Good day, ladies and gentlemen, and welcome to the Agenus Q3 earning report conference call. As a reminder today's conference is being recorded. At this time, I would like to turn the conference over to Ms. Jonae Barnes, Vice President of Investor Relations and Corporate Communications. Please go ahead.

Thank you, Tracie, and good morning, everyone. Welcome to Agenus' conference call to discuss the financial results for the third quarter 2013. With me today is Dr. Garo Armen, Chairman and CEO of Agenus; and Christine Klaskin, Vice President of Finance. During this call, we will review our financial results as well as provide a corporate update. We will then open up the call to a Q&A session. Before we continue, I would like to remind you that this conference call will contain forward-looking statements, including without limitation, statements regarding the company's potential income stream, development and commercialization efforts, timelines, availability of data and potential efficacy and market potential with respect to products and product candidates of the company and its partners. These forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially. Reference to these risks and uncertainties is made in today's press release and they are disclosed in more detail in our most recent filings with the U.S. Securities and Exchange Commission. These statements speak only as of the date of this call and Agenus undertakes no obligation to update or revise these statements. All forward-looking statements are expressly qualified in their entirety by this cautionary statement. While evaluating Agenus' business and securities, investors should give careful consideration to these risks and uncertainties. As a remainder, this call is being recorded for audio replay. With that, I will now hand the call over to Christine, who will review our financial results for the third quarter 2013.

Thank you, Jonae. Good morning, everyone, and thank you for joining us on today's call. Some of the statements I will be making are also contained in the press release issued this morning. The company's net loss attributable to common stockholders for the third quarter of 2013 was $7.4 million or $0.24 per share compared to a net loss attributable to common stockholders of $5.9 million or $0.24 per share for the third quarter of 2012. For the nine months ended September 30, 2013, the company recorded a net loss attributable to common stockholders of $27.4 million or $0.99 per share compared with a net loss attributable to common stockholders of $6.5 million or $0.28 per share for the nine months ended September 30, 2012. Our cash and cash equivalents were $30.2 million as of September 30, 2013. Based on our current plans and activities we expect sufficient financial resources to fund operations through 2014. As a result of various corporate transactions, our net loss for the nine months ended September 30, 2013, increased compared to the net loss for the same period in 2012. This was primarily due to $6.2 million of non-recurring, non-cash charges encouraged during 2013 compared to one-time payments of $13.4 million received during 2012. In the first quarter of 2013, the company's preferred stock restructuring, which reduced the dividend requirements for its Series A-1 preferred securities resulted in a non-cash deemed dividend of $2.9 million. In the second quarter of 2013, the company retired its outstanding $39 million 8% senior secured convertible notes due August 2014, resulting in a non-cash loss on extinguishment of this debt of $3.3 million. In the first quarter of 2012, revenue of $13.4 million was generated primarily due to one-time payments received through an expanded agreement with GlaxoSmithKline and through a license of non-core technologies. This concludes the financial portion of the call. Dr. Armen, will now provide a corporate update.

Thank you, Jonae and Christine. During the quarter and into October we achieved important milestones. These include, firstly, the positive Phase 3 data from GSK's RTS,S, the world's first and most advanced malaria vaccine, for which regulatory application is expected to be filed next year. This will be the first QS-21 Stimulon containing program to advance to regulatory filing. GSK also initiated another Phase 3 trial for the prevention of shingles during the quarter. I am also pleased to report that our Prophage Phase 2 study in newly diagnosed glioblastoma continued to show durable and improving outcomes in progression free survival as well as overall survival. I will now provide additional details on these milestones. First let me begin with GSK's Phase 3 program for the RTS,S for the prevention of malaria. During the quarter, new 18 month data for GSK's RTS,S malaria vaccine candidate, which contains our QS-21 Stimulon adjuvant were presented at a malaria conference in South Africa. The data showed that RTS,S help protect young children and infants from clinical malaria for 18 months post vaccination. RTT,S is the most advanced malaria vaccine candidate in the world and the first vaccine candidate to show efficacy. These Phase 3 trial demonstrate that it can help protect young children and infants living in malaria-epidemic areas against clinical disease and infection. As you maybe aware, Malaria claims over 600,000 lives a year, most of which are children in Sub-Saharan Africa. And these findings indicate that RTS,S has the potential to help prevent millions of malaria cases. Clearly, we are very pleased that our QS-21 adjuvant is a key component of this vaccine. And this will be the first case that a QS-21 Stimulon containing products will advance to regulator filing. During the quarter a Phase 3 GSK MAGE-A3 cancer immunotherapeutic…

Operator, we'd like to open up the call for Q&A at this time.

