Welcome to the Cerulean first quarter 2016 conference call. This call is being recorded. My name is Terence and I will be the operator today. With us today from the company are Chris Guiffre, CEO, Gregg Beloff, CFO, Adrian Senderowicz, CMO, Alejandra Carvajal, GC and Scott Eliasof, VP of Research. Mr. Guiffre, you may proceed.

Good afternoon, everybody and thank you for joining us. Let's start with a comment from Alejandra on forward-looking statements that may be made during the call.

Certain remarks that we make during this call about the company's future expectations, plans and prospects constitute forward-looking statements for purposes of the Safe Harbor provisions under the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors, including those discussed in the risk factors section of our most recent quarterly report on Form 10-Q, which is on file with the SEC and can be accessed on our website. In addition, any forward-looking statements represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. While we may elect to update these forward-looking statements at some point in the future, we specifically disclaim any obligation to do so, even if our views change. Therefore, you should not rely on these forward-looking statements as representing our views as of any date subsequent to today, May 2, 2016.

Thanks, Alejandra. In the first quarter, we continued to demonstrate progress for our platform and the clinical candidates it created. The Mark Davis PNAS paper published in March is a good example. Mark is a member of the National Academy of Engineering, the Institute of Medicine and the National Academy of Sciences and he published groundbreaking clinical data that demonstrate how our platform does what it is intended to do, that is concentrate anticancer payloads in tumor tissue while sparing healthy tissue. The PNAS paper is a major milestone for Cerulean, because it represents the first proof of mechanism in human cancer patients for our NDCs. Because of the paper's importance, I asked our VP of Research, Scott Eliasof, to join this call to share some highlights from the paper and to take your questions. Scott?

Thanks, Chris. These clinical results clearly show drug accumulating in tumors but not in adjacent healthy tissue. We believe this is the first clinical evidence of a phenomenon known as the enhanced permeation and retention effect or simply EPR. This clinical demonstration has important consequences for our platform because targeting tumor tissue while sparing healthy tissue should result in better antitumor activity and lower side effects, thereby enabling more effective combination regimens. I think it is quite remarkable that all nine of the patients showed the payload in the tumor and not in the adjacent tissue. These clinical results also provide important pharmacodynamic proof that the CRLX101 inside the patient's tumors is knocking down its intended targets topo 1 and HIF. We were able to analyze tissue from six of the nine patients and saw in all six patients that 101 inhibits topo 1 and CA9 which is a marker for HIF. If anyone has any questions about the PNAS paper or its implications for our platform, I would be very happy to take them in the Q&A portion of the call.

Thanks Scott. Another example of progress for both our platform and its clinical candidates occurred shortly after the end of the quarter. We had an active AACR where five presentations showcased progress for CRLX101 and CRLX301, including preclinical data that open up two new frontiers for 101, that is combinations with DNA damage repair agents and combinations with IDO inhibitors. I will mention the AACR presentations as I update you on both 101 and 301. So now let's turn to CRLX101. Last quarter, I outlined the four frontiers of our 101 clinical development program with each frontier representing a unique drug combination opportunity. Three of the four frontiers were highlighted at AACR. The first frontier for 101 is combining it with antiangiogenic drugs. Here, we are combining 101 with Avastin to treat RCC and ovarian cancer. With respect to RCC, we have an important update to our guidance for when to expect a readout of our blinded study in third and fourth line RCC. You will recall that the readout is event driven. We plan to unblind the study when we see a total of 70 events. Events are either patient death or disease progression. Of course, our ability to predict the rate of events is limited. Previously we had estimated that we would have seen 70 events in Q2. However, the rate of reported events appears to have slowed down recently causing our third-party CRO to update its forecast last week. We now expect to unblind this study in Q3. I must remind you that our study is blinded, so we cannot draw conclusions at this time about the reason for the rate of events in this trial. If the results of this study are compelling, we now expect to launch a Phase 3 trial in the first half…

Thank you Chris. At TAT, we presented clinical data for the once every three weeks dosing schedule that allow us to declare the MTD at 75 milligram/meter square. 301 appears to be generally well tolerated and show hints of antitumor activity in highly refractory patients. At AACR, we presented detailed pharmacokinetics data. 301 showed a higher retention of drug in plasma, slower clearance and controlled slow release of docetaxel payload from the NDC. At equivalent dose of 75 miligram/meter square, we observe that 301 stays intact in circulation for an extended period of time, resulting approximately 100 times greater plasma exposure of the intact NDC relative to published data for docetaxel. These safe PK results appear to be better than commercial docetaxel leading to much lower distribution from the plasma to normal tissues. This differentiated PK profile may allow for improvement in tumor activity and tolerability of 301. Finally, the Cmax of released docetaxel in plasma after 301 administration was 21 for lower than that for commercial docetaxel, which may result in lower toxicity with 301. With early data like these, we look forward to seeing how the Phase 2 study matures and presenting more data at ASCO. Now I will turn the call over to Gregg.

