Alex Abuin - VP, Alliance Management & Corporate Communications Arthur Sands - President & CEO Pablo Lapuerta - SVP, Clinical Development & Chief Medical Officer Brian Zambrowicz - EVP & Chief Scientific Officer Jeff Wade - EVP & CFO

Matt Lowe - JPMorgan Liana Moussatos - Wedbush Alan Carr - Needham & Company Nicholas Bishop - Cowen and Company Kevin Kedra - Gabelli & Company Stephen Willey – Stifel Nicolaus

Thank you for holding. Welcome to the Lexicon Pharmaceuticals’ Third Quarter 2012 Conference Call. At this time, all participants are in a listen-only mode. There will be a question-and-answer session to follow. Please be advised that this call is being recorded at Lexicon’s request. At this time, I would like to introduce your host for today’s call, Alex Abuin, Vice President, Communications and Alliance Management. Please go ahead Doctor Abuin.

Good morning and welcome to the Lexicon Pharmaceuticals’ third quarter 2012 conference call. I am Alex Abuin, and with me today are Dr. Arthur Sands, Lexicon’s President and Chief Executive Officer; Dr. Pablo Lapuerta, Senior Vice President and Chief Medical Officer; Dr. Brian Zambrowicz, Lexicon’s Executive Vice President and Chief Scientific Officer and Jeff Wade, Lexicon’s Executive Vice President of Corporate Development and Chief Financial Officer. We expect that you have seen copies of the press releases that were distributed this morning regarding our third quarter earnings and the presentation of additional LX4211 Phase 2b results at the American Heart Association Annual Conference. During this call, we will review the information provided in the releases, provide an update on our clinical programs and then use the remainder of our time to answer your questions. The call will begin with Dr. Sands, followed by Dr. Zambrowicz and Lapuerta who will provide an update of our clinical programs, and by Mr. Wade who will review our financial results for the third quarter and discuss our financial guidance. We will then open the call to your questions. If you would like to view the slides for today’s call, please access the Lexicon website at www.lexpharma.com. You will see a link on the homepage for today’s webcast. Before we begin, I would like to state that we will be making forward-looking statements, including statements relating to Lexicon’s research and development of LX4211, LX1031, LX1033, LX2931, LX7101, and telotristat etiprate, also known as LX1032, and the therapeutic and commercial potential of those drug candidates. This call may also contain forward-looking statements relating to Lexicon's future operating results, financial arrangements, cash and investments, discovery and development of products, strategic alliances, and intellectual property. Various risks may cause Lexicon’s actual results to differ materially from those expressed or implied in such forward-looking statements, including uncertainties related to the timing and result of clinical trials and preclinical studies of our drug candidates, our dependence upon strategic alliances and ability to enter into additional collaboration and license agreements, the success and productivity of our drug discovery efforts, our ability to obtain patent protection for our discoveries, limitations imposed by patents owned or controlled by third parties and the requirements of substantial funding to conduct our drug discovery and development activities. For a list and description of the risks and uncertainties that we face, please see the reports we have filed with the Securities and Exchange Commission. I will now turn the call over to Dr. Sands.

Thank you Alex and good morning everyone. We would like to spend most of this call discussing two important new sets of data relating to our lead programs, LX4211 in diabetes and telotristat etiprate in carcinoid syndrome. So the first part will be focused on LX4211 and a detailed analysis of the very recent presentation of our data at the American Heart Association Annual Conference, which was today. For that discussion, I will turn Brian Zambrowicz and lets go ahead and begin with that. Brian?

