Oct 27, 2009
Executives
Arthur Sands - President & Chief Executive Officer Philip Brown - Senior Vice President, Clinical Development Ajay Bansal - Executive Vice President of Corporate Development & Chief Financial Officer Brian Zambrowicz - Executive Vice President & Chief Scientific Officer Jason Ray - Manager, Corporate Communications & IR
Analysts
Allan Corn - Unidentified Company
Operator
Thank you for holding. Welcome to the Lexicon Pharmaceuticals third quarter 2009 earnings 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 taped at Lexicon’s request. At this time, I would like to introduce your host for today’s call, Jason Ray, Manager of Corporate Communications and Investor Relations.
Please go ahead Mr. Ray.
Jason Ray
Good morning. I just like to apologize quickly for the extended wait time.
We were experiencing some technical difficulties with the call, but I’d like to welcome you to Lexicon Pharmaceuticals third quarter 2009 earnings conference call. I’m Jason Ray, and with me today are Dr.
Arthur Sands, Lexicon’s President and Chief Executive Officer; Dr. Brian Zambrowicz, Executive Vice President and Chief Scientific Officer; Dr.
Philip Brown, Senior Vice President of Clinical Development; and Ajay Bansal, Executive Vice President of Corporate Development and Chief Financial Officer. We expect that you have seen a copy of our earnings press release that was distributed this morning.
During this call, we will review the information provided in the release and then use the remainder of our time to answer your questions. The call will begin with Dr.
Sands, who will discuss our key accomplishments for the third quarter. Dr.
Zambrowicz and Dr. Brown will then discuss the status of our drug development programs, and Mr.
Bansal will review our financial results for the third quarter and discuss our financial guidance for the reminder of the year. We will then open the call to your questions.
If you would like to view the slides for today’s call, please access Lexicon website at www.lexpharma.com. You will see a link on the home page 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 LX1031, LX1032, LX2931 and LX4211. This call may also contain forward-looking statements relating to Lexicon’s future operating results, financing 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 results of clinical trials and preclinical studies of our drug candidates, our dependence upon strategic alliances and ability to enter into additional collaborations 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.
Arthur Sands
Thank you Jason and I’d like to thank everyone for participating today. We’ve had a very busy quarter here in the third quarter and I think much was accomplished.
Some of the highlights that we’ll discuss today include LX1031, our drug candidate for irritable bowel syndrome having completed the enrollment for the Phase 2a trial, and that was completed significantly ahead of schedule, and we will be discussing the timeline for that. It includes an expectation of our top line data in November, so next month.
The second point, during the quarter it was very exciting to initiate a new Phase 2 trial of rheumatoid arthritis, LX2931 and this was initiated first in the United States. I was happy to be able to participate in the investigator meeting that took place in August.
I think there is real enthusiasm for that program and we’ll be discussing the progress of that today. Then third, we completed our Phase 1 trial of LX4211, and also initiated the Phase 2a trial in patients with type 2 diabetes, so two important initiations in the third quarter.
Then lastly most recently in October, we completed a public offering of stock of following offering, which resulted in net proceeds of $55.2 million invested in the company. That was a very important event.
I think a significant step in our financing strategy, and it really allowed me and our management team to branch out and meet with new investors. We have significant new investors involved in the financing, as well as very significant current investors that have an ongoing strategy by investing in Lexicon.
It did allow us to share our mission and strategy more broadly, and of course we were very fortunate to find investors who wanted to participate in bringing new mechanisms of the action into drug development, which is our mission. As well to take the portfolio approach which we’ve taken, to have multiple candidates moving through in our clinical development and multiple drug discovery candidates as well.
So we remain on track with our mission and strategy to discover breakthrough treatments for human disease, and we now have a broader investor base participating. The pipeline is proceeding and we now have four drug candidates in Phase 2 clinical trials, with the two recent advancements that I mentioned, LX2931 in RA and LX4211 in diabetes, and we’ll focus the call on these update.
If we look at the upcoming milestones anticipated over the next 12 months, each of these four programs we believe will have important data readouts from these first in patient trials, these proof of content trials. So around the corner is LX1031, again, the top line results anticipated in November.