Thank you. Adrian. I will briefly highlight our financial results for the first quarter of 2016, which are included in the Form 10-Q that was filed after market closed today. For the first quarter, we had a net loss of $13.5 million compared to a net loss of $8.4 million for the first quarter of 2015. The increase in net loss for the period was due principally to expenses associated with our clinical development programs and related CMC. We ended the first quarter with cash and cash equivalents of approximately $60.5 million. We believe will have the cash necessary to fund operations into Q2 2017. We expect to achieve a number of milestones within that period. In the first half of 2016, we have already achieved two of our previously stated milestones. We presented 301 clinical data at TAT and AACR and we reported top line data from the ongoing ovarian trials with the GOG Foundation of 101 plus weekly paclitaxel. In addition, in the remainder of the first half, we expect to achieve three more milestones. We will present additional 301 data at ASCO. We will dose the first patient in the Phase 1B2 trial of 101 and Lynparza and we will dose the first patient in the Phase 2a portion of the 301 trial. Finally, we expect to report the following milestones in the second half of 2016. Top line data from the randomized Phase 2 trial of 101 plus Avastin in RCC in Q3, data from the weekly dosing trial of 101 alone and in combination with Avastin and additional interim 101 data from the ovarian and rectal ISTs. With that, let's open up the call for Chris, Adrian, Scott and me to take your questions. Operator, please prepare the queue.

[Operator Instructions]. Our first question comes from Debjit Chattopadhyay of Janney. Your line if open.

Hi. Good afternoon gentlemen. Thank you for taking the questions.

Hi Debjit.

Hi. Good afternoon. So on the ovarian cancer side of things, what's your gating factor in terms of Avastin combo versus the paclitaxel combo? And where does the once weekly dosing for of CRLX101 fit in?

Okay. So a couple of questions there. The first part is, I think you said what's the gating factor? I would argue that both combos have already cleared the gate, meaning that both of them are very interesting to us, but we don't have unlimited resources here and we would like to pick what we think the most beneficial combination will be for patients and if we can make that decision based on the data we have from these two single arm studies, we will. That's our plan. So gating, they have already clear the gates. Which one we would move into a pivotal study, I can't comment on that now. I think they are both off to very promising starts and I am more than happy to let Adrian add to that if there is anything he would like add.

Thank you Debjit for the question. I think it's a very important question. It's a data driven exercise and we have multiple shots on goal. As you heard, we presented at AACR the combination with Avastin. We are going to be presenting in a couple of weeks the data with paclitaxel, then the Phase 1 is very exciting. The other shot on goal, I would say, is the data that we will have with 101 and olaparib. That will open another angle in the ovarian cancer world. We can tell you summaries that we are very excited about ovarian cancer and one of the three combinations we will explore soon, hopefully at the end of the year, we want to move forward for pivotal study of ovarian cancer.

So what I meant by gating factor, if I look at the data from the AURELIA study, Avastin plus paclitaxel, I believe the PFS number there was about 6.9 months. So where is your comfort level, as you your current data evolve in terms of PFS that will compel or that will make it a compelling pivotal study candidate?

So it is a great question and we really understand the AURELIA study. It's a very important study for the drug that has activity in ovarian cancer. But maybe if you want to go forward thinking about the AURELIA study, it's a study that has some limitations. Basically it was not a randomized trial with different tumor agents. And it was in a very peculiar population where many patients were excluded, whether they have prior Avastin first or maybe they have some CAT scans that were suggesting that the patient could have an obstruction, bowel obstruction or patients who have anti-coagulation. So we believe that that patient population was in better shape than the patients that we are treating ourselves. And while we can tell you that we are very excited about these almost 60% response on including one complete responder in ovarian cancer study and you will see in a couple weeks, we are adding more patients to it. And we are, at least for the Avastin and 101 combination, we have at least that PFS in, we believe, a more advanced setting when patients who have multiple prior therapies as opposed to ovarian studies or AURELIA prior therapies. So I think AURELIA is important. Avastin is important, but with the data we have, we can beat that benchmark.

