Check http://seekingalpha.com/article/2543705-resverlogixs-rvxcf-ceo-don-mccaffrey-hosts-corporate-update-conference-call-transcript?page=2

1. At this time I would like to turn the conference over to Mr. Donald McCaffrey, President and Chief Eexecuitive Officer of Resverlogix. Please go ahead.

1. Good day. My name is Don McCaffrey, I’m the president and CEO of Resverlogix. It is my pleasure to once again review some of our 2013 and 2014 milestones, and discuss our ongoing biomarker and genetic analysis program. As part of this review we will be discussing the analysis of our clinical data, our ongoing mechanism research, and the design and launch of our clinical trial. We will also touch on some of the exciting new opportunities afforded us as a result of our world leading BET bromodomain program. In conclusion we will also have a look at some of our projected milestones and inflection points, at which time we will open up for questions from the audience.

1. On slide three you will note that our 2013 and 2014 year was a busy development year. We announced exciting new data such as plaque regression in high risk CVD patients, which was announced in November. And then most recently in September at the European Society of Cardiology, we announced a 77% relative risk reduction in MACE events in diabetic patients. MACE events are major adverse cardiovascular events. As you will learn in today’s presentation, our analysis and planning have led to faster and less expensive trial options. During this twelve month period we also completely turned around the company’s financial position, starting with an insider led equity round and followed by a thirty million dollar financing dedicated to clinical trial development, which was a direct result of our strong data set. The Australian trial was enrolled and completed, and during the coming year we will have future publications and abstracts highlighting positive data learned during that trial. We also had patent approval in Europe, and we had many peer-reviewed papers published on the attributes of RVX-208.

2. On slide four, some of the recent publications regarding RVX-208. These publications include very prestigious groups such as the Cleveland Clinic, the Structural Genome Consortium, Oxford University, Harvard Medical Group, and our own world-leading scientists. This is a testament to the growing acceptance and knowledge of BET inhibition and the Resverlogix world lead in this epigenetic space.

3. Slide five leads us to the next section covering our biomarker and genetic pathway analysis.

4. On slide six, let me start this section with this cartoon and by discussing a little bit about the discovery path that we have been on with RVX-208. Although we have an eight year head start on any other program in this space, we may have been a little bit too APO-A1 centric in the past. However, our clinical data and our growing mechanism of action understanding have enabled us to look outside the lighted area, and greatly expand the value of our assets.

5. Slide seven. It’s a brief description of what we have worked on over the past year. The knowledge from this work will lead to faster and less expensive drug registration. That is what we want. That’s what pharmaceutical companies want. That’s what stakeholders want. The three key steps for development start with analyzing the existing clinical data from Sustain, Assure and the Australia trial. Exciting information is being generated from all three trials. All three studies currently have papers and abstracts being generated for presentation in 2015. The second step toward a probability of success was a further delineation of the mechanism of action that’s driving the MACE reductions that we have witnessed. So we’re looking at micro-arrays of relevant cell types, analysis of blood markers, algorithms for identifying patient groups most likely to respond to treatment, and proteomic analysis (of archived clinical samples). The third step is to design and launch the upcoming clinical trials based on utilizing knowledge gained from steps 1 and 2. We’ll be hiring some new staff. Additional smaller trials are being planned that may add value, We’ll talk about those shortly. And we are confirming clinical sites and principle investigators. Over the next few slides I hope to give you a glimpse of some of the highly complex work that we do. And how it will soon translate into value. We own the only BET bromodomain clinical blood bank samples in the world. That’s a huge asset that will start to pay off soon.

1. Now on slide eight. Slide eight represents some of the most successful data that was generated in the first step, the clinical analysis. The 77% relative risk reduction of MACE in patients with diabetes was a remarkable find. This data has allowed us to better position our drug in future trials. CVD patients with diabetes mellitus are the very patients that we want to move forward with in our next trial. And that was confirmed in both Sustain and Assure.

2. Slide nine is a continuation of the knowledge gained from the clinical trials. The p value which represents a test of absolute change, clearly showed up versus patient’s own baselines. RVX-208 has a very consistent effect with all of these biomarkers showing a p value of 0.0001. This is one of the many reasons we know this drug works, and it works very well.

• HDL

• Apo A-1

• Total HDL particles

• HDL particle size

• Large HDL particles

• hsCRP

• Alkaline phosphatase

1. Slide ten highlights more than sixty biomarkers that we studied in both ASSURE and SUSTAIN. We utilized them in a pooled analysis to better understand what it is the RVX is doing that % relative risk reduction. These categories included reverse cholesterol transport markers, inflammatory markers, metabolic markers, chemistry, liver safety markers, atheroma markers, hematology and vital signs of the patients.