Then we see LX4211 our type 2 diabetes compound proceeding with results in the first quarter of 2010. Then we turn to LX1032 in carcinoid syndrome results anticipated there in mid 2010, and LX2931 on a similar timeframe mid 2010.
So a very important 12 month period as we look to readout from these four drug candidates operating on our mechanisms in the clinic. So with that introduction, I’ll turn the call over to Dr.
Zambrowicz and Dr. Brown and the format we’ll use here is a slightly different one form past calls.
I’m going to ask Dr. Zambrowicz to give a brief scientific overview of each program and then Dr.
Brown will proceed with the clinical development updates. Brian.
Brian Zambrowicz
Thank you, Arthur. I’m on the slide entitled LX1031, a new drug candidate for irritable bowel syndrome.
LX1031 is an inhibitor of tryptophan hydroxylase, the rate limiting enzyme in serotonin synthesis. Most of the body’s serotonin is produced by enterochromaffin cells that are dispersed along the lumen of the GI tract or EC cells as you can see in the diagram to the right.
One of the unique characteristics of the LX1031 compound is that, it was designed to be locally acting on the GI tract, where it can hit the EC cells and inhibit serotonin synthesis without giving systematic exposure. This was important we thought to maximize the safety of the compound in this indication, and that safety has been supported by both our pre clinical and clinical data today.
The function of serotonin in the GI tract is both to increase the motility, as well as to signal feelings of GI’s comfort to the brain, and so by decreasing serotonin one would expect both deceased motility as well as decreased feelings of GI comfort. On the next slide, there is growing evidence that abnormal serotonin signaling may play a role in the irritable bowel syndrome.
This graph was taken from a paper by acting cyanidol, and in this study what they did is, they measured serotonin levels in the blood on the Y axis after a meal, and they did their study in IBS-D patients in the closed circles, and helping normal in the open and triangles and in IBS-C patients in closed. What you see is, after a meal IBS-D or diarrhea predominant IBS patients had elevated levels of serotonin relative to healthy normals, while IBS-C or constipation predominant IBS patients have lower levels than the health normals.
This suggests abnormal signaling, but it also suggests that bring these IBS-D patients their serotonin levels back into the normal range to benefit them. On the next slide, there is also generic data that support this concept, that abnormal serotonin signaling may play a role in IBS.
In this study, they looked at polymorphisms in the serotonin 5-HT3E receptor, and they found that there was a polymorphism in this receptor or gene for this receptor that was associated with IBS-D in females. It turns out that this polymorphism is thought to up regulate the expression of this receptor for serotonin in parasites that line the GI tract, and one could imagine that this would make them hypersensitive to serotonin signaling.
The final bit of generic evidence on the next slide is the association between polymorphism and the serotonin trial quarter [ph] and IBS-D, and what they found in this study was that polymorphisms that resulted in decreased expression of the transporter were associated with IBS-D. The decreased expressions would cause enhanced or up regulated serotonin signaling in the GI tract, again, together between the biomarker data and the generic data suggesting this up regulation of serotonin signaling in IBS-D patients.
With that, I’ll turn it over to Dr. Phil Brown.
Philip Brown
Thanks very much Brian. Well, clearly IBS represents a very common disorder.
Some estimates suggest that up to 20% of the US population is affected or experiencing symptoms consistent with IBS. As Brian just described, LX1031 really represents a novel approach to influencing a number of the symptoms that these patients experienced, and it’s first in class compound, and we believe that by reducing serotonin we have the opportunity to influence motility and/or the subjective aspects of the disorder, all of these being very important in the symptom complex of these patients expedience.
IBS really represents an unmet medical need. There are two emerging therapies that are gaining some evidence of utility in both the diarrhea and/or the constipated predominant forms of IBS rifaximin and linaclotide.
Interestingly these are completely different mechanisms or actions for 1031, but they also act locally which underscores, I think the necessity safety profile that’s required to develop drugs in this area. So again, the development goal around 1031 has been to focus on this localized activity of reducing serotonin.