And just for clarification, on the paclitaxel combo, the 56% partial response rate, how many of those patients were at the MTD as opposed to the 12 milligram per meter square does?

It is interesting. We have responses in both. We have three patients at 12 and six patients at 15. We have activity in both. And again, this complete responder is something almost unheard of in this heavily [indiscernible] patient population. We have discussed with the GOG. We are very excited. We are putting many more patients to ensure that we can maintain this level of response and we have been talking to different PIs who are willing or thinking about the next steps for these combinations.

Just to be clear, Debjit, I am sorry a bit. The old lawyer in me jumps up right now. I heard Adrian say complete responder and I want to be clear that we are specific and don't speak loosely. It is a complete responder by recessed criteria. It is not a complete responder by the GOG ovarian response guideline. So I just wanted to clarify that.

And there is another question we didn't answer. I apologize. You asked about the question about the weekly. And we are actually studying the weekly administration for paclitaxel and 101 and we are in the amendment process. We believe that the weekly especially 101 is going to be even more active. We are obviously waiting to test that in the clinic and we are going to have results, as Gregg mentioned, in the second half of next year.

And how many centers are involved in the GOG study?

I will it's around eight to nine centers.

Great. Then moving on to the pushout in the RCC readout. If you look at the historic data, what's the fat tail in terms of the long term responders with, say Avastin monotherapy or any of the TKI monotherapies?

Yes. So basically what we expect in this patient population is around 3.5 month median PFS.

Yes. But right now, since it's an event driven readout, obviously some patients are doing better than your point estimates. Now traditionally what will you expect, what percent of patients traditionally do fairly well at any of these monotherapies?

Well, again, the median meaning 50% of patients will do 3.5 and then you have patients who do worse and some patients who do better. So I don't know 50%. So if you one standard of error, we can start speculating but 50% of patients will have a median PFS of 3.5.

Great. Thanks so much.

Thank you Debjit.

Our next question comes from Joe Pantginis of Roth Capital Partner. Your line is open.

Hi guys. Good afternoon.

Hi Joe.

Hi there. A couple of questions if you don't mind. First, still sticking with the ovarian program, assuming you go past your, I would call it, your multi pronged decision tree with regard to your different combinations, what could the potential regulatory path like because this represents such an unmet medical need? Obviously you have to most likely have the combination arm. I don't necessarily see you being able to do a single arm study. I am assuming you would need a Phase 3. And any other color you would be able to add, would be great.

Okay. So I am going to start and I am going to Adrian jump in, if he thinks there is anything I missed. The first thing I need to do, unfortunately Joe, is say that I don't like to speculate about things that I am not certain about. So I am going to try and be responsive to your question without getting into any undue speculation. So number one is, I think it's fair to say that we would go forward with a pivotal study that would be head-to-head with a comparator as opposed to a single arm study. I agree the unmet need is very high there and single arm studies are not unprecedented in certain tumor types. But our base case expectation and therefore I think your base case expectation should be comparative study. What we don't yet know is what the comparator would be and that could largely depend on what our combination will be. The size of the study, I think you should expect that it would be larger than the RCC study that we are running now, but the exact numbers that we have, I don't know them. Adrian doesn't know them. So I don't think we can guess at that. Beyond that, I am not sure what else we could say at this point.

This is Adrian. Probably as you know, it's that PFS is unacceptable for full approval in ovarian cancer in particular unmet medical need and I agree with Chris completely that the most likely scenario will be a randomized trial unless that we are improving further the response rate and the duration of response that we have seen with the small Phase 2 trial that obviously I worked there at the FDA. So it's always good to talk to my former colleagues and see whether they we would be impressed with a high response rate in this tumor refractory population with longer duration. Sort of that, we want to go for a Phase 3 trial pivotal study and we are excited about the data exactly as it sounds like you are.

