http://wsw.com/webcast/rrshq25/rvx/

SLIDE 1

OK everyone, we’re going to start with our next presentation. We have Resverlogix who are investigating the use of an epigenetic modulator to control cardiovascular disease. So with us to tell us more is CEO Donald McCaffrey.

Thank you very much and welcome everybody in the room as well as those on the accompanying webcast.

SLIDE 2

We’ll start today by going over today’s agenda. We’ll talk about the problem we’re addressing, the solution as we see it, our clinical data presentation, we’ll touch on some very important Phase III planning and trial updates and we’ll go over our mechanism, as well as our market opportunities.

SLIDE 3

So in today’s review, we will highlight that RVX -208 is very soon entering Phase III clinical trials. We’ve already finished all our drug production and we’ve got our facilities all lined up. We’re actually within a very short few weeks from starting enrollment. So we will announce that when we do. We’re getting very close; it’s getting quite exciting. It is a first in class BET bromodomain inhibitor, and we basically have an eight-year head start on anybody else in this area. So other BET bromodomains are out there, however they are focused primarily on oncology. This epigenetic mechanism allows us one target and multiple indications. So we will also very soon be announcing an orphan indication that we will be proceeding on planning with. With this very same drug, we have almost a thousand patients already dosed. So we have a very strong safety profile, and look forward to sharing that as well.

SLIDE 4

So let’s talk about what the problem is. The problem is addressing the 70% unmet need in cardiovascular management. So if you look at the pie chart here, the 30% that’s covered by mainly statins. Your Lipitors, your Crestors. Good drugs, but they only address 30% of the needs. Other drugs are being developed such as the PCSK9s. They will take a small sliver of that remaining 70% unmet needs, leaving a huge market. They are good at lowering HDL. Their weakness so far seems to be pricing. They have a lot of kick back from payer groups. Ours being a small molecule, it will fall in line with normal pricing ranges.

SLIDE 5

The 70% unmet need extends beyond cardiovascular disease. It extends into other indications such as diabetes, which is closely related to cardiovascular disease. The amount of people worldwide with diabetes is huge. And more importantly, 68% of these people will die from cardiovascular disease. That’s an alarming number. And no matter how well their glucose is treated, they will die at the same rate. That was proven definitively in the ACCORD study by Dr. Henry Ginsberg from right here in New York. And Henry was very impressed with our data and has actually joined our clinical steering committee, so we’re very pleased to have him on board.

SLIDE 6

Now, the 70% unmet need also extends beyond diabetes into chronic kidney disease. So type II Diabetics often morph into different levels of renal disease. So it’s an extension of the disease. Now in our last study we had patients of both categories, diabetes and chronic kidney disease. That has provided us with some very invaluable information.

SLIDE 7

So let’s talk about the solution.

SLIDE 8

The solution is our drug, and it’s RVX-208, which has now been named apabetalone. So it’s the first in the class, all future drugs that follow us, those that are eight years behind and more will presumably be called betalones of some kind. Now we are first in class. The drug is a BET inhibitor. And it is a specific BET inhibitor. The guys at Harvard and Oxford and the structural genome consortium have published on this that it is a selective BRD4-BD2, so this has allowed us to get outside just the oncology curve. And our supporting safety data from nearly a thousand patients backs that up.

SLIDE 9

To date the drug has been tested in nearly a thousand patients. Our next trial will be two to three thousand patients. So we’re getting some very good numbers and good results. The drug has been approved in eleven countries around the world already for testing. (From slide: U.S., Canada, Belgium, Poland, Russia, Holland, Hungary, Brazil, Argentina, South Africa, Australia).

SLIDE 10

Now the clinical data I’d like to present is regarding MACE.

SLIDE 11

So MACE is major adverse cardiac events. And in our past two trials, we used a mid-level MACE which included death, heart attack, stroke, revascularization and rehospitalization. Some companies use much broader than that, chest pains and others, there can be up to eight-point MACE. We used five. In our future trials, we will use a three-point MACE, only including death, MI or heart attack and stroke. So as you can see in this past collection of trials, in the dark colored lines, blue and red, we had a relative risk reduction of MACE of 55% (p=0.02). That is a very high number. When you look at one of the most successful drugs in history, being Lipitor, their relative risk reduction is 37%. So we’re pretty pleased with that. But it got even better. When we broke down the 40% of the patients who are diabetic, we actually showed a 77% relative risk reduction, and that has a p value of 0.01.