(Operator Instructions) And our first question today comes from Mike King with JMP Securities.

Just wondering if you might be able to talk about follow-up timing on some of the GSK programs. I unfortunately was not able to listen to the GSK calls. So I was just wondering what they've said both as far as timing for the follow-up on MAGE for melanoma, as well as perhaps, topline for MAGE in non-small cell.

The guidance from GSK for the gene signature analysis is expected to be in 2015. That's what they have officially indicated. In terms of guidance for the non-small cell lung cancer readout, that's again by from GSK is indicated to be the first half of 2014. That is the first half of next year.

Is there a genetic signature or subgroup in lung as there is was for melanoma?

There is. Actually the history of this dates back several years, but it was post the initiation over the trial. And in a number of Phase 2 trials, both in lungs and in melanoma, both retrospectively defined trials as well as prospectively defined trials. Gene signature seems to correlate exceedingly well with immunological activity and outcomes. And so what they have done is meet with the FDA sometime ago, several years ago and come up with an analysis, which is considered again, a primary endpoint. So there is some confusion about this is, this is secondary endpoint or a primary endpoint. It is a primary endpoint, that's why they call it co-primary endpoint. And they incorporated this analysis in a way that would keep the integrity of the trial intact, again with the blessings of the agency. And it is this analysis in melanoma that will be available in 2015. And with lung cancer, the topline data without the gene signature analysis will be available in the first half of next year and the gene signature analysis will be subsequent to that. So there is a gene signature analysis also incorporated into the lung cancer trial. Now, the differences between those two trials are quite stark. One is that melanoma patients represent sicker patients and they have an average time to recurrence of about nine months, whereas lung cancer patients are much healthier patients and the time to recurrence for those patients exceed three years. And historically, we have known that cancer vaccines are most appropriate in the healthier patients. So if you go by that criteria lung cancer trial represents a better patient population for targeting with a cancer vaccine. Now, having said that because of the significant differential of the gene signature positive patients in melanoma, we're hopeful that the outcomes maybe positive.

And then I had a quick follow-up on HerpV and then I will jump back in the queue. And that is just, can you help us calibrate what meaningful difference would be in both viral shedding and viral load when you going to report those results later this quarter?

So in terms of viral shedding days, the guidance has been that a 30% to 50% reduction in viral shedding days would be considered clinically important. But the trials have two elements: one, that the results be statistically significant, so our trials are designed to generate potentially statistically significant outcomes; and then second thing, is a reduction in viral shedding days and the secondary outcome is reduction in viral load, which is still unknown in terms of what would be a relevant number. Now, one of the reasons we incorporated a loaded booster shot into the trial is because it takes time for the immune system to give up, to produce results. So first after vaccination, you will have to wait a bit to make sure that the immune system is kicked up and then that activated immune system comes and does its job appropriately. So we will have two readouts back-to-back within a few months of each other. The significance will be both statistically significant outcomes and also reduction in viral shedding, but this reduction may come in two stages because of the booster shot.

But one should only, will expect a reduction not an elimination, I mean it's not reasonable to think that. You would have patients that would go to undetectable on their viral load, is it?

I mean this is unknown. That's not the expectation of the trial. Perhaps, at this early stage of development that maybe an unrealistic expectation. Although, one of the very relevant parameters here is viral load and we will do all kinds of analysis obviously, but in some patients, it wouldn't surprise us if viral their viral load decreases by a very substantial margin.

Our next question comes from Jason Kolbert with the Maxim Group.

So I'm going to just speak up right where Mike left off. And I'm going to bet that Mike's next question would have been on G-100 and G-200. So can we talk a little bit about what the expectations are in rGBM since the prior data set showed 10.9 months versus 7.5 in control? If that data is reproduced in the Phase 2 clinical trial, what's its significance and what do you think it means in terms of the need for a pivotal program?