Thank you Arthur and just to remind everyone, LX4211 is a first-in-class dual inhibitor of two glucose transporters, SGLT1 and SGLT2; and SGLT2 is the major transporter involved in glucose re-absorption in the kidney. SGLT1 is the major transporter involved in glucose uptake in the gastrointestinal tract after a meal. And it is SGLT1 component of the mechanism of action of LX4211 that differentiates from the selective SGLT2 inhibitors. Next slide. I would like to remind you again that design of the Phase 2b study was done in patients with uncontrolled diabetes on metformin monotherapy. There were 299 patients enrolled and there were five arms, placebo and four different doses of LX4211 were explored; 75 milligrams once a day, 200 milligrams once a day, 200 milligrams twice a day and 400 milligrams once a day and it was a 12 week dosing period with the primary endpoints being changed from baseline in HbA1c at week 12. Next slide. These are few slides to remind you the topline data, first of all, the effect of LX4211 on hemoglobin A1c overtime. We are going to focus in these slides specifically on the 200 milligram dose group in blue and the 400 milligrams once daily dose group in black. We are very pleased to see a robust effect on hemoglobin A1c particularly with the high dose group in black where we have 0.95% reduction relative to a minus 0.09% reduction in green for placebo. We saw a minus 0.52% reduction in the 200 milligrams once daily dose group in blue and we are really struck by this large improvement in HbA1c between the 200 and 400 milligrams once daily dosing groups and an additional 0.43% reduction in hemoglobin A1c. If we go to the next slide, we saw a very similar pattern for the effects of LX4211 on fasting plasma group care, so again if we focus on the blue line which is the 200 milligram once daily dose group and the 400 milligram once daily dose group in black, you can see that we got a jump from 17.5 milligram per deciliter drop in fasting plasma glucose in the 200 milligram dose group to minus 28.1 mgs per deciliter in the high dose group; yet again, a very nice improvement as we saw what HbA1c in the fasting plasma glucose as we move between these two doses. On the next slide then, the last of the topline data that I will show you, we had looked in every patient using a spot check at the ratio of glucose to creatinine, and what we have seen is in green a very low glucose to creatinine ratio as expected in placebo, where we are not inducing urine glucose excretion. And very little effective low dose group in gold, but what was quite apparent is that we got a maximal effect on this glucose to creatinine ratio with the low dose group in blue, 29.64 grams per gram. And as we pushed those to 200 milligrams BID in red or 400 milligrams once daily in black, there was no further increase in the effect on SGLT2. So we had a maximum effect on SGLT2 in the 200 milligram dose in blue with pushing the dose giving no further SGLT2 benefit. And If we then contemplate what we just described for the effects of LX4211 on both HbA1c and fasting plasma glucose, we got a very nice improvement, an additional improvement in both measures as we move between those two doses; suggesting that that improved benefit between the two doses was mediated by in addition of SGLT1. We go to the next slide now, on the new data we presented today inferred very importantly additional measures that we used to measure the effect of LX4211 on SGLT2 in addition. So in addition to the spot check I just described to you, we did a sub-study including about a third of the patients in each arm with 24 hour urine glucose collection. And in this slide, we have done the same glucose to creatinine ratio, but it’s done on the full 24 hour urine glucose collection. In green is the baseline measure, in grey is the day one measure, they want the dosing in, in red is the week 12 measure. What stands out very clearly is if you look at either in grey, the day one measure or in red the week 12 measure we are seeing the exact same pattern as we had previously observed with the spot check of the glucose to creatinine ratio. We are seeing a maximal effect at the 200 milligram once daily dose group, and as we push the dose there's no further effect on this glucose to creatinine ratio, no further effect on SGLT2. If you go to the next slide we also measured the total 24 hour urine glucose excretion in grams. And again if you look at the pattern overall with green being base line, gray is day one of dosing and red is week 12 of dosing. Again with this total urine glucose excretion measure we are again seeing the same pattern of maximal effect at the 200 milligram once daily dose. And as we push the dose to 400 milligrams, if anything there’s a reduction in urine glucose excretion over 24 hours. With the total urine glucose excretion for the 400 milligram dose group being about 56 grams on day one and 57 grams at week 12. This is very intriguing because it represents about half of the urine glucose excretion that is achieved with some of the selective SGLT2 inhibitors, and again now we believe this confirms and builds the data, the top line data demonstrating that LX4211 provides a clinically meaningful benefit through the inhibition of SGLT1. And this SGLT1 effect continues to differentiate LX4211 from the selective SGLT2 inhibitors. I do want to emphasize that this effect on the SGLT2 is in spite of systemic exposure increasing dose proportionally as we move between the 200 milligram once daily dose and 400 milligram once daily dose. We believe that we do have a full inhibition of SGLT2 in the kidney, but this low urine glucose secretion is due to the profound effect of SGLT1 inhibition and post-prandial blood glucose levels, and because of these much lower post-prandial blood glucose levels there's simply less glucose to be filtered in the kidney and released in the urine. If you go to the next slide, we also use the 24 hour urine glucose measure to look at the total urine volume and what we see here is in gray is the day one measure and in red is the change from base line to week 12. We first looked at the measure on day one in gray, where you can see its clearly the 200 BID and 400 milligram dose groups have a transient elevation in total urine volume on day one. But if we then focus on the red, the week 12 measure, we see that both of those high dose groups particularly the 400 milligram