2. On slide eleven, we show that as a result of the analysis of the last slide’s biomarkers, we ranked the most predictive biomarkers. To our surprise HDL and ApoA-1 ranked very high, but not at the top. The top one was alkaline phosphatase, which I will refer to as ALP from here on. ALP it turns out is a very useful biomarker and one that we may utilize as our primary endpoint in future trials. In reviewing the last five trials, including the Australia trial, ALP had highly significant reductions and the p value was 0.0001 in all five of the trials. ALP has been gaining prominence of late and has been used as a biomarker in Intercept’s Nash trial and in Amgen’s Cinacalcet trial. Most importantly it helped us to better understand how exactly RVX-208 was delivering such strong results.

• Alkaline Phosphatase

• HDL

• Apo-A1

• Glucose

• Large HDL

• HDL Particle Size

• Total HDL particles

• hsCRp

1. On slide twelve, this slide shows a small fraction of the research linking ALP to mortality in cardiovascular disease and patients with diabetes.

1. Slide thirteen is the start of our second step of work, where we delineated the mechanism of action and the pathways involved in RVX-208’s successful clinical data.

2. In slide fourteen, we move on to some of the mechanistic work that was done over the last year in order to further understand how RVX-208 was achieving the MACE results. This work is very important to pharmaceutical companies and agencies, as it further distinguishes safety and efficacy aspects of our drug. The slide shows you several published BET bromodomain compounds, most of them are in oncology, and it shows their relationship to the corresponding binding sites on the BET bromodomain itself. BET is the blue bubblegum-looking item on each of the graphics. Four interaction sites between the molecules and the bromodomains have been circled and highlighted in purple, red, green and blue. These interaction sites determine what epigenetic changes will occur as a result of the compounds’ interaction with the bromodomain. As you can see RVX-208 is the only one that does not touch on the red (WPF) shelf, and the only one that interacts with the light blue area (peptide channel). These are unique characteristics. They’re responsible for the positive epigenetic actions and selectivity.

3. Now on slide fifteen, the story gets a little complex here. However this is very important information, so I will try to explain it properly. The top portion of the slide shows you a sample of a gene expression array. These are used by us to study the effects of RVX on various genes. Each of the six red or blue boxes lined up from top to bottom, they represent a specific gene. So there are over sixty genes being tested on this array alone. I have blocked out the names of the genes for IP reasons, but a blue signal means you are turning the genes down. A red signal means you are turning them up. We have done numerous arrays, and as with this particular one, the blue genes o the top left three lines are turned down by RVX-208. Based on which genes they are, we now know new indications that RVX could possibly treat. The absence of corresponding negative gene interaction is also very good news for us. Genes are in turn part of a particular pathway or network of genes as depicted on the bottom half of the slide. These pathways can regulate all kinds of events in the body, such as statin metabolism, triglycerides, blood clotting. In conventional or old-school drug development, you would target just one of the genes that are seen here as blue and white colored boxes. Working together in a cascade or a domino effect, they cause positive or negative effects in the body. The reason they would target just one gene in the past is that if they were affecting several genes, you would most likely have some negative effects caused along with the desired positive effects. However, in our case the epigenetic mechanism that is activated by RVX-208 has numerous positive effects, and have not been over-shadowed by corresponding negative effects. This positive cascade effect appears to be unique to BET bromodomains, which are acting as master regulators of these networks. This is the missing link, the holy grail of drug development. This is why Dr. James Watson is so excited about BRD research. We have already identified several gene pathway cascade networks that are positively affected by RVX-208. Resverlogix leads the world in this research, and we have recently been demonstrating our knowledge to various pharmaceutical companies. The reactions have been very encouraging.

1. Now in slide sixteen let’s have a much simpler look at what this master regulator of gene networks really means. The complex science behind the previous slide has led us to understand that BET inhibition is involving numerous factors that are collectively responsible for our observation of our observation of a 77% reduction in MACE events. Our original hypothesis was that the Apoa-1 increase and the reverse cholesterol transport were solely responsible. Now we know it is much more complicated. It involves not only reverse cholesterol transport, but vascular inflammation, thrombosis and metabolic factors. Among these pathways we have also witnessed combined events involving reduction of alkaline phosphatase, proper lipid parameters, glucose reduction, weight loss, renal function improvement and thrombosis improvement.

2. So slide seventeen is the start of our third step which is the clinical planning. This is where one of the biggest mistakes in drug development occurs, which is rushing this stage.