So let me just address this in two parts. As you know, there is historical skepticism about single-arm trials outcomes. Now, to address this skepticism, in GBM, when you talk to the key opinion leaders, people who treat this disease day-in and day-out and operate on patients, there is essentially unanimous opinion that the variability between patients in terms of outcomes in this disease is much narrower than in other cancers. So that's basically normalizes the issue of patient selection in single-arm trials. That's number one. Number two. We have tried as you may know, Jason, to correct for any other variability in terms of, for example, if patients have received resections over 90% of their tumor, the outcomes are better than those who have not. So we've normalized our results based on selecting historical published data that consider also these parameters. So the question then becomes, as you know, in our first line G-100 trial, this is on top over the standard of care. If we can repeat the results that we have seen so far on top of the standard of care in a relatively modest sized trial, we think the product will have very strong prospects for regulatory approval. In the G-200 trial, on top of Avastin, once again if we can repeat our historical one-arm study outcomes in combination with Avastin, and as you know in these patients who are treated with Avastin, the standard of care is Avastin in second line patients, but there is really no survival benefit in these patients, there is time to recurrence benefit, but overall survival has not benefited patients. So we don't really have a huge hurdle to overcome. If we can once again show the kind of outcomes we've shown in our single-arm trials, both in terms of survival, as overall survival as well as recurrence fee to disease.

Can you just touch a little bit on what the time lines are for the two different trials, so that we can understand when that we might start to see topline data from each?

The topline data from the NCI trial, the 222 patient randomized trial, is expected to come approximately 30 months from now. And the topline for a trial in first line patients of Phase 3 trial, that we will have to wait post our discussions, which I mentioned in my formal remarks that we will schedule a Phase 3 trial meeting with the FDA to discuss the trial protocol structure, number of patients and so on. So after that meeting, which should take place shortly, I will give you a better guidance on timelines.

The next question comes from Ren Benjamin with H.C. Wainwright.

Just a quick question regarding the GSK signature. Can you talk a little bit more about it, was this a prospectively design? Is this something that continues to be modified as data is evaluated? Is it looking at five genes or 20 genes? How should we be thinking about this gene signature? And is there any sort of a read-through that we might be able to apply to the non-small cell lung cancer trial. I think you touched based on the types of patients between both melanoma and non-small cell lung cancer trial, but is there something we can glean from the melanoma study that will help us think about PFS and OS in non-small cell lung cancer?

Let me just rewind and address a couple of issues that will answer your question, Ren. One is, this saga of doing trials in earlier stage patients, we are as a company, as you know well-schooled in the art of studying earlier stage patients. And we know what the drivers of this trials are, because historically there has been a lot of skepticism that if these trials take a long time, as that a sign of either positive outcomes or negative outcomes and my answer to all of that is, it's a sign of nothing, because these trials take a long time to readout because you're waiting for recurrence and death of patients who are relatively early-stage. So that is just one. The second issue is, why is the gene signature readout taking a while. Now, GSK has provided guidance about this readout to be completed sometime in 2015. Could it be done earlier, perhaps, but I have had questions as to why can't we have this readout in three months and the answer is simple. And the other question that I've been asked is why couldn't they have done the gene signature analysis in parallel with everything else that was going on the time the results were in parallel out, they would have the results of the gene signature analysis. So unfortunately, that is not possible and I'll explain why? And that's part of the FDA guidance and the decision to make sure that everything done with this analysis is not retrospective analysis, it's all prospective. So the analysis of the gene signature will have two components, two silos, one is to take a certain number of the patients from the trials, randomized the same way, perhaps something like a third of the patients and demonstrate in those patients, the line that separates gene signature positivity from gene signature negativity. Now, this patient sample will set that standard of what is considered gene signature positive and negative, before that is prospectively applied to the analysis of the rest of the patients in the trial in order to demonstrate efficacy in the gene signature positive growth. So that's why this will take a little time, perhaps not as long as the guidance, but it will still take sometime. In terms of what does the gene signature constitute, these are genes over 80 in total that are connected to immunological expression of cytokines and a whole sloop of other drivers of the immune system. And GSK has a proprietary position in identifying these markers and setting this threshold, but suffice it to say in earlier trials they demonstrated quite impressive correlation between the immune response of gene signature positive patients and the outcomes in terms of disease-free survival and overall survival.

Just related to that the read-through question to non-small cell in regards to PFS and OS, I would normally think that in immunotherapy, other therapeutics, the chances of PFS being that is usually lower than OS. I thought historically that's how the field seems to be evolving, that the body just does not have enough time to mount that immune response and show that effect from a PFS point of view. Am I still thinking about that correctly or could that change with non-small cell?

So you make a very good point. However, what you are saying is true in late-stage disease setting, but not true in the early-stage disease setting. So if I were a betting man, I would bet that of the two trials, the melanoma outcomes would have more relevance to the point you made, but the lung cancer trial should not. Because from the Dendreon experience, we know for example, that sometimes by the time the new response kicks in, it may not be able to prevent recurrence of disease, but in that case it has had a positive outcome on overall survival. So that's why I say correlation may be more appropriate for melanoma, but not sure for lung cancer, where patients on average don't recur for a period of about two years plus.