once daily dose group by week 12 has virtually the same urine volume as placebo. And this is the same thing we observed in our Phase 2A study where we saw very transient elevation in total urine volume on the initial day of dosing, but by day 28 of that study we really saw no difference in total urine volume relative to placebo. If you go to the next slide, I just want to remind you of the very favorable safety profile we observed in the Phase 2B study. If you look at overall the subjects with at least one adverse event; you can see that the percentages were vehicle similar across all dose groups and placebo. We saw a 66.7% adverse event rate on placebo and for every dose group of LX4211, we saw the same or lower frequency of adverse events. In fact in high dose group, it was 57.6%. We do believe that this in general lower frequency of [As] on LX4211 is likely [real] and largely due to decreased events such as worsening type 2 diabetes and hyperglycemia. We were particularly interested in FX and GI. There had been concern that SGLT1 inhibition could lead to GI adverse events such as diarrhea and other adverse events, and we're pleased to see in general the GI adverse events appear to be very similar on all the dose on LX4211 and placebo. With a 20% rate of GI adverse events on placebo and a 22% rate on high dose of LX4211 Of course we are also interested in the effects of SGLT2 inhibition with LX4211 on generally urinary tract infections because of the elevated urine glucose excretion. We're pleased to see that we have no signal for urinary tract infections. We had one adverse event on placebo and one on three of the four dose arms of LX4211. We did have a small signal for general tract infection, where we had zero on placebo and three on the high dose of LX4211. But we believe this is a relative low general infection rate relative to the selective SGLT2 inhibitors and now we think there is clearly and firmly a mechanistic reason for this promising safety data and that’s because we have much less urine glucose excretion then is being created with the selective SGLT2 inhibitors. Going to the next slide then to summarize the Phase IIB study; [dual] SGLT1 and SGLT2 inhibition with LX4211 demonstrated the clinically meaningful improvement in glucose control with consistent reductions in systolic blood pressure and body weight without increased risk of hypoglycemia. Clearly now we have solidified this interpretation that the urine glucose excretion was maximized to 200 milligram dose group and clearly suggesting that the further benefits we see in HbA1c in fasting plasma glucose with the high dose 400 milligrams of LX4211 is mediated by SGLT1 inhibition and I think firmly demonstrating that this SGLT1 inhibition is clinically meaningful in this study. We do see a favorable generator urinary and gastrointestinal side effect profile. It appears that we have added the SGLT1 inhibition without adding any significant additional GI adverse events, and we believe that the generator urinary infection safety profile is very promising at this point than again we believe it’s explained mechanistically by this lower urine glucose excretion. We will require a longer term Phase III studies to really nail down and further confirm both efficacy and safety effects of LX4211. Next slide, then I will remind you that we do have a couple of ongoing studies; we have an ongoing re-impairment study. We believe this is a very important differentiating study for LX4211. We do know that selective SGLT2 inhibitors have limited efficacy in this specific diabetes population, because as patients loose kidney function and their glomerular filtration rate declines and they no longer can benefits from SGLT2 mechanics of action. However, the decreased kidney functions should have no affect on the ability to benefit from SGLT1 edition, so we think that this is a perfect copulation to test LX4211, and this is a small study point [station] and we’ll be treating with the high dose of LX4211 placebo over seven days and this will be very important as we - useful in guiding us for Phase III studies to look at the differentiating affect of LX4211 in the patient population. We are also very instead on the next slide, in type 1 diabetes. LX4211 has two important insulin independent mechanics of action. First of all, where we seen glucose in the urine through SGLT2 inhibition does not require insulin, and then much of the affects of SGLT1 edition in blocking glucose up tick from the GI is not dependent our insulin as well. So we believe both of these mechanisms can benefit of type 1 diabetic. We think in oral [region] could be very useful in combination with insulin in enhancing hypoglycemic control and reducing insulin needs, and we believe we can help these patients reach to HbA1c target. Targets with less hypoglycemia and potentially less weight gain and reduced insulin usage. Its 30 patient study we’ve just initiated. We will be treating for 28 days and our primary endpoint is reduction in total insulin usage. Secondary endpoints as it relate to improved glycemic control. And just to summarize, our goals of establishing a differentiated profile for LX4211. We believe the Phase 2B data again differentiates LX4211 in showing very robust glycemic control, very robust effects on HbA1c. We've already spoken to, we believe we will be in an ability to differentiate in the renal impaired and Type I diabetes. In addition because of these unique dual mechanisms of actions and effect of LX4211 and SGLT1, we do believe we have a unique synergy with DPP-4 inhibitors due to our ability to elevate the release of GLP-1 from the gastrointestinal tract and the effects of DPP-4 inhibitors inhibiting the breakdown of GLP-1. Of course, we’ve demonstrated that in mechanistic study in Type II diabetics and we are eager to further those studies in Phase III. We do have this very favorable safety profile to-date both good GI tolerability, no hypoglycemia and a very favorable genitourinary safety profile. And we think there is a good potential to demonstrate cardiovascular benefits due to the effects of LX4211 both on glycemic control but also the effects on improving blood pressure and body weight. And we are continuing to be on track to initiate Phase III in the first half of next year. With that I'm going to turn it over to Pablo Lapuerta who will cover our most recent data on (inaudible) in carcinoid syndrome.

