Mani Mohindru - SVP of Corporate Strategy Ali Fattaey - President & CEO Michael Gray - CFO and CBO.

Adnan Butt - RBC Capital Markets Joe Pantginis - Roth Capital Partners Boris Peaker - Cowen.

Good day, ladies and gentlemen, and welcome to the Fourth Quarter Curis Inc. Earnings Conference Call. At this time all participants are in a listen-only mode. [Operator Instructions] I would now like to introduce your host for today’s conference, Mani Mohindru, Senior Vice President of Corporate Strategy, please go ahead..

Thank you, Christy. Good morning everyone, and thank you for joining us. During today's call, we'll provide you with an update on corporate developments and plans and also discuss fourth quarter and full year 2015 financial results.

Before we begin, I'd like to advise you that this conference call contains forward-looking statements including, without limitation, statements relating to our strategy, future operations, future financial position, future revenues, projected costs, prospects, plans and objectives of the management; the potential therapeutic benefits of our drug development program and our plans to advance the development of drug candidates within these programs, as well as our expectation about Genentech and Roche's continuous development and commercialization of Erivedge.

Actual results may differ materially from those indicated by forward-looking statements in this conference call as a result of various important factors, including those risk factors described in our quarterly report on Form 10-Q for the quarter ended September 30, 2015 and in other filings that we periodically make with the SEC, and we encourage you to review these risk factors carefully.

We caution you that forward-looking statements we make in this conference call only represent our views as of today and that we may not update any of these statements even if events and developments subsequent to the date of this call cause our estimates and expectations to change.

I'd now like to introduce Ali Fattaey, our President and CEO, who will provide an update of the Company and our development programs. Following Ali's remarks, Mike Gray, our Chief Financial and Chief Business Officer, will review our financial results for the fourth quarter and full year 2015, after which we will open the call for questions.

Ali?.

Thank you, Mani and thank you to the conference call and webcast participants for joining us this morning. We remain focused on building Curis by advancing our pipeline with the aim of eventual commercialization of innovative and effective drugs for the treatment of patients with cancer.

We’re pleased to put our clinical stage drug candidate CUDC-907 on a path to registration with the recent initiation our Phase 2 clinical study in patients with MYC-altered relapsed refractory diffuse large B-cell lymphoma or DLBCL.

Also during the fourth quarter of 2015, in our collaboration with Aurigene we in licensed two drug candidates, the first in the immuno-oncology is an orally available small molecule antagonist of PD-L1 and VISTA, checkpoint proteins that we’ve named CA-170.

And the second is a potent and selective inhibitor of the IRAK4 kinase which we’ve designated CA-4948. We expect to file IND applications and to advance both of these drug candidates into clinical development in 2016. I’ll now provide additional details regarding these programs today. Now, I’d like to begin with CUDC-907.

As I mentioned we recently initiated a Phase 2 trial to determine CUDC-907’s efficacy in patients with relapsed refractory DLBCL with cancers harboring alterations in the MYC oncogene. The design and patient population of the Phase 2 trial was driven by the promising efficacy and safety data presented by our lead investigator Dr.

Anas Younes from the Memorial Sloan Kettering Cancer Center at the American Society of Hematology's annual meeting held in early December last year. In this presentation CUDC-907 was shown to be well tolerated with diarrhea, fatigue and non-symptomatic thrombocytopenia being the common adverse events of note.

Those limiting toxicities of grade 3 diarrhea and grade 3 for hyperglycemia were only observed at the higher or more frequent doses and no dose limiting toxicities were observed with the 60 milligram dose that was given on the five days on, two days off schedule which we determine to be the recommended Phase 2 dose and the regiment that is being used in the Phase 2 study.

On the efficacy front 25 of the total 72 were patients with relapsed refractory DLBCL and of these 18 were evaluable for response assessment. Now 8 of these 18 patients achieved an objective response including three patients with complete responses. At the time of the presentation all but one of these responses were still ongoing.

A retrospective analysis of the molecular pathology of these patients showed that a majority of them, responses were observed in patients whose DLBCL tumors harbored alterations in the MYC oncogene including tumors from all three complete responders that had an increase in MYC gene copy number.