And just one question on HerpV. Are we supposed to be expecting both a B-cell response as well as the T-cell response, when we see the data. And what has in the past, why haven't people just kind of like what we've done with polio, heat kill, let's say HSP, and try to mount the immune response that way to protect patient?

So this is obviously a very complex question. And I'll answer it in the following way. The first generation of herpes vaccines that were developed very early on by companies like Chiron, were prophylactic vaccines. And for prophylaxis, B-cell activation is certainly relevant. But unfortunately those efforts did not come to a positive conclusion. And for a long time, you had a drought in the field, until we picked up the ball several years ago and moved into this field. And that's one of the reasons, we're one of perhaps only or two most advanced vaccines in this indication right now. In terms of our particular vaccine, it certainly is primarily a T-cell vaccine. What's been impressive about the earlier results is that it's been the only vaccine up until the publication of our people that has shown both CD4 and CD8 positive activation of T-cells. Now, because of the components in our vaccine, which include certainly QS-21, the antigens bound to heat shock proteins and because of the known activity of heat shock proteins, irrespective of their binding to peptides or antigens, heat shock proteins as well as QS-21 prime the immune system and generate the secretion of certain cytokines. And it's very possible that in addition to activating CD8 cells because of the involvement of the CD4 arm, it's entirely possible that you would also get some antibody activation.

So just extrapolating that, could that mean, based on these results that you may also explore the prophylactic indication or do you think you'll stick with just the therapeutic?

Because of our size and capacity right now, to do a prophylactic trial would be a huge undertaking. And so that's one of the reasons and because of the fact that this is a primarily T-cell vaccine, we have done after the therapeutic indication in herpes and there's a huge, obviously, huge need for patient treatment in this area. But there is very little doubt in my mind that should this vaccine show efficacy in the therapeutic setting, that it would make much sense to take it to the prophylactic setting, perhaps in connection with a partner.

Our next question comes from George Zavoico with MLV & Co. George Zavoico - MLV & Co.: A couple of questions, first one about the malaria vaccine. There is a component to the trial with a booster shot as well I believe, is that going to be -- when it goes to regulatory, for regulatory filing, is the booster part going to be separate thing or is it going to just to go ahead with a first shot as a vaccine product.

The guidance from GSK that's provided is that the information that's been generated is sufficient to file. However, given the fact that without the booster this vaccine has shown efficacy over this longer period of time. It would be very surprising to any one, if the booster shot does not provide additional benefit. So while I don't think the booster shot outcomes or readouts are needed for filing, I am also very bullish on what the booster shot will do. George Zavoico - MLV & Co.: So you'll file without the booster and the booster you could file perhaps as if you need to a supplemental BLA. With regard to the new trial that GSK is starting with its seasonal flu vaccine and herpes zoster. The seasonal flu obviously is a highly mutatable virus and it requires seasonal immunization. That's not necessarily true for the zoster, so will this be a one-shot seasonal for the elderly and then they would go back to the just a seasonal flu. How is GSK going to position that product in that regard?

I haven't had a chance to discuss these details with them. But my assumption would be that the influenza vaccine of the season, whatever it is, would be compatible with the use of this product on an ongoing basis. That would be my assumption, but I have not discussed this specifically with GSK. George Zavoico - MLV & Co.: No, I mean combining vaccines in a single shot obviously is very convenient and it helps a lot with complaints. I'm just wondering whether, you just need one shot of zoster and then the next few years just go back to whatever the seasonal vaccine is in the next year.

I mean, we'll certainly get some color on this George, and get back to you. It's a very good point. And since we talk to GSK quite frequently, we'll get back to you properly on this.

Thank you. And there are no further questions at this time. Please continue.

Thank you for your interest in Agenus. We hope that you have found this update to be helpful. And I will now conclude the remarks. I would like to remind listeners that a replay will be available approximately two hours after the call through midnight Eastern Time on December 23, 2013. The replay number is 416-915-1035 and the access code is 402191. The replay will also be available on the company's website approximately two hours after the call. If you have any additional questions after today's call, please call the Investor Relations at 781-674-4538. Thank you very much.

Ladies and gentlemen, this concludes the conference call for today. We thank you for your participation. You may now disconnect your line and have a great day.