.The ones that we missed on that mattered the most were the primary, the two in green.So overall the trial did do exceptionally well.And we’re pleased with the data, especially what we learned from it.

This slide I would say is the real meat and potatoes of that trial.I think it speaks very well.Our endpoint as I’d mentioned earlier was .6 of 1% plaque regression.As you can see here, in the intended to treat population of low HDL patients, we actually had 1.43% plaque regression on patients with rosuvastatin.The atorvastatin showed exactly what atorvastatin would normally do, only on the highest dose, meaning 80 mg of atorvastatin can you see plaque regression in an IVUS study.There are two studies that have been done that have minor plaque regression, I believe one of them is .2 of 1 percent and the other one is a little higher than that.

So we did very well, and so if you add all four of these columns together, you get our announced primary endpoint of .04 which missed statistical significance as well.Here, when you do what we intended to do in this trial with low HDL, obviously we were correct – and we do have some very solid theories as to why atorvastatin and rosuvastatin behave different, and it’s a lot to do with the abc-a1 transporter and how each one of those actually affect it.

So when you look at this particular slide here, it’s the statins themselves, it’s rvx vs. the placebo, and these are patients on rosuvastatin.So we had a very strong “placebo” effect, but regardless, even above placebo we would have met the endpoint with statistical significance.

Here’s a lot more numbers for you to look at. We’re not shy about showing this data because we thinkit’s extremely good. We didn’t, as I say just pick little pockets of good data and put them up there, this data is very good. So in the purple, you see the below 39 column, and it’s pretty exceptional, especially the large HDL.That’s the fully matured plaque accepting particles.

And now here you’re seeing the rosuvastatin-rvx and placebo, so rosuvastatin only, and again some pretty good numbers in our favor.

So we decided to look at it a little further.The green bar is the (we’re on slide eleven), the green bar is what our announced primary end point was, the one that missed by .2.And all the other bars are….right here this first purple one, is showing rvx and all of the statins.This is all, including the high HDL, and now we’re looking here at rosuvastatin, just with some of the higher ones, so trying to see if there was indeed a dose impact on this trial, and the answer is quite clearly yes.So now this bar in the middle, the 1.43, that’s what the trial was intended to do, the below 40 mg/DL HDL population on rosuvastatin.I’d say that is a highly successful result right there.Then if you look at the 10 and 20 mg, even better.If you look at the 20 mg alone, even it is 2.04% with statistical significance.So we’re very encouraged about this data, and it has been certainly getting the telephones ringing.

Going forward, we threw placebo up there, so you could see that the effect of placebo does kind of wane as you get further into the analysis and the dose dependency. And again this trial was not powered against placebo.There were all kinds of confounding factors that were even discussed and mentioned at the European Society of Cardiology last week, including the non-balance of plaque burden in this trial.The placebo patients had 35% less plaque overall than the treated patients. So there were some interesting issues there.

Now let’s compare it against rosuvastatin alone and some of their own trials.This is the ASTEROID trial. That’s two years and forty mg.So in a quarter of the time and a quarter of the dose we’re doing 1.43. We’re doing higher than theirs in a quarter of the time and a quarter of the dose. So we’re pretty excited about that, we think that’s pretty strong data. We filed a patent around that information.So that particular patent will not expire ‘til 2033.And Crestor, or rosuvastatin expires in 2016.So it’s aninteresting market opportunity, not only for Astra Zeneca, but also for any pharmaceutical company, because it will be a generic by the time this drug gets to market.

So this particular slide is judging it against a few other trials that were done in the past; the reversal trial,asteroid, periscope, illustrate.And then you look at our breakdowns that I’ve just shown you. The blue one here is atorvastatin.It for some reason it’s just acting normal, and I think it’s blocking the action of our drug – which, our drug was designed to enhance reverse cholesterol transport.And atorvastatin is known to interfere with the abc-a1 transporter system.So it looks like that may be the issue there.And it sure makes for a pretty simple solution: change statins.The bottom line is by having this in combination with rosuvastatin, we don’t lose a single person in our intended population.Our intended population is low HDL patients on a statin. So this makes for a pretty good opportunity for a fixed dose combination programgoing forward.