If you move to the next slide, the Phase 2 study which Arthur has just mentioned, completed enrollment ahead of scheduled focused on patients with non-constipating forms of IBS. So it would be either diarrhea predominant or mixed form of IBS.
We randomized 150 patients, in a one-to-one-to-one fashion to placebo, exploring two dose levels of LX1031, 250 mg or 1000 mg given four times daily over a 28 day treatment period, and we are following a number of the symptoms associated with IBS to determine how the drug maybe affecting these parameters. If you move to the next slide, the overall outline of the analysis which we’re currently involved with, obviously the primary objective is to confirm the safety and tolerability profile of the compound that’s been observed today.
So it’s going to be a very important facet for the compound in IBS. We are also obviously tracking a number of both, subjective and objective symptoms associated with the disorder.
We have the opportunity here to continue following the biomarkers of serotonin and its metabolic urinary 5-HIAA, which has been very helpful in our normal healthy studies today, our Phase 1 studies, but as Brian just alluded to, the evolving literature suggesting the generic basis for classifying these patients, we have samples, pharmacogenemic samples that they believe will help identify patients that maybe most likely to benefit from those type of approach. The real purpose of this study of course is to identify the symptoms that maybe influenced by LX1031 and the size of that affect, so that we can better define and plan for future studies.
We are currently in the process of finalizing the data set and we hope to have results from this towards the end of November. The final study report which will involve the very comprehensive analysis that will include both of biomarkers, the pharmacogenomic assessments, as well as the various symptoms will be available in the first quarter of 2010.
Brian, I’ll hand it back to you for 1032.
Brian Zambrowicz
Thank you. I am on the slide entitled LX1032, a new drug candidate for carcinoid syndrome.
A little bit on carcinoid syndrome; it’s a result of neuroendocrine tumors. These tumors typically start in the GI tract, and therefore they contain these enterochromaffin cells which are making large amount of serotonin.
Once they metastasize to the liver, the serotonin is able to reach the GI tract where it causes very severe GI symptoms, as you might imagine, of diarrhea and cramping and discomfort. Now LX1032 is an inhibitor of tryptophan hydroxylase, however it’s a unique chemical entity from LX1031, and it’s also unique from 1031 and that it does gives systemic exposure, which is critical in order to reach the tumors that are typically in the lever.
So this is an interesting program, and serotonin is clearly the driver of the symptoms in carcinoid syndrome, and for unique opportunity to hit its emphasis in the periphery without getting into the brain. We do have fast track status from the FDA, an orphan designation from the EMEA.
On the next slide, is the unique case where there is actually a proof of concept for this target and this mechanism of action for carcinoid syndrome. This is the New England Journal of Medicine Article from 1967, and in this study and in other studies by these authors, they tested a compound called pCPA, parachlorophenylalanine, which is an inhibitor of tryptophan hydroxylas in 16 patients with carcinoid syndrome, and this was effective on 13 of the 16 patients in both decreasing abdominal cramps and pain, as well as decreasing bowel movements.
So it had a good, excellent response. Now the problem with this compound was that it caused depletion of brain serotonin, because it crossed the blood line barrier and so it wasn’t progressed.
If you look at the left on the graph, I think one of the interesting things is the biomarkers that they are tracking here, a biomarkers we’ve already discussed, 5HIA, which is a breakdown part of serotonin. This is in one of those carcinoid patients that gave a response, and you can see that it’s decreased following treatment by about 50%, which is very similar to what we’ve seen with our inhibitor in clinical studies.
Moving to the next slide, I think there is further support again for this mechanism, as far as especially related the discomfort and nausea. pCPA was also tested in humans undergoing chemotherapy, and its prevented chemotherapy and just nausea and vomiting.
In fact Arthur has described it is being a good as if not better than drophram [ph] in controlling those symptoms. On the next slide, more recent data suggests that there may be an actual anti tumor benefit for these carcinoid syndrome patients by treating with the tryptophan hydroxylase inhibitor, and that’s based on this study, where they took nacomiapher [ph], the target tryptophan hydroxylase, and they put colon cancer tumor cell lines into those.
Those tumors were very slow in a lot of animal, however if you rescued the animals by allowing them to produce serotonin, those tumors start to grow again. Phil.