We defined MYC alteration as either a trans-location of the MYC gene locus, an increase in MYC gene copy number or increase in MYC protein levels all of which are well accepted criteria used in the field to assess MYC status in tumor samples.

This potential correlation between clinical responses in patients and MYC alterations observed in the patients’ tumor samples is consistent with our recent preclinical findings were CUDC-907 treatment of DLBCL cell lines in culture can effectively and rapidly eliminate MYC protein levels in a dose dependent manner and at very low nanomolar concentrations.

The in vitro data are also consistent with anti-tumor activity of CUDC-907 that we observed in in vivo animal models of MYC altered DLBCL [lymphoma models]. We expect that we will be presenting our preclinical findings at upcoming scientific conferences this year.

I also want to mention that in addition to the data presented at ASH in late 2015 interim data from CUDC-907 phase 1 trial were also presented earlier at the ASCO Annual Meeting last year at the European Hematology Association Annual Meeting as well as at the International Congress on malignant lymphoma at the Lugano Conference earlier in 2015.

So based on the totality of the Phase 1 data as well as our preclinical findings we believe that CUDC-907 is well suited for further investigation in patients with MYC altered DLBCL. A very aggressive disease with very poor prognosis and for which no approved or optimal treatment options exist.

This also represents a sizeable population which MYC gene alterations reported in up to 19% of DLBCL cases and increased MYC protein expression reported in up to one-third of all patients with DLBCL and there is some overlap between the genetic alterations and protein expression levels of course.

In January of this year we initiated the Phase 2 trial of CUDC-907 in patients with MYC altered relapsed refractory DLBCL disease. The trial is designed to evaluate the efficacy of CUDC-907 with or without rituximab. Patients with relapsed refractory DLBCL with MYC alterations will be treated with either CUDC-907 or in combination with rituximab.

Both treatment groups are designed to enroll up to 60 patients each with overall response rate being the primary end point in progression free survival, overall survival, duration of response and safety being key secondary end points.

The monotherapy arm is designed to assist the single agent efficacy of CUDC-907 and if the data are consistent with our Phase 1 observations there is potential to expand the monotherapy arm after discussion with the FDA in consideration for accelerated approval in this indication.

The rituximab combination arm is designed to inform a randomized trial of CUDC-907 which is expected as a combination treatment regimen which will be supportive for full approval. We will provide further updates on the status of the Phase 2 trial over the course of this year.

In addition to the Phase 2 trial [indiscernible] NMC which is known to be a MYC driven cancer. In preclinical models of NMC as well as in models of other solid tumors with genetic alterations of MYC, CUDC-907 has shown significant anti-tumor activity.

We are also in discussions with clinical investigators to evaluate CUDC-907 in pediatric patients with MYC altered cancers such as neuroblastoma and medulloblastoma both of which are known to be dependent on MYC alterations. These studies are possibly as investigator sponsored trials.

I would now like to provide an update on CA-170 our orally bio-available small molecule immune checkpoint antagonist drug candidate that we in licensed in October under our broad collaboration with Aurigene. CA-170 is a first in class oral small molecule that targets the two checkpoint regulators PDL-1 and VISTA.

CA170 was selected as a developing candidate based on its compiling in vitro and in vivo profile in preclinical studies as well as its pharmacokinetic, pharmacodynamic and safety properties in vivo.

All IND enabling studies including GLP toxicology have now been completed and we expect to file an IND and initiate the Phase 1 trial in advance cancers within the first half of 2016. Now CA-170 targets PD ligands as extracellular domains.

Within the tumor micro environment the PD ligands appear to be expressed predominately on tumor cells whereas a VISTA expression is restricted mainly to cells of the hematopoietic origin including cells of myeloid origin such as myeloid drive suppressor cells within the tumor microenvironment.

Origin scientists have shown that CA-170 can selectively rescue T-cell proliferation and function that have been specifically inhibited by PD ligands or VISTA but not inhibited by other checkpoint regulators such as MS or CTLA-4 or others suggesting the specificity of CA-170’s mechanism of action.

CA-170 is active in multiple syngeneic tumor models such as those of melanoma, colon and breast cancers and including some models that are not responsive to anti PD-1 alone.

This is in agreement with what has been reported pre-clinically by others that PD and VISTA pathways are non-redundant and that inhibition of both may synergize in mediating anti-tumor effects.