That's very fair. Thank you. And if I could just switch gears quickly to the IDO program. I guess my question is two-pronged. So first, in your prepared comments when you talked potentially looking at mechanistic data, just curious to see how you might the able to or might not be able to look at the mechanism of action regarding the chemotherapy aspect providing many more tumor antigens presented to the immune system or epitope spread and is that part of your mechanistic analysis? And then the second question is, are you looking and this goes to the study design, obviously there's some open-ended questions in immunotherapy still with regard to what might be better and I think it's almost on a case-by-case basis regarding having sequential therapy or concurrent therapy because of the role of chemotherapy in at least perceived abuse in muting the immune system? So thanks a lot.

So thank you, Joe. I think I am going to let Scott jump in. I am glad to have his help on answering the question. I am going to again sort of, I hate to do this, but say that there is a limit to how much we can talk about our plans on the studies that Scott is planning to do to further understand the mechanisms and so forth. So we may not be able to give you quite as much of an answer as you are looking for, but he can certainly talk at a high level about some of the studies he is planning and what he is going to do there. Go ahead, Scott.

Yes. So with respect to the mechanism of action, we are doing immune profiling type of studies in multiple models that are just span the range of sensitivity and PD-L1 levels baseline. We are going to be also definitely looking at the relative timing of sequential versus concurrent. We haven't yet presented any of those data, but that's a very important question.

That's great. Fair again. Thank you very much, guys.

Thank you, Joe.

And our next question comes from John Newman of Canaccord. Your line is open.

Yes. Hi. Thanks for taking my question. The first question I have was, do you think that the prior use of PD1 or the potential prior use of PD1 over the course of the RCC study has changed at all? And the second question that I have is, regarding the observation that the event where it seems to be slowing down, has that been something that has been developing over time? Or has it been a specific time point where the CRO really noticed that there was a lengthening in terms of the time between events? Thanks.

Sure. So let's take the prior PD1 question first. If I understood you correctly, you are asking whether there is a change in PD1 use over time and the answer to that certainly is yes. We have, I believe, a small number of patients on the current study that had experienced prior PD1. And in fact, the Phase 3 study that we have tentatively designed and discussed with the FDA assumes PD1 prior exposure. So that would be a difference between the Phase 2 and the Phase 3. In the phase 2, we had very, very few patients with PD1 and in the Phase 3 every single one of them would have prior PD1 as part of the protocol design. So that's the first question. The second is about the rate of events slowing down. I am not sure I know how to answer your question with specificity. I can tell you that up until last week, the CRO was forecasting that we would have our 70 events in the second quarter. We would be very close to the 70 events now. We are apparently behind that. And so last week they updated us as they regularly do and told us that they thought that the 70th event would not occur this quarter and was more likely to occur next quarter. As I said before, there is a limit to how much they can predict how long a patient will stay on a treatment, especially an investigational drug. So I understand there is some limitations in their ability to forecast. And I think moving the events out two or three month is something that we just have to live with when you run studies. But I don't think I know how to answer your question of, is there a particular date and time where it started to change. If there is, I don't know that, but it seems like in the last couple months, things have started to slow down.

Okay. Great. Thank you.

Thank you.

[Operator Instructions]. Our next question comes from Michael Schmidt of Leerink Partners. Your line is open.

Hi. This is Varun Kumar, calling for Michael Schmidt. So I have a question on CRLX101. So for the ongoing trial in ovarian cancer for CRLX101 with weekly paclitaxel, can you remind us if there was a prior study with 101 and every three week paclitaxel in ovarian cancer? And if so, what kind of response rate was observed?

Thank you for the equation. No, this is the first study that we you are doing in combination with paclitaxel. And as you know, every three weeks paclitaxel is skewing as a first line therapy. These are patients who have relapsed platinum resistance. So for those patients generally we give more dosing than with paclitaxel. So there is none. So this is the first study ever with paclitaxel.

Okay. Great. And again, continuing with ovarian cancer, you have guided to move either with Avastin combo or paclitaxel combo after the final data. How much the safety profile will play a role if you get to see kind of similar response rate? Is one combo more tolerable over another?

Yes. I think it's a very good question. And the safety is very important for Cerulean and for patients in oncology. However, as you know, the primary endpoint and all the sample sensitivity is based on efficacy and assuming that both have the same efficacy and the same safety, that's going to be unlikely because in general, you have some differences. We will go with the more efficacious antitumor agent. So actually I would say that if one has PFS objective response rate over that one that has only PFS, I will take think that combinations that has both a response rate and PFS, while I assume that we have PFS safety. By the way, we haven't discussed in detail the safety profile for the combination of paclitaxel, you will see that in the next 10 days. But the safety is great.