Thank you Brian. (inaudible) is a serotonin synthesis inhibitor. To understand, added (inaudible) the Tryptophan hydroxylase enzyme that produces serotonin. It’s absorbing to the peripheral circulation but does not cross the blood brain barrier. And that gives the opportunity for Tryptophan hydroxylase to be used in the treatment of carcinoid syndrome. This syndrome resulting from metastatic carcinoid tumors that’s a life threatening tumors that produce large amounts of serotonin causing diarrhea and flushing pain and cardiac vascular disease. So let's just elaborate it as Fast Track and Orphan Status from the FDA, as Orphan status from the European Medicines Agency. We also have a (inaudible) on going with telotristat etiprate and ulcerative colitis. Recently, we presented at the North American Neuroendocrine Tumor Society results of the open-label Phase 2 study in patients with carcinoid syndrome. This was a 12 week open-label dose escalation studies, patients started on a 150 milligrams three times a day and over the course of the trial increased to 500 milligrams two times daily and spent the last six weeks of the study on the 500 milligrams two times daily dose. The patients have been offered an open-label extension. 15 patients are studied; these are patients of carcinoid syndrome and a minimum of (inaudible) per day. On the next slide, I have the results for bowel movement frequency and the new bowel movement frequency in the patient population was around 6,000 units per day. There were some benefits that were statistically significant even in the first one to two weeks with telotristat etiprate but over time as patients continued on therapy and as the dose escalated, the bowel movement reductions increased an increase in magnitude until we reach a point where the bowel movements reductions goes over 40% patients starting with about 6,000 units per day and then the upwards 3.3. The next slide has individual patient bowel movement treatments response in (inaudible). What you can see is that the vast majority of patients had drug reductions in bowel movement frequency and our experience with telotristat etiprate patients with carcinoid syndrome with a reduction of 25% in bowel movement frequency and frequently the vast majority of patients achieved that by week 12. The next slide has (inaudible). The improvements in still consistency followed post in the reductions in bowel movement frequency and so patients sensored with (inaudible) this 20% improvement from baseline to weeks 11 to 12 is clinically meaningful. We also saw in the next slide good reductions in the urinary 5-HIAA. We saw some results in the first two to four weeks but as patients stayed on the therapy longer and as the dose increased, the reduction in urinary 5-HIAA improved until it reaches a point at 72% at weeks 11 to 12, which is a good evidence of inhibition at serotonin synthesis. Patients also saw a reduction in flushing. We saw a patient flushing and we saw a 37% change from baseline in weeks 11 to 12, we saw the same pattern. Early results will give us statistical significance and yet they (inaudible) totally duration of therapy. The main abdominal pain and discomfort this was rated on a scale that will led up to 10 points and the baseline is around two points. So the less abdominal pain in this calculation as an average was not very prominent and the results were not statistically significant but followed the same overall binary trend that’s almost a 20% reduction in abdominal pain and discomfort on this rating scale. The next slide has the efficacy summary for open-label study. A newly profound reduction in bowel movements per day from 5.9 to 3.3, reductions in (inaudible), improvements in still form from (inaudible), reductions in urinary 5-HIAA and adequately reported by patients. At the end of the study, nine out of 12 patients reported adequate [release] for their syndrome gastrointestinal symptoms. Perhaps most importantly was the safety experience in this study with more patients going for a longer-term treatment? Here we have the overall summary of adverse events; these patients had many gastrointestinal symptoms and a lot of diarrhea from the carcinoid syndrome. So most outpatients had at least one treatment modules of adverse events. However, only half of those had adverse events that the physician felt it might be related to the therapy. There were three that were serious that were gastrointestinal related and before that were rated severe. However, although these are gastrointestinal adverse events, the serious and severe from physicians felt they were not need to telotristat etiprate treatment. There were no events that led to the discontinuation and there is no (inaudible) in the study. So overall, the safety experience are encouraging. The next slide gives a little bit more color on the adverse events during the study. Organizing this into adjust gastrointestinal disorders and vascular disorders, we paid special attention to diarrhea, we saw a very little diarrhea during the study and we see a general pattern where there might be one or two adverse events in week one or two I mean generally as the study progresses and even cure. This is the sign of good tolerability. We look at vascular disorders because of flushing and there was only one case of flushing that was considered in adverse event. Moving onto the next slide, we have some more information in terms of investigations, these patients have metastatic disease often have [infusions] and enzymes, but we saw no constraints with the use of telotristat etiprate in this population. It was like another system disorders, and mostly telotristat etiprate does not cause the blood brain barrier and we wanted to make sure that there was no issue with anything like depression and we just had a few case of dizziness and headache. So on the next slide, we have our summary, telotristat etiprate is well tolerated in all those levels and 11 to 12 weeks, and patients spending half the time at this 500 milligram of two times daily dose. There were treatments casted along those events, they were not (inaudible) intensely they are consistent with the profile of patients having intestine carcinoid syndrome and were not related to study drug. We look at improvements in clinical symptoms and we saw a very consistent picture of evidence of patients responding to therapy and clinical symptoms and urinary 5-HIAA levels. I mark it as serotonin synthesis inhibition. And this 12 weeks study is generally consistent with the results of our four week study. We experienced in the first four weeks of the placebo-controlled study in the US, match very well with the first four weeks of this open label study that we conducted in the EU. Almost all the patients are continuing into long-term extensions, continuing to receive our telotristat etiprate. This open label study in Europe is as we produced the favorable benefit gross results, as we saw in our placebo controlled study in the US and so together, this open label study and our placebo controlled study support advancements in pivotal registration trial. On the next slide, we have initiated our Phase 2 study. We are very pleased to hold our investigator meeting recently to have site open in screening patients. We plan a pivotal study for Phase 3 with a 12 week treatment period amassing the experience what we saw in the European open label study. The telotristat etiprate have three arms, there will two doses 250 milligrams two times daily, 500 milligrams two times daily and placebo. We hope to improve to approximately 105 patients and we will be focusing on the reduction in the number of bowel movements. Essentially there are endpoints to look at still consistency in urinary 5-HIAA which in our experience have trended in the same direction. As a reminder, I would like to provide a brief update of our telotristat etiprate Phase 2 study in ulcerative colitis, that's on the next slide. We want to see if we can establish proof-of-concept. We have favorable preclinical data suggesting that telotristat etiprate maybe beneficial in ulcerative colitis and we started enrolling patients into parts of Phase 2 study of the relationship between starting time and efficacy of ulcerative colitis. These are patients with mild to moderate ulcerative colitis treated through placebo 500 milligrams once daily and 500 milligrams two times daily. All these patients have ulcerative colitis that merits (inaudible) and they continue on the (inaudible) throughout the study and we are looking at standard efficacy measures for ulcerative colitis program. Enrollment is progressing very well and we are satisfied with the conduct of the study so far. On the next slide, we have some of our upcoming clinical milestones. We have had a very busy year in 2012 as we settled some important stats with our Phase 2b results in diabetes. Results that we announced previously in rheumatoid arthritis and glycoma and telotristat etiprate continue Phase 2 and starting Phase 3. In 2013, we will have more results from LX1033 our drug for the treatment of irritable bowel syndrome. We will have results from ulcerative colitis studies, the telotristat etiprate and more results from LX4211 diabetes because of ongoing impairment and Type I diabetes studies we will be reading out. With that I would like to hand the call over to Jeff Wade.