As I mentioned earlier all IND enabling studies including GLP toxicology with CA-170 have been completed now and we are pleased that thus far CA-170 appears safe with a high therapeutic index in both rodents and primate safety models.

We expect to file the IND application and initiate a Phase 1 trial within the first half of 2016 and we expect to initiate the first inhuman trial with CA-170 in patients with advanced solid tumors including those that are now used to immunotherapy as well as patients that are refractory or have relapse on anti-PD-1 ways therapies.

In addition to CA-170 during the fourth quarter of 2015 we selected a second preclinical program within our immune oncology collaboration with [RAG]. This program is focused on evaluating small molecule antagonists that target PDL-1 and TIM-3 immune checkpoints.

TIM-3 is also an independent inhibitory checkpoint molecule that is generally co-expressed with PD-1 on highly exhausted cytotoxic T-cells in the tumor tissue as well as being expressed on certain regulatory T-cells and plays an important role in immune suppression.

The lead compounds within this program show potent and selective rescue of T-cell proliferation and function that is induced by either PDL-1 or TIM-3 but not by other checkpoints again indicating a selective profile.

We expect that our colleagues at Origin will present preclinical data from the CA-170 program as well as the PDL-1 TIM-3 program at scientific conferences this year. With regards to our other collaboration program with Aurigene, we in licensed the IRAK4 inhibitor in October of 2015 and have designated the development candidates as CA-4948.

IRAK4 is a serine/threonine kinase that is important mediator of Toll-like receptor and IL-1 receptor signaling and plays an important role in innate immune signaling. Based on its function in this pathway IRAK4 has been a target of interest for a generation of drug candidates for treatment of various inflammatory diseases.

Additionally, in certain human hematologic malignancy such as a subset of diffused large B-cell lymphomas oncogenic mutations in this pathway have been identified that result in constitutive activation of IRAK4.

Now Preclinical data with CA-4948 and other program compound show potent anti-tumor activity in cell base and in vivo tumor model assays especially those tumors models that have activating mutations in the IRAK4 pathway.

In addition to the cancer models, some of compounds from this program also demonstrate activity in in vivo inflammatory disease models indicating the potential of targeting IRAK4 in both oncology and inflammatory disease with our compounds.

We expect that our colleagues at Aurigene will also make presentations on additional preclinical data from this program at upcoming scientific conferences this year. We continue to work with Aurigene to complete the IND enabling studies for CA-4948 and expect to file an IND application for its clinical testing in hem malignancies in 2016.

We remain resolved to building the company through advancement of our pipeline. In 2016 our focus will be on executing the progression of CDUC-907 through Phase 2 clinical testing in patients with MYC altered relapsed refractory DLBCL and its further testing in patients with solid tumors including patients with NMC.

We are committed to filing the IND for CA-170 to initiate its clinical testing in patients with advanced cancers. And we continue to work closely with our Aurigene colleagues to complete the IND enabling studies for CA-4948 for its advancement in into the clinic in 2016.

We also anticipate that the optimization work will continue to advance in order for us to select the development candidate from our PDL-1 TIM-3 checkpoint antagonist program leading to the exercise of our option to license compounds from this program in the collaboration.

I will now like to turn to Erivedge which is being developed and commercialized globally by Genentech and Roche under our collaboration. Roche continues to concentrate on the global commercialization of Erivedge for the treatment of advanced BCC in key territories worldwide.

We recorded royalty revenues of approximately $2 million for the fourth quarter of this year as compared to $1.9 million for the fourth quarter of 2014. For the full year 2015, our Erivedge royalty revenues were $8 million as compared to $6.8 million for the full year of 2014.

We are pleased to note that Roche continues to invest in Erivedge and has recently initiated two trials with Erivedge.

One in patients with intermediate or high risk myelofibrosis where Erivedge is being studied in combination with ruxolitinib which is a JAK inhibitor as well as the second study in idiopathic pulmonary fibrosis or IPF where Erivedge is being investigated in combination with pirfenidone the standard of care for IPF.

I would now like to turn the call over to Mike Gray for his discussion of our financial results after which we will open the call to Q&A..

Okay, thanks Ali. For the year ended December 31, 2015 we reported a net loss of $59 million or $0.48 per share for basic and fully diluted rather as compared to a net loss of $18.7 million or $0.22 per basic and fully diluted share in 2014.