Now lets talk a little bit about the safety.We again had a very good safety profile, we’re pleased with it.In the last trial we saw the exact same thing that I’m showing you here.We see a very small rise percentage wise in ALTs between week four and week eleven in this case.Last trial it was between week six and week twelve.In both trials they resolve themselves, they’re transient, they go away, they don’t come back as you can see. We don’t even have them starting beyond a certain point.So we’re very careful about this, but we have not had any issues with bilirubin or Hy’s law or any of those issues. We have seen other drugs that are on the market that actually do the same thing, and interestingly enough, they do it between week six and week twelve.Tacrine, an Alzheimer’s drug, is a perfect example.Their incidence is a lot higher. Now any other drug that’s on the market with ALTs, they’re a lot higher than ours, and they’re a very different version.This is basically the liver just temporarily turning on and checking to see what this new compound is, and it appears to go away.But the interesting part, is the drugs that are on the market that do have high ALTs, their half life can be, in many cases, six to nine months.The half life of RVX ALTs is three to five days.So that’s pretty much the half life of an ALT themselves.

We’ve seen interesting cases with these ALTs.In that in this category here in the above eight, we had a patient who went above eight. Doctors could not contact him for three days.He had come in, still taking drug, he had come in and he had already resolved all on his own.We did have to take him out of the trial, because that’s part of the protocol if you’re over eight in a phase II.You can go up to twenty or thirty in a Phase III.But it was very interesting.And all of the lower ones in the three were all adaptable.All of the ones in the 5 to 8 – you stop them and rechallenge them – all adaptable.And in every single case in both studies, which between the two of them is almost 600 patients, not a single person had a new ALT onset beyond week twelve, all the way through to twenty six.So we’re really happy about that.

Now this is an interesting finding in this trial as well.Between the SUSTAIN trial, which was176 patients in South Africa, and the ASSURE trial, which was 324 patients in eight countries around the world, we saw the exact same thing, or very close to the same thing.So we looked at MACE events, assuming in our case MACE is death from myocardial infarction, MI without death, revascularization procedure and/ or hospitalization for cardiac reasons.So…Sometimes people throw in stroke as well, but we didn’t in this case, I actually don’t believe we had any strokes either.So look at that MACE difference.The relative risk reduction was 46%. And that’s pretty impressive.I heard recently that one of the most impressive cardio drugs ever is Lipitor, and it sits there at the 37% risk reduction.So if this holds true in a larger trial where you can actually get statistical significance, that would be pretty impressive.

So then we took that very data and said OK, how does that look in the intended population of the low HDL and just patients on Rosuvastatin, where we know it worked the best. Well, I think that pretty much confirms it, 17.4% to 1.6%- that’s an incredible difference.So we’re very excited about moving this drug forward and seeing where it goes next.

Now, if you look at - this chart is just showing where those were, deaths, non-fatal MI’s etc. You notice here I have a 17 here instead of an 18.I like to point that out because one of the patients here in the non-fatal MI infarct, actually had a heart attack during his last IVUS on the last day of the trial, and was a supposedly dosed patient who had zero PK trough levels of our drug in his body the entire time he was in the trial.So if I had my way I’d move him over to the placebo side, but we can’t do that.But our numbers look pretty good even with that in there.

And here’s the chart between the last trial, SUSTAIN and the current trial we’re talking about ASSURE – even the combined total, they’re both six months, they were both on the same statin, so you get a fairly good comparison there, same dosage etc., you get a 43% relative risk reduction.That’s pretty impressive.

Now the intellectual property estate continues to grow.Just last week we announced in this announcement on September 3rd , that we had added two more patents to our estate. Those are the two on the bottom dealing in plaque regression.And of course they are combination patents dealing with our drug’s unexpected advantages of working with rosuvastatin.So having that tied up moving forward into fixed dose combinations has some very large potential value.

So other than what we’re working on here, RVX-208 is actually in another ongoing clinical trial in Australia.It’s a pre-diabetes trial.And we’re almost fully enrolled. Half of the patients are already completed.And so we should have data out on that trial in about the first quarter of 2014. And this trial working for diabetes is dependent on the drug’s ability to raise functional HDL.That has been confirmed in all three of the last clinical studies that we have done. Very solid high statistical significance of increasing functional HDL.

Now we’re also considering an Alzheimers program, because Apoa-A1 which is one of the key biomarkers that we raise has a very profound positive impact on the brain’s health, including the integrity of the blood-brain barrier.And when beta-amyloid is in conjunction with Apolipoprotein a1, it’s non-toxic.So as you get older and your Apoa-1 levels drop off, you have an exact inverse curve of increase of Alzheimers.So we have a very different approach to Alzheimers than anybody else and we have made application to the NIA for funding to run that trial.Seems to be accepted very well, but we’ll see how that goes, and hopefully in the next few months we can announce that there will be a trial going forward sponsored by the NIA.