SLIDE 12

Now I mentioned earlier that we had diabetics and CKD (chronic kidney disease) patients in the trial. So that last slide was showing that we had 40% of the patients were actually diabetic. Well by natural levels, about 15% or more of those are going to have CKD. In this case, that was 48 patients. So we were able to get some very valuable data in moving forward, whereas you can see, in the treated patients, which there was 35, we had a statistically significant increase in estimated GFR, which is your glomerular flow rate (eGFR) of the kidney. So you’re increasing the improvement of the kidney. Whereas in the placebo group, you had a continued decline, which is what you would expect in this type of sick patient population. So we were very pleased to see that, we shared it with some key opinion leaders in the renal area, in particular Dr. Kam Kalantar of UCLA. He was very impressed with the data and he has actually also joined Henry Ginsberg on our clinical steering committee. So he will be working with us going forward as well.

SLIDE 13

These two are just to show that we’ve been getting a lot of publications and presentations. These are just two that I highlight, one with the Cleveland Clinic and one at the European Society of Cardiology. However, I can state that in both publications and abstracts, there are between nine and ten in each category for the year. We’ve had a very good year and a lot of material being published on our results from BET bromodomains. We have a couple of very impressive publications coming up that should be in early 2016.

SLIDE 14

So let’s talk a little bit about the Phase III clinical data.

SLIDE 15

The trial here is going to be called BETonMACE. And as I mentioned all of the packaging and the CMC (chemistry, manufacturing and control), and the organizing the clinics, the PIs (principal investigators), doing the safety reviews, that’s already completed and we are moving forward with this trial quite quickly. The patient population will be patients with low HDL, below 40 (mg/dL), that’s where about 70% of the cardio events take place. And they will have diabetes. All of the patients this time. We will still be testing both Rosuvastatin and Atorvastatin as a request by the agencies. But it’s really designed to show that the one does work better than the other, and that will allow us to move forward in the future with a fixed-dose combination with the superior one, which we do believe is Rosuvastatin. So the average length of the trial will be about 18 months. The first patient will stay on-drug until they have completed two years, and the last patient enrolled will stay until they have been on-drug for twelve months. Therefore, we’re estimating that the average will be about 18 months on drug. The location of the trial will be around the world. Mostly in Europe, but we’ll also include some countries like Israel, Australia and Taiwan. The trial is an event-driven trial. So we’re estimating that it will be about 2,400-3,000 patients. But we will keep enrolling until we know that we’ve hit a curvature that will provide at least 250 severe adverse events, which will be death, MIs and strokes. So the exact number of patients and length of trial, we’ll try to keep people updated as we move forward, but we don’t have a definitive number at this point. The primary endpoint is the reduction in MACE. Three point MACE, which will be death, ischemic stroke, and non-fatal MI. So we’re looking for a relative risk reduction of 30%. And in the last few trials, we’ve averaged somewhere around 45-50%, in all of the trials in all of the patient populations, so we do believe this is an attainable goal.

SLIDE 16

Now moving forward, as I mentioned, we are going into a bunch of new countries. There will be thirteen countries included here. So that will be a total of eighteen countries that this drug has been approved to test in. As you can see most of those countries are in Europe, and then we do have Israel, Australia, Argentina and Taiwan. So it is a very broad based trial and we’re very excited to get it started. (per slide: Mexico, Germany, Bulgaria, Hungary, Serbia, Israel, Slovakia, Croatia, Taiwan, Belgium, Poland, Argentina, Australia).

SLIDE 17

Now the epigenetic mechanism, I’d like to focus on this a little bit, because it really is quite intriguing, and it is what sets us apart from the other approaches in this field.