The 2015 net loss includes a onetime charge for in process research and development expense of $24.3 million associated with our issuance of 17.1 million shares of Curis common stock to Aurigene under the terms of our January 2015 collaboration agreement.

For the fourth quarter of 2015 we reported a net loss of $13.5 million or $0.10 per basic and fully diluted share as compared to a net loss of $5.7 million or $0.07 per basic and fully diluted share for the same period in 2014.

The fourth quarter 2015 net loss includes $6 million in payments to Aurigene for our exercise of options to license the CA-170 and CA-4948 programs. Revenues for the year ended December 31, 2015 were $7.9 million as compared to $9.8 million for the same period in 2014.

Substantially all of our revenues in 2015 and 2014 were recorded under our collaboration with Genentech. The decrease in revenue for the year ended December 31, 2015 was primarily due to a decrease in license fee revenues associated with the $3 million milestone payment that we earned during the year ended 2014.

Revenues for the fourth quarters of 2015 and 2014 were $2.1 million and $2 million respectively and were comprised almost entirely [in vivo, in vitro] two revenues. Operating expenses were $64.4 million for the year ended December 31, 2015 as compared to $25.7 million for the same period in 2014.

Operating expenses for the fourth quarter of 2015 were $15.3 million as compared to $6.8 million for the fourth quarter of 2014. As noted earlier we recorded a one-time charge in 2015 for in-process research and development expense of $24.3 million associated with the issuance of common stock to Aurigene.

Research and development expenses were $26.7 million for the year ended December 31, 2015, as compared to $13.7 million for 2014. The increase was primarily due to increases in spending on our CUDC-907 clinical development program as well as our programs under collaboration with Aurigene.

These increases were partially offset by decreases in spending on other programs including CUDC-427. R&D expenses were $12 million for the fourth quarter of 2015 as compared to $3.5 million for the same period in 2014.

We incurred $6 million in milestone payments under the Aurigene collaboration during the fourth quarter of 2015 in connection with our option exercises to license the CA-170 and CA-4948 programs.

G&A expenses were $12.9 million for year ended December 31, 2015 as compared to $11.7 million in 2014 and were $3.2million for each of the fourth quarters of 2014 and 2015. The increase in annual expense was primarily due to increased spending on legal costs, consulting and professional services as well as stock based compensation.

Other expense was $2.5 million for year ended December 31, 2015 and $2.9 million for the year ended 2014 and is primarily comprised of interest expense associated with the loan made by BioPharma-II to Curis Royalty which is a wholly-owned subsidiary of Curis.

Other expense was $215,000 for the fourth quarter of 2015 as compared to $878,000 for the fourth quarter of 2014. As of December 31, 2015 our cash, cash equivalents, marketable securities and investments totaled $82.2 million, and there were approximately 129 million shares of our common stock outstanding.

Turning to 2016 financial guidance, we expect to end 2016 with cash, cash equivalents and investments of between $27 and $34 million, excluding any potential future payments from new or existing collaborators. We expect that 2016 R&D expense will be between $40 and $45 million and the G&A expense will be between $12 million to $14 million.

These expense expectations include approximately $1 million and $2.5 million of estimated 2016 stock-based compensation expense in R&D and G&A expense respectively, based on awards that are outstanding as of today. With that, I will turn it back to Ali..

Thank you, Mike. Before we open up the call to questions I would like to certainly not least but last, would like to thank Mike Gray and [Jay Rayner] as you know you’re all aware of are leaving the company to pursue their other opportunities.

We thank Mike especially for the many significant contributions that he has made during his tenure as the Chief Financial Officer and Chief Business Officer at Curis and we wish him well in his future endeavors.

I would also like to thank Jay for her contribution in building the clinical development organization and bringing the clinical expertise at Curis as we prep ourselves for our expanding clinical pipeline to its instrumental and taking CUDC-907 through the Phase 1 testing and determining the dose and path forward for the drug candidate in patients with diffuse large B-cell lymphoma.

We wish Jay well in her future path as well. The company has benefited greatly from both Mike and Jay's experience and insights and I join the board and the employees of Curis in thanking them for their years of valuable service.