Thank you Pablo. I will provide a brief financial update. As indicated in our press release today, we had revenues for the three months ended September 30, 2012 of $0.4 million consistent with the prior year period. Our revenues of $0.9 million for the nine months ended September 30, 2012 reflected a 42% decrease from $1.5 million for the prior year period. Our research and development expenses for the 2012 third quarter decreased 2% to $19.2 million from $19.7 million in the prior year period. The decrease was primarily attributable to decreases in lab supply personnel and preclinical costs, partially offset by an increase in clinical development costs. Our R&D expenses at $61.6 million for the nine months ended September 30, 2012, reflected a 3% decrease from $63.7 million for the prior year period. A connection with our acquisition at Symphony Icon we made an initial estimate of the fair value of our liability for base and contingent payments. Changes in this liability based on the development of the programs and the time until the payments are expected to be made are recorded in our consolidated statements of operations. During the third quarter, we exercised our option to pay the full $35 million balance of the Symphony Icon base payment in shares of Lexicon stock. As you may recall, we have the obligation to pay this amount on or before July 30, 2013, and we have the right to make a payment a 100% in stock through July 30, 2012. After that time, we would have been obligated to make at least half the payment in cash. The stock price used to calculate the number of shares issued $2.644 cents was the average of the closing prices of our stock over the 20-training day period ending immediately preceding the second trading day before the July 30th, payment date. Based on that stock price, we issued 13.2 million shares of stock in satisfaction of the $35 million dollar balance of the Symphony Icon base payment. The only remaining payment obligations we have under the Symphony Icon arrangement are contingent on certain success based milestones either on our receipt of partnership proceeds in which they are eligible to receive the share, or on our receipt of U.S. regulatory approval for products that were funded by the Symphony Icon partnership. The associated increase in fair value of Symphony Icon Purchase Liability was $5.8 million in the third quarter and $10.1 million for the nine months ended September 30, 2012. Our general and administrative expenses for the 2012 third quarter were $4.4 million, an increase of 8% from $4.1 million in the prior year period. The increase was primarily attributable to increases in personnel, legal and patent related costs. Our G&A expenses of $13.1 for the nine months ended September 30, 2012 reflected a 2% decrease from $13.3 million for the prior year period. Our net loss for the 2012 third quarter was $29.5 million or $0.06 per share compared to a net loss of $26.1 million or $0.08 per share in the prior year period. Our net loss for the nine months ended September 30, 2012 was $85.3 million or $0.18 per share compared to a net loss of $82.4 million or $0.24 per share for the corresponding period in 2011. For the three and nine months ended September 30, 2012, our net loss included non-cash stock based compensation expense of $1.6 million and $4.9 million respectively. For the three and nine months ended September 30, 2011, net loss included non-cash stock based compensation expense of $1.4 million and $4.4 million respectively. Let me now turn to our cash and investments. As of September 30, 2012, we had $206.8 million in cash and investments as compared to $231.5 million as of June 30, 2012, and compared to $281.7 million as of December 31, 2011. After the end of the quarter, we completed the public offering and sales of 17.5 million shares of our common stock at $2.25 per share. The net proceeds of the offering after deducting underwriting discounts and offering expenses were approximately $37.2 million which will bolster our cash position going forward. Now let's turn to our forward looking financial guidance for 2012. We continue to expect contractual revenues from existing agreements in 2012 of around $1 million. Consistent with our past practice, while we are in conversations with pharmaceutical companies about potential collaborations and alliances, we are not including forecasted revenues from those potential arrangements in our guidance. That said, we believe our productive pipeline provides Lexicon with attractive opportunities for future alliances. We continue to expect operating expenses in 2012 to be in the range of $110 million to $120 million. Non-cash expenses are expected to be approximately $21 million of this total, including $11 million in increase in fair value of Symphony Icon Purchase Liability, $6 million in stock based compensation and $4 million in depreciation and amortization. Taking into account cash received under existing contractual relationships only, we expect our 2012 net cash used in operations to be in the range of $93 million to $98 million consistent with previous guidance. I will now turn the call back to Arthur.