Philip Brown
Thanks Brian. So 1032 really represents the unique opportunity in the setting of carcinoid.
As Brian just described, serotonin’s a primary mediator of the symptom complex that is experienced in carcinoid syndrome. This novel approach will allow a reduction of serotonin in the periphery, which is completed different from current standard of care.
The current standard of care, the metastatic analogs which are injectable proteins, that also influence symptoms but patients develop, they become refractory to this therapy over time, so their symptoms begin to reoccur despite this therapy. Therefore, LX1032 we believe will meet a nice need that’s currently unmet for these patients in helping to moderate their symptoms that reoccur after they develop resistance to this metastatic analogs.
As Brian mentioned, we have recently gained orphan designation by the EMEA, and that has opened Europe as an opportunity for us to take advantage of. So we’re currently evaluating opportunities within Europe, and determining if and how we might be able to further continue the development of 1032 in that study.
As Brian also mentioned, there is an evolving literature base suggesting that serotonin plays a significant role in a variety off disease settings, which we believe may represent opportunities for 1032 as we gain additional information about its utility in the clinical study. If we go to the next slide, these are data from our normal healthy volunteer studies.
Utilizing the biomarker of urinary 5-HIAA, the primary metabolite of serotonin. What we noticed in that study was at the mid dose level of 500 milligrams given once daily, up to the maximum dose we explored 500 mg three times daily, we saw a very similar reduction of urinary 5-HIAA over the 14 day treatment period.
So this is a nice suggestion of what the potential of the drug does in terms of its pharmacodynamic activity, and importantly the mid dose level, and above, all achieved the same degree of reduction, about a 50% to 60% decline of serotonin production, relative to what is observed in placebo randomized subjects. So that’s in the basis for which we’ve identified the dosing going forward into our carcinoid proof of concept study.
This is the double blind randomized placebo controlled study in patients were symptomatic carcinoid syndrome, who have become refractory to the standard of care. The study design is a serial dose escalation in which we’ll asses for both, safety tolerability as well as effectiveness of the compound on a variety of the symptoms these patients experience.
Once that optimal or maximum dose is identified, then we’ll expand the cohort, and each of these dose levels is being explored over a 28 day treatment period. We are currently enrolling patients and the study is progressing at present.
Brian, back to you for 2931.
Brian Zambrowicz
Alright. Then on the slide entitled LX2931, drug committed for autoimmune disorders.
Our LX2931 is an inhibitor of an enzyme called sphingosine-1-phosphate lyase, and to give you a feel for the past where I’ll referred to the cartoon on the right. This is the cell and this pathway, S1P pathway has become I think a pathway of very high interest of weight, especially due to the progress of FTY720 or single limit in multiple sclerosis.
FTY720 is an S1P receptor agonists. Now we had a different plan with the pathway, the lyase as I already mentioned.
The lyase’s function is usually to breakdown the endogenous second messenger sphingosine-1-phosphate. So by blocking the lyase function, one would increase the naturally occurring second messenger.
By hitting this point in the pathway, we think we kind fire our unique sensitivity of action relative to receptor agonists, and we believe that may translates into an improved safety profile. There is clearly an affect of modulating the lyase by trafficking, but there is growing data that suggests that increased S1P levels have affect on the information that go beyond the trafficking effort.
If we go to the next slide, this is an animal model of autoimmune disease caused in mice, and well you can see on the left is, we are measuring the response in this model by the slowing of the ankle or the change in the ankle thickness. In the treated animals and animals treated with LX2931 you can see that our compound is able to block inflammatory response in this model.
What’s very important is, if you look on the right, that’s the lymphocyte counts in animals in the study. What’s I think very important to note is that, in spite of a very modest reduction in circulating blood lymphocytes, we have a very profound effect on getting stimulatory response, and we believe that LX2931 has the opportunity to benefit patients with arthritis, without causing severe immunes oppression.
On the next slide, this is a similar arthritis model, but this is now in the lab. It’s the rate as in this arthritis model, and in this study we did the treatment starting after the disease had reached about 50% maximum inflammatory response.