I also want to take the opportunity to introduce David Tuck, our Senior Vice President of Clinical and Transnational Sciences who will be leading the clinical developments activities at Curis.

David has been with the company since the first half of 2015 and brings a wealth of experience in the field of immune oncology and drug development as well as biomarker development. For example, during his tenure at Bristol Bristol-Myers Squibb he was involved in the development of ipilimumab as well as other immune checkpoint inhibitors development.

He has been an important addition to our team and will be leading the clinical efforts at Curis. I would now like to open the call to questions..

Thank you [Operator Instructions] our first question comes from line of Adnan Butt of RBC Capital Markets. Your line is open..

Thanks and nice progress on multiple [end shares].

First on 907 in terms of taking the Phase 2 that's ongoing into a registration enabling study has, what is the threshold that Curis is looking for and when would it hope to discuss those thresholds or the ability to do so with the regulators?.

Thank you Adnan and thanks for the question. So far as I indicated, let me just re-ash just some of the Phase 2 design in the patient population it gives you a good sense of timing as well.

The patient population is literally the same population that we enrolled for the Phase 1 trial so relapsed refractory patients with diffuse large B-cell lymphoma with the exception that the Phase 2 will select patients based on their MYC alteration before treatment.

We do intend to enroll up to 16 patients in the monotherapy arm of this study that's an open label study which means we will able to view the data and we have certain looking points that we have established for ourselves during the enrollment process.

We expect the enrollment to take somewhere in the 12 to 15 months timeframe for the study and as I indicated if the data as we go forward are consistent with what we have observed in the Phase 1 trial meaning that similar levels of response rate then we expect to discuss that with the FDA and ask for an expansion of this Phase 2 trial of the monotherapy arm to put the drug on registration path again using objective response rates as the primary end point..

Okay and maybe I can ask one on CA-170, the therapeutic window appears pretty wide so when would you expect to reach therapeutically relevant doses in the Phase 1, how quickly could you assess activity?.

This is a good question.

So, we feel quite comfortable that the drug is obviously safe in the models that we observed and again this is consistent both with other checkpoint inhibitors anti-bodies that have gone into the clinic and it's also consistent with the mechanism of relieving checkpoint inhibition in that these kinds of drugs are able to relieve repression of activated T-cells, they are not really intended to activate T-cells that's part of the reason that we think that we have such good therapeutic index, certainly with the oral small molecules as well.

Having said that as we indicated majority of our data in the in vivo activity models indicate that the drug is somewhere active in the 10 mg per kg dose level whereas in the safety models we have taken the drug all the way up to 1000 mg per kg per day administration and has remained safe.

This does allow us to initiate the Phase 1 trial at a comfortable dose one that we think based on calculation should result in repression of the immune activation but again the first study in patients in the Phase 1 trial will be a dose escalation, will start at a healthy dose for the patients but we will see as we go.

First safety, first and foremost but as we escalate we will do both evaluation of the biomarkers that we intend to look at and of course any of the clinical activity that may emerge as part of the study.

So I couldn't exactly tell you Adnan which dose or which cohort we expect to see it, we just feel as if that starting dose should be a good dose for the patients, we will look at safety first and then expect to see both immune activation and hopefully benefit for the patients in clinical form soon as well..

In terms of update would be just hear that it's moving from cohort one to two to three or you would be able to update on activity at some point?.

I think the later Adnan, I don't think this is the case where every dose cohort we would make an announcement that we have gone to the next cohort. I think, we better think for the shareholders and for the drug candidate is allow us to experience how to actually give the drug.

Our expectation is overall daily dosing and it continues those escalations, but these things yet we have to go into the clinic first and get that experience before we come out and describe what types of activities and safety and everything else that we think so. I doubt that we will do this cohort by cohort..

Thanks. If you can just let me ask Mike a question since this is his farewell call. Hi Mike, so does guidance assume exercise of any future programs from Aurigene and that's it? Thanks..

Yes, the guidance assumes exercise of one future program in immune-oncology which is a $3 million option exercise in 2016..

Okay thanks..

Thank you. Our next question is from the line of Joe Pantginis of Roth Capital Partners. Your line is open..

Hey guys good morning, thanks for taking the question and Mike good luck on your future plans as well.