Thank you, Jeff and we can now take questions.

(Operator Instructions). Our first question comes from the line of Cory Kasimov with JPMorgan. Matt Lowe - JPMorgan: Matt Lowe, in for Cory today. Just a couple of questions. The first one is just around the partnering talks of 4211; I am just wondering how those talks are coming along; any specifics you can share with us in terms of what you might be looking for from a partner, timing or anything like that? And then secondly, if you could just outline the market opportunity for carcinoid syndrome that would be great? Thank you.

Thank you Matt. I will just lead off by saying that the whole process is proceeding very, very well. It’s a robust process and I think for some of the more color and detail we can turn to Jeff who is actually leading the process on our behalf. Jeff?

So as Arthur mentioned, we've been very pleased with the process overall and with it’s progression. And it continues to be our objective and expectation to complete a partnership before Phase 3 launch and we are continuing to work towards Phase 3 launch in the first half of 2013 from that perspective.

There was also a question about structure and…

Yeah, we are talking with companies about, we are still talking to companies about different types of structures at this point and so our key is to progress the program forward. We are obviously expecting a partnership to be a big driver in terms of funding that development program going forward.

And then the next part was on carcinoid syndrome.

So carcinoid syndrome is a disease that affects approximately 10,000 patients in the US and it’s proportionately similar in Europe. There are a sizeable proportion of those are refractory to existing therapy which is a octreotride therapy and our trials have been designed to address that refractory population. So we are going in on top of octreotride therapy. Typically, we are told that people who have carcinoid syndrome get some relief initially usually from octreotride therapy and then with then 12 to 24 months on average they cease to get relief from that and it’s a long disease that people suffer with for a long time and they continue on octreotride therapy for a number of years and we will be going on top of that in the patient population that is not achieving adequate relief. So we think it’s a meaningful and substantial market opportunity for Lexicon and one that we can address on our own and which is why we are taking it forward in Phase 3.

Your next question comes from the line of David Friedman with Morgan Stanley.

(Inaudible) Just a follow-up on the last question regarding your partnership for 4211, it sounds like you guys are planning to go forward into Phase 3 no matter what, is that correct, and if that's the case do you feel like securing a partner while the Phase 3 is ongoing is a possibility or if we don't see a partnership before that Phase 3 starts are we then going to wait for the Phase 3 data to potentially see a partnership. Thanks.

So I think our expectation and our plan is to have a partner in place before we launch Phase 3. It’s an expensive development program and that's our plan and that's our expectation, and we will expect to have that in place before we actually launch the studies.

Your next question comes from the line Liana Moussatos with Wedbush. Liana Moussatos - Wedbush: Can you give us an idea when we would expect data from the Phase 2 LX4211 in renal impaired and the Type 1 diabetes Phase 2, and then also, I know it's longer-term but the Phase 3 for carcinoid and the Phase 3 for diabetes, would that be more of end of 2014 or 2015?

Okay, So Pablo I know you that your remote location there at the AHA meeting, would you care to comment on the first part of that regarding the 4211 results and renal impaired and type 1?

Yes. For real impairment, we're actively recruiting several size, it's up and running, and we hope that we can recruit within the next four months and so patients are treated for only about a week. So we would have results for you in the first half of 2013. The same thing with LX4211 and type 1 diabetes. We recently initiated a study, we got several sites up and running and it's a study of a similar size to that in renal impairment and hope we can have results in the (inaudible) timeframe. So sometime in the spring of 2013.

Excellent. And then the second part of the question was regarding the completion, the enrollment period for carcinoid syndrome, we're forecasting 18-months of enrollment period from initiation, which would make the total study time to completion approximately two years from now. And then the 4211 Phase 3 plan Pablo in terms of that’s a farther out to forecast, but you want to comment on the planning with regard to timing and the completion of that study of 4211.

Yeah these Phase 3 programs in type 2 diabetes have generally taken around 3.5 years, and we’ve looked at our program which is a similar size to others and these really can be done in a similar time frame. And so that means that we will have a filing sometime in 2016. Liana Moussatos - Wedbush: Any new products coming in the clinic next year?

Brian do you want to comment on those (inaudible).

Sure. We believe we will have one; we have a diabetes programs that’s come along it’s an SGLT1 inhibitor that remains in the gastrointestinal track produces virtually no systemic exposure and new urine glucose excretion. And we think it may be a particularly a [peeling] agent for the renal impaired where since I can’t benefit really from the SGLT2 inhibition there is no sense in bringing drug on board. And then in addition we think that there may be patients who don’t tolerate the SGLT2 inhibition due to increased infection susceptibility. So that compounds working really good. We have currently IND enabling studies. Liana Moussatos - Wedbush: Do you have an LX number for that.

Yes, it’s LX2761.

Your next question comes from the line of Alan Carr with Needham & Company. Alan Carr - Needham & Company: A couple of them; one of them in your discussions with pharma. I am wondering, if you can give us a sense of where their priorities are in terms of get around a doubled SGLT2, SGLT1 inhibitor, are there certain parameters where you’ve realized your HbA1c that ranked higher than others. And then also I am wondering in your longer term extension for Telotristat and carcinoid syndrome and extension trail their, can you comment on any of the efficacy trends in the longer term and did they flattened out or are there continued improvement since some of those parameters?