Okay. Great. And my last question is on 301. Do you think it's going to be all common design or will you have selection bias for a few indications? I know you mentioned bladder cancer. But do you have any few indications in mind?

Yes. And obviously we have several. One, as we shared with you, that makes a lot of sense and bladder cancer is a tumor type where taxanes, particularly docetaxel is active and we are going to explore patients who are taxane-naïve. I can tell you the other one that is going to use for docetaxel is to triple-negative breast cancer. So these are a couple that we can share with you. And certainly, at least these two tumor types, we will be expecting a significant number of responses. And we are expecting that's going to be the case and then we are going to move forward. We want to continue with a weekly Phase 1 trial. And as soon as we have the recommended phase for the weekly, we are test these indications and then we are going to have an interesting discussion which of the two we want to move forward for a pivotal.

Okay. Great. Thank you for taking my questions.

Thank you.

Thank you.

Our next question comes from Jon Eckard of Barclays. Your line is open.

Hi. Good afternoon. Thanks for taking my questions.

Hi Jon.

Sorry about the background. Hi. How are you doing? So I have two kind of like big pictures strategic questions. First one, scenario is that the RCC data comes out and its clearly positive. Chris I think in the past you have talked about exploring potentially expedited ways of getting this drug approved, if that were the case. Do think that that's still a possibility, given some of the changes in the landscape? I know they are early aligned, but do you think that is still a possibility if the data was very strongly positive for some sort of an expedited pathway to this drug?

Yes. So, thank you for asking the question. It's a very fair question in light of all the changes that have been going on in the RCC paradigm. But I will remind anyone on the call that when we started this program, we not only thought those changes were possible, we expected them and we have been predicting them for quite a while. So we predicted NEVO, we predicted Cabo, we predicted lenvatinib and so far we are two for three and I expect will be three for three with lenvatinib. All of those changes are in first and second line. We intentionally did not go into the middle of that. There are other companies who are developing drugs in second line, very reasonable things to do and it's just a very crowded space and highly competitive. There is really nobody else, at most you would say there is one other person in third and fourth line. We will be the only folks who have a data set in third and fourth line that includes patients who have been treated with at least two or in sometimes three cases, TKI and/or an mTOR. And what I can tell you is that if we see 9.9 months in this study, like we saw in the U Penn study, that would clearly be, I am trying to find the word that is even more exciting than exceptional, that would be outstanding data and we would believe that that data would warrant approval based on a single trial and we would talk to the FDA about that. Even if we saw something in the seven month range, that would be in third and fourth line, what Cabo saw in second line. So I think that there is some argument that even there you might want to move forward. But I don't get to decide that. The FDA gets to decide whether we need this study or an additional study. And our base case plan has always been and continues to be that this study will tell us whether this combination is active in late stage kidney cancer patients who would currently only get about 3.5 months benefit and only about a 4% response rate, if we can do much better than that then I feel we have done something very good for our patients and we will run a Phase 3 and get it done as fast as we can and get the drug approved in that indication.

Yes. So let me add one thing to Chris and we agree completely. When we visited the agency last year in October, we asked the same particular question to them. And they say that they are open, assuming that these are quality well data or they knocks the socks off data. So still we believe that if that's the case, we want to go there and I am sure that they will be open because it will be potentially unethical to not to approve a drug like that, that is helping patients so much and doing and repeating a new trial will not be ethical for patients for the possible patients. Thank you.

Great. And then if I could just ask another questions, it was on the flip side. I am not sure how much you are willing to divulge. But if the trial is negative for RCC, now early in the call here you mentioned how you see a path forward in ovarian, what do you see the optimal way strategically to monetize or to recognize the maximum value for 101? Could you run a trial with combination with paclitaxel or Avastin, while still potentially leaving open partnership opportunities with PARPs, IDOs and so on and so forth? So again, just big picture wise, again under the assumption that the RCC is negative, what's the best way to maximize the value of 101 thereafter?