So it’s in a treatment mode clearly, and what we did is three separate treatments. We on the left treated with methotrexate alone, which are of course used in humans and it’s effective.
We resorted to 3101 in the middle, and then we used the combination of methotrexate for LX2931 on the far right. What you can see is that, neither methotrexate alone or LX2931 alone was able to block the further inflammatory response, but on the right in red, you can see that together they were very effective in blocking the further inflammatory response once treatment again.
The reason we really like this model is because we think it mimics what we are trying to do in our Phase 2a study. We are moving in patients that are feeling on methotrexate, and there quite our symptoms are breaking through, and we’ll be treating on parts of methotrexate LX2931.
Phil.
Philip Brown
Alright. So clearly rheumatoid arthritis represents a very large market opportunity, and we believe the 2931 is uniquely positioned as an oral agent, not only for RA, but for a number of autoimmune or inflammatory conditions, due to its novel immunological inventory types of effects.
Being in oral, we believe it has the opportunity to be utilized prior to moving into the more aggressive biologic therapies that currently represent the standard of care. So we recently presented data at the American College of Rheumatology meeting, relative to our drug-drug interaction study of 2931 with methotrexate.
These data were presented at a poster by Dr. Roy Fleischmann who’s been our primary investigator in this study, and this is a very important study for us, and that it has allowed us to move into the Phase 2a study.
The finding of this is, that there were no clinically significant changes in the pharmackinetics of either methotrexate or 2931, and this underscores the lack of a drug-drug interaction, which was anticipated based on our preclinical studies. In the study 2913 was given over a 14 day treatment period to patients with stable rheumatoid arthritis, who were on incumbent methotrexate.
It was well tolerated, they were very mild, events reported including abdominal pain, nausea and headache, but there are really no clinically significant trims observed with regard to AE profile laboratory assessments or vital signs or electro-cardiogram. So this was a very important next step for us to position the compound to go into the proof of concept study.
It was a very exciting opportunity for us that this meeting and I think based on the traffic we received a poster, and I think that reflects the novel approach to modulating the inflammatory process in this setting, and really the lack of emerging therapies in this area. Our Phase 2a study is designed as a double-blind randomized placebo controlled study, that’s looking at 2931 in combination with methotrexate.
We are anticipating enrolling up to 120 patients. As Arthur mentioned in his introduction, this is being conducted both in the US, as well as Eastern Europe.
We are exploring three dose levels of LX2931 70 milligrams, 110 milligrams and 150 milligrams, all given as once daily over a 12 week treatment period. This is a very standard study design at this stage of development with the primary efficacy on point being the ACR20 at week 12.
We are evaluating a number of secondary endpoints that include all the ACR assessments, ACR 2050 and 70, as well as the DAF 28 scoring at weeks four, eight and 12. We are anticipating the study being completed in mid-2010.
As Author indicated, we’ve had a good initiation of this program, and we believe that it should be able to achieve that sort of timing goal. Now to LX4211.
Brian Zambrowicz
Thanks Phil. I’m on the slide entitled LX4211, a mid drug candidate for diabetes.
I will point out that this is the only program that we are working on, where we are not first and fast either in the clinical pipeline, and I’ll try to explain why that is. We believe this is an extremely compelling mechanism for treating type 2 diabetes.
If you refer to the picture on the right, it describes SGLP2’s function. So the kidney normally filter the blood and removes impurities which are then excreted in the urine.
Typically glucose passes right through the glamelioila [ph] and it’s the SGLP2’s job as a glucose transporter to re-uptake that glucose so it’s not lost in the urine. So by blocking its function you can excrete excess blood glucose in the urine.
Now, I think one of the things that’s very unique about this target is, its function is very specific. Its job is really only to re-uptake that glucose in the blood, and so if you have a compound that’s quite specific, you would imagine a very clean mechanism that it’s working on and its seen effect.
That’s supported by the knockout data in mice that we’ve seen, as well as by human mutants who are completely lacking this target. Both mice and humans completely lacking the target are quite healthy, never show hyperglycemia.