Okay, Brian. We want to take the first of that.

Sure I can comment. I think that in our discussions with pharma, I think that at this point quite convinced of the meaningful affective SGLT1 edition and obviously I think they are pleased with the robust effects we get with LX4211 on glycemic control. Obviously they consider the blood pressure and [late] affects of peeling as well. But I think what stands out is that we have multiple opportunities for differentiation, that there is clearly the opportunity to straight up differentiate based on overall glycemic control on HbA1c effect. There is an opportunity to differentiate on safety and I have given you the mechanics of reasons why on any adverse events way to here in glucose excretion should be less with LX4211 and with the selective SGLT2 inhibitor. And then we have these other opportunities in the renal impaired that can back [safe] from SGLT2 in addition in type 1s with the two and mechanism of LX4211 and it’s the unique synergy with DPP forum. And I think, so overall it’s a very appealing package and I would even argue that not only do we have multiple opportunities to differentiate, but I think we have a very strong possibility on differentiating on every one of those.

And I think the second part of the question was on the durability of the activity of telotristat etiprate in carcinoid syndrome at least as we see it currently in 12 weeks which is the same treatment period for our Phase 3 program. Pablo do you want to comment on what you see in the trends.

Yeah, so the overall trend that we saw upto 12 weeks is an improvement in efficacy over time as patients went up in dose and took the drug along the (inaudible). We do have some experience now with long term extensions and there is one patient who has even taken telotristat etiprate for over two years it’s a long term extension, and from that we are comfortable with the profile that we are seeing and it seems that patients are maintaining benefits. Alan Carr - Needham & Company: So from 12 weeks and beyond you see the same benefit maintained.

Yes.

Your next question comes from the line of Nicholas Bishop with Cowen and Company. Nicholas Bishop - Cowen and Company: I have a question around the telotristat phase 3 trial design and that is I am not sure that I see an example in your Phase 2 experience of challenging patients immediately with 500 milligram dose and so I am wondering what elements of the trial there are that gives patients the ability to switch arms perhaps or dose deescalate if they have difficulty tolerating the 500 milligrams and just what elements of the trial are on the (inaudible) issue.

Pablo would you like to clarify some of the design points in the trial and regarding dose.

Yes. In the 500 milligram arm patients spend a week first at 250 milligram. It was not fairly necessary, but we chose to do that because we have such good experience of titrated medication in the open label study. In the placebo controlled study, we thought there might be some nausea with an issue being just at the 500 milligram dose and we really didn't see much nausea in the titration regime. So as patients continue on the 500 milligram dose, in the Phase 3 trial we will give the option to [anti] titrate based our discussions with the medical monitor and consideration of issues with tolerability. With the European experience there was only 1 patient that was titrated down from 500 milligrams out of 15. So we feel most patients would be staying at 500 milligrams two times daily. Nicholas Bishop - Cowen and Company: And then just one follow-up, regarding the glaucoma data that you reported in August. Just curios as to whether in your view this rises the level of proof of concept, should we expect to see more data from this compound in the future.

Brian, you want to comment on that.

Sure. First of all we are really pleased as far as the mechanism of action working. So as we went in based on the macro data, we of course have hypothesized that LX7101 would lower intraocular pressure and it did and it significantly lowered intraocular pressure. And secondly our hypothesis based on the genetics was that it would be safer as far as tolerability and than the low kinase inhibitors. And we in fact saw an extremely favorable safety profile. So I think again I think its another example of the (inaudible) predicting what the small molecule inhibitor would do. So we think there is still room to work on the magnitude of the effect. Because of this nice safety window and we will be talking to potential partners and considering what might be the best way to proceed.

Your next question comes from the line of Kevin Kedra with Gabelli & Company. Kevin Kedra - Gabelli & Company: I have a question around partnership talks. Given that, it sounds like it's going to be more of a first [effect] of 2013 event if you guys try to partnership, is the upcoming FDA decision on (inaudible) playing any role there or company’s waiting to maybe read out how the FDA is looking at that product before they instead of making an investment in another drug in the SGLT class?

Yeah, I don’t really think so. I think that the data that they presented so far is not really totally relevant because we're operating on to different mechanism with the dual mechanism but I think that and so I think that progression of discussions don’t really, are not really affected by the timing of the J&J, but we don’t expect them to be affected by the timing of the J&J regulatory process.

I want to say that from our discussions, I would say in there is general an acceptance of the fact that the SGLT-2 class is coming and it's inevitable and there is, we never really gotten into a discussion that those sort of events would getting, for what we're talking LX4211? Kevin Kedra - Gabelli & Company: Okay, and in regards to the recent cash raises, I was wondering if you could just give a little bit more clarity I want know what your motivation was for that, was there specific upcoming trials that you were thinking about or was this just sort of an opportunistic raise? And perhaps along that line when you think about LX1033 I know that we are going to get the read on the Phase II next year but if that data come in positive and you like what you see is that a program that you would consider taking to Phase III yourself or would that be partnered out?