Okay. Thank you. I am happy to chat about that. So if the trial were to be negative, that would be a disappointment and a surprise, given what we have seen about this combo in prior studies, both in ovarian and RCC. But anything is possible, especially in oncology and I think it is fair to discuss what the path forward for 101 is. In that situation, we would still be sitting on a drug that is clearly active and clearly well tolerated in multiple combinations and at least in my view and I believe in Adrian's view and I believe in the view of my Board, is the drug that is likely to be approved. It's just a matter of when and in what indications and how many indications and which combinations. So I think it's important to note that this drug is much more than just an RCC drug or it's much more than just a drug that helps Avastin to do its job better. We talk about our four pillars of our clinical development program or the four frontiers. The first is antiangiogenic drugs of which Avastin is of course one and I would like to think that the $5 billion or $6 billion a year of antiangiogenic drugs that are being sold year could provide better outcomes for patients if those drugs were combined with our drug. And we will look to various ways to either work ourselves or in combination with partners to try and get this drug approved in combination with other antiangiogenic agents. But again, the RCC trial is in the first frontier. So let's say, in your hypothetical that we were to miss the endpoint in this study for whatever reason. In that case, we would still have combinations with chemo and…

Absolutely. Generally I just wanted to hear your response to the fact there's many potential paths forward even if there was a disappointment in RCC. So thank you very much.

Thank you Jon.

And we have a follow-up question from Debjit Chattopadhyay. Your line is open.

Hi Debjit.

Hi. Thanks for letting me back in again. When you compare your underlying technology with everything else that's being done to encapsulate chemo to make it more tolerable and potentially better, including the recent success from a competitor in AML, how should we differentiate your platform technology versus the rest?

Sure. So I am going to invite Scott to chime in a little bit, but I am going to start off by saying something that you know, because I have talked to you about it many times, which is that we conjugate where other companies entrap. That is very, very important and that is why our molecules are called NDCs, nanoparticle drug conjugates and other folks talk about nano therapeutics or nano medicines or whatever. There is a very big advantage from a commercial standpoint with conjugation, that is that we are able to get composition of matter IP, not just dosing patents, like entrapped molecules are and we believe there are certainly multiple advantages from a therapeutic standpoint with conjugation, including the ability to stay intact in the bloodstream, the ability to stay in fact in the tumor tissue while we penetrate deeply, the ability to be taken up inside the cells through macropinocytosis and very importantly the ability to have a slow release of the payload over time, which is the only reason that our topo 1 inhibitor is also a HIF inhibitor. No other topo could make that claim. So I think there are a lot of differences. We do not view other nanoparticles as competitors. That's a term you used. We are excited for them because we want them to deliver medicine to cancer patients as well. We are happy for Celator. We are happy for other good technologies the space. We just do something a little different and we think it's very important. So with that said, Scott, is there anything else that you would like to jump in on?

Yes. So I would echo everything that you said. I think conjugation is really a major part of the secret sauce and it also gives us, in addition to all the advantages that Chris mentioned, it also gives us the ability to control PK very, very exquisitely because we can put different linkers in there and then thereby control the rate of release, both in the plasma and also in the tumor as well. And then the other thing I would add is a couple more things. One is that the PK that we have seen clinically is very, very compelling. It is a very robust and reproducible PK that you don't see often with other nanoparticles because typically like liposomes and these larger polymeric nanoparticles have a PK that can vary quite a bit from patient to patient because they are rapidly recognized by the immune system and removed pretty quickly whereas our PK has been very, very reproducible from patient to patient and we have shown that in a 2013 PNAS paper. And then the other thing I would mention is along the lines of translatability. I think one of the real key strengths of our platform is how well it has translated from animals to humans and I would specifically point out the recent PNAS paper that we published in which we demonstrated that CRLX101 accumulates in tumors but not in adjacent healthy tissue. And we have seen that not only in the gastric cancer paper that we just published but we have also see it again, which we just presented at AACR in ovarian cancer patients where six days after a single dose of CRLX101 we saw that the nanoparticles were diffused throughout tumor. In other words, they are not hanging around by the vasculature, which is what most other nanoparticles and liposomes do and we saw sustained DNA damage six days after a single dose. So I think this translatability of our technology is also a very, very important aspect of what we do.

Awesome. Thank you so much.

Thank you Debjit.

I am showing no further questions in the queue at this time. I would now like to turn the call back over to Chris Guiffre, CEO for any closing remarks.

Thanks for joining us today. We look forward to reporting on continued progress in August. Have a good night.

Ladies and gentlemen, thank you for your participation in today's conference. This concludes the program. You may now disconnect. Everyone have a great day.