Then it’s happens to be the one of the strongest anti-diabetic effects we are seeing, having looked at almost a quarter of all protein encoding genes to-date. Now we have a realized biomarkers in the clinic which is glucose, but two of the most appealing aspects of this mechanism are one that unlike all of our mechanisms for treating type 2 diabetes, glucose is being lowered in the blood through a non-insulin dependent mechanism, and what that means then is that you are sparing pancreatic data cells.
Ultimately the pancreas would result from type 2 diabetes and they require insulin therapy and as one could imagine, they allow them to function longer without requiring insulin. The second thing that’s very appealing is that, all the other mechanisms for controlling blood glucose in type 2 diabetes, resulted in storage of the glucose, in fact in other tissues, whereas this in fact dumps very large amounts of glucose and provides the opportunity for weight loss.
That too have potential benefits for cutting back to metabolic benefits. Phil.
Philip Brown
Well clearly type 2 diabetes represents a very large market with plenty of space we believe for market for the agents that are going to be required to ultimately manage the symptoms that these patients experience, and the outcomes that they experience as a result to their diabetes. If we move to the next slide, as Arthur mentioned, completed our Phase I study.
What we observed in this, utilizing the biomarker of urinary glucose, was a dose dependent increase in urinary glucose excretion up to a 300 mg dose level. Importantly, all the dose levels that we explored in normal healthy volunteers were extremely well tolerated.
We had no serious adverse events, and there is no evidence of dose limiting toxicity that emerged within this study. The pharmacokinetic and pharmacodynamic data, both support once daily dosing regime, which I shared with you on the next slide, and we believe that this represents a very favorable safety profile and efficacy profile as we continue to produce the compound.
If you move to the next slide, these are our urinary biomarker data. If you’ll bear with me as I walk you through it, you’ll note that on the far left of the slide is the individuals randomized placebo, and of course there is no glucose within the normal healthy volunteers, who has a normal blood glucose.
So there is obviously no urinary glucose detected in those individuals. You’ll note that as we increase doses from 25 mg, up to the top dose of 500 mg, we see a dose dependant increase in the glucosuria or the urinary glucose which excreted.
What I’d also like to note is that, these are cumulative data over 72 hours. So following a single dose of LX4211, we achieved a fairly robust glucosuria response that occurs over a three day time period, and this really underscores the once daily dosing regimen that we believe is going to be required to be an attractive agent in the setting of diabetes, and was a development goal for us, prior to moving it into its proof of concept study.
I think it’s also important to note again, that these are normally healthy volunteers, who have completely normal blood sugars, and we are achieving this fairly robust response in glucosuria. So we have just recently moved this compound into a proof of concept study in patients with type 2 diabetes.
We’re exploring two dose levels for 4211, 150 milligrams once daily or 300 milligrams once daily, versus placebo over a four weak treatment period. We are obviously evaluating a number of the biomarkers that are associated with diabetes, including fasting blood glucose or glucose tolerant tests, but based on this very nice biomarker that exist for the target, we are continuing to follow urinary glucose excretion to begin to correlate its effects Pharmacodynamically with the laboratory parameters.
Obviously safety and tolerability remain paramount, and that’s an ongoing confirmation of those observations in this study as well. This study is ongoing at present.
We have initiated it, and we hope to have it completed in the not too distant future, with the results available in the first quarter of next year. So with that, I’ll hand it over to Ajay Bansal.
Ajay Bansal
Thanks Phil. Let me just take a brief moment to provide you some financial update.
Lexicon’s revenues for three months ended September 30, 2009 were $2.1 million, a decrease of 72% from $7.5 million for the corresponding quarter in 2008. The decrease was primarily due to reduced revenues under our alliances with Bristol-Myers Squibb, Organon and Genentech, partially offset by increases in revenue under our collaboration with the chronic form.
For the nine months ended September 30 2009, revenues decreased 64% to $9.3 million, from $26 million for the corresponding period in 2008. Overall this decrease in revenues reflects the shift in our business model, from drug discovery collaborations, to developing our drug candidates to clinical proof of concepts, before forming new collaboration.