And that’s pretty much it for the day.Just to review what we’ve talked about, the PAV, the percent atheroma volume reduction of these patients of the intended trial population of below forty was exceptionally good in the rosuvastatin group, and it’s not a small population finding, it’s our entire population we were trying to confirm with the first study.

Now we haven’t talked yet about the virtual histology ‘cause we just got it.It’s fresh off the press, and it’s exceptionally good.We’re going to be rolling that out shortly.Now the VH is the plaque composition, so did we turn the lipotic core to more fibrotic? Did we stabilize the plaque build-up problem that may rupture? And the answer was a resounding yes.And we stabilized it very well.Another trial was run by GSK on a drug called ? Deroplavit ?.And they decided to go into a Phase III based on their VH results. Our VH results are considerably stronger than theirs. So we’re pretty excited about that.It’s just further confirmation that this drug in the right population works very well.

The MACE events again, very solid, and we’re continuing with the programs in cardiac, alzheimers and diabetes, and we’ll keep the market updated as we go forward.Thank you very much.Pleasure to be here today.

Moderator:We have a few minutes for Q & A.

Don:Does anybody have a question?

Q: Can you remind us what were the effects on Apoa-1 as far as[…..?...]

A:The Apoa-1 was up from baseline which was the target of around 12 or 13 percent, which was quite large.And in the placebo group it was also strong, but when you break it down into the Rosuvastatin and the low, again the charts are very much in our favor.Cause we know where our drug works, and the last two trials really helped us determine that.I think that’s two of three trials where the APOA-1has had statistical significance.So we’re creating new functional HDL.

QWhat is your financial situation?

AWe have just done a small financing a couple months ago.We also have an ATM facility equity distribution.And our burn rate has just dropped considerably, because this was a very expensive trial.It was about 25 millon dollars. So our burn rate has dropped from 3.5 million per month to under 350,000 per month. So we’ve got over a year to work forward.Yes

QWhat have the KOLs like Nicholls said about the [….?subsequent?...]analysis?

AWhat any KOLs will say any time of the day any week, which is that the only thing that counts is primary endpoint.And I wholeheartedly disagree. I know why KOLs feel that way. Because too many people try to slip in too much stuff.But when you can just simply change the drug that the patient is on, it’s pretty solid results.They agreed with us, and they actually presented some of that data including the MACE and the VH data as far as solid advancement.Nicholls himself presented it at the European Society of Cardiology in Amsterdam in front of 4,500 people in the audience.I wish the end point was … He’d have been dancing on his chair if the endpoint was .2 higher, but none the less, it was an exploratory trial, and for us to be able to see those results in the rosuvastatin group, we definitely learned a lot from this trial.Yes

QWhat’s the[?size of?]your next trial …. [….](will you be working with rosuvastatin, and will it be a phase….????(not sure what he says)

AI think if I gave you a number right now, my Chairman of the Board over here would throw a shoe at me.But no, we just really just came off getting this new data like days before the European Society of Cardiology and we just got our virtual histology data.So we have put together four or five strategies moving forward, we have a board meeting here in New York tomorrow. We’ll discuss it more there. But as I mentioned In my last web cast, it’s going to be a month or two before we get to the market with our plans going forward.

QWhat is so different about the drugs, the Lipitor, vs. the Crestor?

AWe’re not positive yet, but what we think just from looking at the initial literature out there -There are four or five papers out there that show that the rosuvastatin acts differently on the abca1 transporters than any of the other statins. It actually enhances it.And that kinda makes sense because the abc-a1 transporter is the first step of reverse cholesterol transport, exactly what we’re trying to do. Lipitor inhibits it.So if you’re inhibiting what we’re trying to put up at the same time, you’re gonna get what you saw here - a flat tire.You mix it together with the Rosuvastatin data, and you miss your endpoint.If you work with rosuvastatin only – and all of these extra points like the virtual histology, all of it, says it works exceptionally well with rosuvastatin.

QDid you have any patients that weren’t on a statin?

ANo, every patient was on a statin.We really had to do that because a new drug going into the statin market, especially one of the most successful drug markets that has ever been, they’re all going to be on statins by the time they get to, you know, an ACS population, and for us it just made sense.And I’m glad we did it because now we know, well, which way to put it and we’ve got a very valuable patent out of it that doesn’t expire until 2033.

QWere there any peculiarities about rosuvastatin vs atorvastatin that […..?] [something about study population?]

AWe didn’t see any.No we did not see any but our last trial that was very successful was actually higher rosuvastatin use vs. atorvastatin, so that’s very interesting as well.But we’ll continue to do some work on the mechanism there, but I think the abc=a1 transporter is the smoking gun here.

Thank you very much.Appreciate it.