SLIDE 18

So epigenetics has been in clinics and around our radar for about the last dozen years. Most of what people like us in this room and other people studying in these fields…. Most of what we’ve heard about in the past is the writers and erasers. So this is adding a chemical component on or off of the end of a histone tail, and therefore creating an interaction. Early days they had a lot of tox issue to work out. I think the newer programs are very well designed and handling the tox issues. But anyway, with the chemical-to-chemical interaction, they were more prone to having to solve those problems early on. Whereas we are the newer end, being the eraser. So this is a protein-to-protein interaction, so a much more natural flow here, and therefore we haven’t seen a lot of high-end tox. A lot of that is probably because of the selectivity. So in the structural genome consortium paper I mentioned from Harvard and Oxford, we are the first ones to be selective. So there is a BRD2, BRD3, BRD4, and BRDT. Each one of those four has a BD1 and a BD2 endpoint, so you basically have twelve targets there. The other firms are working on oncology because they’re pan-inhibitors; they hit everything. We are selective to BRD4-BD2, which has allowed us to move into these long-term chronic programs. And the king of all is always clinical safety, it is already there and proven, so we’re very excited about that.

SLIDE 19

Now being an epigenetic mechanism, it acts different than a normal small molecule would in the past. In the past, you would target a gene in a pathway and try to shut it down and affect a cascade below. However, epigenetics works in a different fashion. You’re cooling down a pathway. So instead of shutting something off and affecting what’s below it, you’re cooling off many targets, and our science has shown that the targets are almost the entire pathways. You’re cooling them down 10, 20, 30 percent - whatever the attempt is, and you’re having a very profound impact on more than just our original target. Our original target was reverse cholesterol transport. So our goal was to find something that transcriptionally increased apolipoprotein A-1. Well we did and we did it very well. Because not only are we doing that, we saw such profound results with those relative risk reduction numbers - we went back into the science and the blood samples that we had and really analyzed what was going on. Because even we believed that with the increase in ApoA1 that we were having, that that was a rather remarkable relative risk reduction we were seeing. So we knew other things were going on. And we’ve been able to go in and confirm this. That we have a very profound impact on vascular inflammation, on the metabolic system and on thrombosis. And we have recently rolled this new data out to our clinical steering committee in London a week ago at the European Society of Cardiology. And they were very thrilled with the results. As a follow-on to that, here in New York on September 25th, coming up in a couple weeks, we will be back here hosting a large group of analysts at the Yale Club, and we will be rolling that material out to them. We believe we are eight to ten years ahead of the field in understanding the biology. Now we kind of had a short cut there, because we have the only blood bank available to study. So we have several hundred patients’ blood banked for up to six month’s treatment. We were able to go in and see exactly what effect the pathways were having from BET inhibition treatment. So now, we know what indications to go after. So at this analyst day at the Yale Club, and anybody in the room or on the webcast who would like to attend, Susan Noonan is in the room here, she will be organizing that, please feel free to give her your card at the end, and we will gladly have you attend as well. But we are pretty excited about where we are going with this. It really did confirm our first goal, which was to show, reverse cholesterol transport, and now it has greatly expanded our potential in the market.

SLIDE 20

That segues into this slide. Some of the earlier indications that we’ve always talked about, were…we can definitely now look at chronic kidney programs, and we can also go in for peripheral arterial disease. We’re still very excited about the Alzheimer’s approach, and now with this new material, especially with the new excitement in a pathway called “complement” and its relationship to Alzheimer’s, we have one more reason to believe that RVX-208 will have a profound impact in Alzheimer’s. And of course, very soon, within a matter of a couple weeks, we will be announcing an orphan indication that we will be moving forward with with RVX-208. Our future orphan indications will be with follow-on molecules, however in this first one we have such an advantage time-wise by using 208, that it seems to make a lot of sense to do that.

SLIDE 21

Now let’s talk a little bit about the market opportunities.

SLIDE 22

They are huge. This number here of eighteen million plus is simply the diabetics with low HDL. Of course, we will look and investigate beyond that in the future, but it is a very very large market, and it is an unmet-needs market. As I mentioned earlier, there is no drug, until this one came along, that has been able to show a MACE reduction in a diabetic patient population. It’s interesting because in FDA guidance, existing FDA guidance, you are allowed to receive approval for a diabetes drug, as long as you can show a 0.5 or greater reduction in HBA1C Hemoglobin, and that you do not increase MACE by more than thirty percent. And yes, I said increase. That includes death, heart attack and stroke. I am glad we’re not on the increase side of that line. So we’re very excited. And yes, we do. In a very narrow patient population, our sick patients who have diabetes and low HDL, the very group we’re going forward with, we already show a very strong trending to also showing the HBA1C reduction. So we’re pretty excited about the results that have come our way in the last two years.