So I think I can address both those questions. So, one of the reasons for doing this capital raise was to allow us to pursue a more robust Phase III program for carcinoid and to continue to have a good cash position post the Phase III data for that program. So that was one of our motivating factors in proceeding with those offering. The other thing that it allows us to do is to progress with Phase III preparations for 1033 during the period after we get the data and in parallel with partnership discussions but without delaying the progress to Phase III. I think that our expectation at this point anyway would be that we would partner that program. Ultimately, I think that it is an indication where partnership makes a lot of sense and I think our current expectation would be that we have partner that before we get fully into the Phase III program, but this does allow us to make those preparations without having to delay while we are having those partnership discussions.

Thank you for your question. Are there any other questions?

Your next question comes from the line of Stephen Willey with Stifel Nicolaus. Stephen Willey – Stifel Nicolaus: I know you guys are doing some preliminary work in terms of trying to sketch out some at Phase III program for 4211, but I was wondering in your conversations to various potential partners at this point. How much had (inaudible) is there in terms of what people perceive they want to have done in terms of a Phase III program, I guess that is one question and kind of a couple of subparts of that, one, do you get the sense that there are partners that would potentially want to dose escalate beyond 400 mix once daily, just given the fact that you still seem to have decelerating HbA1c and not a facility and kind of dose dependency related [AEs]. And then two, the strategy for exploring a DPP-4 combo, would that be something that would try to be developed using a fixed dose combination or would you imagine that you would be essentially taking two separate pills and maybe lying a quick little bit of bridging study to try to get something fixed dose into the clinic?

Okay, so the three parts. The first part Pablo, if you care to comment on any of the consensus around the Phase III program and our stage, I know you have been directly involved with the EMA discussions and remember coming up on our FDA meetings but go ahead on the overall plans of Phase III first.

Sure, with the Phase III we have seen a lot of agreement among potential partners. And I think part of the reason is because we’ve had so many regulatory interactions. And we started to do this early on in a proactive manner by going to the United Kingdom to Germany and Austria, (inaudible) which questions about the Phase III program and the program that was well outlined, and that gave us a lot of good feedback and it was something that we shared with partners as well. They [start] regulatory minutes, supporting our overall direction including the cardiovascular outcome study in Phase III and since then we've had very recently just two weeks ago are into Phase II meeting with the European Medicines Agency and so we have our own minutes from that and we will be expecting official minutes soon from the European Medicines Agency and we were very satisfied with the interaction and that's something we are sharing with our partners and that's helping both consensus around the program. The interaction with EMA was very favorable in the sense that there were no issues from the bar going forward into Phase III. There was overall acceptance of the program, the dose selection. There were no comments about significant efficacy or safety issues of the 400 milligram dose. So we are waiting for a formal advice and the minutes from the European Medicines Agency but we have a good interaction that helps us go forward in both consensuses with our partners.

The next part of the question was regarding the dose and [outlined] forward with the single dose of 400 milligrams and I think that's actually fairly easy to answer. There really has not been any discussion around that being different and the 400 looks like the logical dose to take forward in the Phase III program. Our partners seem to agree with that and as Pablo indicated so far the regulatory interactions has been consistent there. So that's good I think in the future and later stages of the Phase III program our post filing one could consider exploring other doses but that would be for another day. Then the last part of the question was on the accommodation of DPP-4 and our staging of that in the Phase III, current Phase III plan and any potential plans for fixed dose combinations. Pablo, do you want to talk about the staging of the initial trials?

Yeah in Phase III we do want to have data on we are comparing efficacy and safety versus a DPP-4 inhibitor and so we have that in the program but when we compare ourselves to the DPP-4 inhibitor, we also have a dose sign that will have a combination of LX4211 and the DPP-4 inhibitor. So we hope we’ll able to show synergy as we've done in a smaller mechanistic study that we released last year. And we think that will help us prepare for the eventual development of other fixed dose combination.

In Phase III those would be given as separate agents but certainly given the general dosages of DPP-4 inhibitors and 4211 one could contemplate fixed dose combination in the future. Stephen Willey – Stifel Nicolaus: And I guess along those lines, is it kind of safe to assume that a number of the parties that you are speaking to at this point also have a bit of a budding interest in the DPP-4 space as well?

Yeah, so it’s safe to assume and it’s obviously something that we are navigating as well. So it’s another interesting dimension of the whole set of discussion. So I think you can start to see each of these avenues of opportunities from 4211 when you look at the multiple indications that Type 1 diabetes, renal impairment, the positioning in Type 2 diabetes and then also then the combination of opportunity. It opens up a number of lines of discussions that have to be thought through very carefully and we are progressing those.

(Operator Instructions) Your next question comes from the line of [Zick Bigelow], a Private Investor.

My question was recently answered, I think somebody else asked. I was just trying to get some added color on the capital raise and I think you just talked about it. So thanks.

Okay, listen, thank you all. It's been a very robust question and answer period. A lot of excellent questions. We covered a lot of data today and I think we've taken up a lot of time. So at this point, I think we would like to thank you all and say good bye.

Thank you. This concludes today’s conference. You may now disconnect. Speakers please hold the line.