Now a brief look at our expenses; R&D expenses for the 2009 third quarter were $19.3 million, a decrease of 29% from $27.3 million for the corresponding period in 2008. The decrease was primarily due to lower external pre-clinical research and development expenses, as well as lower salary and benefit costs.
For the nine months ended September 30, 2009, R&D expenses decreased 26% to $62.4 million, from $84.9 million for the corresponding period in 2008. G&A expenses for the 2009 third quarter were $.46 million, a decrease of 8% from $5 million for the corresponding period in 2008.
The decrease was due primarily to lower consulting expenses. For the nine months ended September 30, 2009 G&A expenses decreased 10% to $15 million, from $16.7 million for the corresponding period in 2008.
Lexicon’s net loss for the three months ended September 30, 2009 was $19.1 million or $0.14 per share, compared to a net loss of $23.5 million or $0.71 per share in the corresponding period in 2008. Net loss for the nine months ended September 30, 2009 was $60.8 million or $0.44 per share, compared to a net loss of $61.4 million or $0.45 per share for the corresponding period in 2008.
For the three months ended September 30, 2009, net loss included non cash stock based compensation expense of $1.3 million, compared to $1.4 million in the corresponding period in 2008. For the nine months ended September 30, 2009 net loss included non cash stock based compensation expense of $4.1, compared to $4.8 million in the corresponding period in 2008.
Let me now turn to our cash and investments. As of September 30, 2009 Lexicon had $87.3 million in cash and investments.
Net of this obligation under credit line secured by the auction rate securities, and including $5.7 million in cash and investments held by (Inaudible). This compares to $106.9 million as of June 30, 2009 and $158.8 million as of December 31, 2008.
Taking into account the recent financing which resulted in net proceeds of $55.2 million, Lexicons pro forma cash and investments net of the credit line would be $142.5 million. We believe that the working capital available to Lexicon, without taking into account funds held in the auction rate securities will be sufficient to meet our cash requirement for at least the next twelve months.
I would now like to turn to our forward-looking guidance for the full year 2009. The revenues are projected to be in the range of $10 million to $11 million, up slightly from our pervious guidance of $9 million to $11 million.
Operating expenses are now projected to be in the range of $102 million to $105 million, down from our pervious guidance of $105 million to $110 million. Non cash expenses are expected to be approximately $11 million of this total, including $5 million in stock based compensation and $6 million in depreciation and amortization.
We expect our 2009 net cash used in operations to be in the range of $92 million to $95 million, down from a pervious guidance of $93 million to $98 million. This will result in an estimated year end cash and investment balance, again net of our credit line of approximately $120 million.
Let me now turn the call back to Arthur.
Arthur Sands
Well, thank you Ajay. We can now take any questions you may have.
Operator
(Operator Instruction) You have your first question comes from the line of Allan Corn.
Allan Corn – Unidentified Company
On your diabetic drug.
Arthur Sands
Well I didn’t hear that, something about drugs, the diabetic drug. Okay, go ahead.
Allan Corn – Unidentified Company
How soon do you think will be available for use, where you have a large trial.
Arthur Sands
Well its one step at a time, lets put it that way. I think what we are willing to forecast at this point is that we’ll get results from our first in-patient trial in the first quarter, which is a big step forward for a new entity, and then we’ll make the judgment call based on the data.
So that’s about all we can say at this time. I’ll put it in context though, that’s fairly rapid for the phase 2a program, because we did compress it by doing a trial a four way trial in patients, these are patients that are sequestered in the units that we are monitoring everything, and so I think in a very reasonable time frame we’ll get those results.
Allan Corn – Unidentified Company
Thank you
Arthur Sands
Thank you.
Operator
(Operator Instruction) And there are no further questions. I would now like to turn the call over to Dr.
Sands.
Arthur Sands
Well thank you. I anticipate over the next twelve months that we’ll have a lot of questions, and I think that’s true because that’s of course the time frame in which we’ll have these results.
We are on stage now to evaluate those, and I’m referring to the slides that have the timeline over the next twelve months for these four trials which we spend a fair amount of time now reviving. So we look forward to keeping you updated as the results flow in, and thank you for you participation.
Bye-bye.
Operator
This concludes today’s conference call. You may now disconnect.