SLIDE 23

Now early revenue opportunities. We have taken advantage of some of this already. We have recently done a licensing deal in China, which included an equity component that ended up being a forty percent premium to market, so we were very excited about that. But the potential of the deal itself has a very large sales milestone component that will reside with Resverlogix, that we believe could produce up to four hundred million over the next fifteen years. So it’s a very very good opportunity. We may look at other regional deals in BRIC countries, and we are looking at that possibility right now. But most importantly, we’re looking at the orphan indications. Now the BETonMACE trial start to finish is going to be about a two-and-a-half year plus process. So we didn’t want to get stuck with two-and-a half-years of no data for our shareholders. So the inflection points will be many, from regional opportunities, as well as these orphan indications, which as everybody knows are much faster and much cheaper than a cardiovascular program. We’re also looking at the potential that one of these will be a pediatrics program, as we do like those coupons that the FDA have been handing out, and we in our case would very much be interested in monetizing one of those should we receive one.

SLIDE 24

Now the China market, we’ll just touch on that briefly. And why I’m excited in it is way back in 2011, China had already moved into the number three spot in the world. And it’s hard to do a deal in China. They have a different type of sales structure; they have a different business philosophy. They don’t like to do up-fronts. I have never heard of an up-front in China more than one or two million dollars. So a lot of deals get announced but don’t get closed in China. We however, have closed ours and we’re very excited about it because that market is very soon going to be number two. And when you look back at my original slide about the three hundred and fifty some odd million diabetics in the world, pretty much half of those reside in China, and those are diagnosed ones. So it is an incredible potential for us. We really look forward to it moving forward.

SLIDE 25

Now a little financial profile overview here. We were founded in 2001. We’re on the Toronto Stock Exchange. We are very actively investigating moving on to the NASDAQ. We’re very keen on doing that, and we believe we have the potential of doing that hopefully within six months. Our current cash position is $64 million dollars. Market cap is $201 million. Outstanding fully diluted we’re about 120 million shares. Current burn rate is about three million per quarter. That will go up as we continue on with the BETonMACE trial; however, we do have plenty of money to move forward with that as well as our orphan indications.

SLIDE 26

And just to touch on the management, we have an extremely strong management team and Board of Directors, both current and past. Past Board members and current board members have included the Chairman of Bayer, CEO of Bayer, past President of Abbot, head of business development oncology for Roche, a gentleman who was CFO for ImClone, (that was for Carl Icahn and not for Martha). And our staff have come from many different places. Our most recent addition was actually Dr. Michael Sweeney here. Mike spent eleven years with Pfizer. He worked on many of the Viagra clinical trials, so he has excellent experience in clinical, and he has also got a very large book of Viagra jokes.

SLIDE 27

So the milestones that we’ve been checking off this year. We have proven MACE reduction in a clinical setting. We’re very pleased with that, with our data that we’ve been collecting in the last three trials. We’ve done a lot of financing in the last year, about eighty-two million. And the clinical team has been expanded, I just mentioned Mike Sweeney a great addition. The BETonMACE Phase 3 is about to launch, so we’ll be able to check off that one fairly quick. Also, the phase 2/3 orphan indication launch, the data information on it is coming up. And we’ve been presenting left right and center. I’ve got four major ones down there (ACC, EAS, ATVB, ERDTA), but we’ve pretty much been at every event. We were accepted in nine out of nine this year, so it’s nice to see. Business development keeps coming. Now we have all this additional information to share with Pharma. They have loved our results, but they have always had the question about where are we genetically, what else is going on with BET inhibitors, because we are the front of the pack, we are the lead. There is not a lot of data to go after, to read in the existing literature because a lot of it is being published by us. So now that we have that in place and we are sharing it, it’s pretty exciting. It’s good to see the look on their face.

So on that note, I’d like to wrap it up on time here. If you have any questions for me, I will be in the hallway. And thank you very much for your time today.