So Ali first, with regard to one, I am sorry, 907 you said Phase 2 status update, can you be a little more granular on that if you can, I mean, with regard to potential data updates at say major medical conferences?.

We certainly, obviously the ASH would be an idea of timing for us to present the abstracts and do for a period of time.

We would certainly like to update at the ASH conference anything that we observe noteworthy wise for Phase 2, but certainly we would be wanting to update on the finality of Phase 1 trial, there are still patients ongoing in the Phase 1 trial in particular patients in the combination with rituximab expansion arm, but it’s still ongoing.

So likely that we will present at ASH again not committing right now just because the abstracts aren’t quite due yet, but certainly ASH can be a conference for CUDC-907 for us..

Well that's helpful thanks.

And if I can just focus one quick question and a little more broader question on the Aurigene collaboration, first on 4948 do you have specific plans yet or are you in wait and see mode with regard to moving into inflammatory indications?.

Our expectations are and where we have been looking at this star candidate and has been in hem malignancies, lymphomas are certainly an area these are malignancies including the DLBCL are an area that we would like to look at as well as other hem malignancies. But it will be predominantly hem malignancies that we will be looking at with CA-4948..

Not sure understood and I guess the broader question with regard to 170 or even just compounds coming from the program as you look to a lot of your pre-activities before getting into the clinic in identifying sites and such activities, could you describe the type of feedback you have been getting from the sites with regard to the general views towards having an oral immunotherapy compound since all the focus is on the biologics right now?.

Yes, I can tell you that there is high interest both in the concept of taking an oral small molecule from multiple centers that David has been in discussion with and investigators that would very much like to take this drug into the clinic for testing in their patients.

There is also level of excitement for taking a drug with this profile, target profile in particular for dual targeting of PDL-1 as well as VISTA. Both of those seem to be very attractive for investigators, the fact that it's an oral inhibitor as well as the opportunity to target these particular checkpoints has been of excitement.

David has been in discussion with multiple centers, several of which we will be entering and enrolling patients in the Phase 1 trial..

Thanks a lot guys..

Thanks Joe..

Thank you. Our next question is from Boris Peaker of Cowen, your line is open..

Great, thanks for taking my questions.

So first maybe on 907, do you have a sense of what or how frequently this alteration, MYC alteration is found, have you done or do you plan to explore various tumor type to just kind of get a sense of the landscape?.

Sure. As I mentioned at least what’s published in the literature with respect to MYC alteration in diffuse large B-cell lymphoma which is the fairly common occurrence up to 19% of patients have gene trans-locations of MYC and roughly third or so patients with diffuse large B-cell lymphoma have up regulation of the protein.

As I mentioned there is an amount of overlap associated with that meaning many patients that have trans-locations have MYC protein up regulations that's obviously the driver, the protein being the driver in this case.

With regards to other malignancies, in solid tumor we predominantly find gene amplifications increasing copy number with respect to MYC. NMC disease is an interesting one simply because that's where we find higher expression of MYC.

In other solid tumor cancers higher prevalence of MYC trans-locations appear to occur in patients with triple negative breast cancer for example, sub-populations of patients with colorectal cancer and hepatocellular cancer.

And then as I mentioned a few different pediatric cancers and in particular meduloblastomas they are driven by [semec] amplifications, high percentage of them especially the prognosis group or the highest risk group. And then, a significant portion of patients, pediatric patients with neuroblastoma that are driven by [indiscernible] amplification.

I hope that answers your question in the DLBCL obviously where we have majority of our data and up to a third of those patients are thought to be altered for MYC in one form or another..

Great, yes now that answers the question.

So one of my other question is for Mike in your last call, I just want to get a sense of what’s the timeline for pain off the royalty debt?.

2019 is what we are currently forecasting..

And the partnership will end…?.

The composition matter IP goes to late 2020s, end of 2028 so there is a lot of royalty life after the debt is repaid..

Got you, alright thank you very much for taking my questions..

Thanks Boris..

Thank you and that does conclude our Q&A session for today I will now like to turn the call back over to management for any further remarks..

Yes, thank you and lastly I would like to extend the thank you to all the employees of Curis for their hard work and bringing our programs to the state that they are in and allowing us to progress the company to one that is focused on developing effective drugs for patients with cancer and our eventual goal of commercializing some of these drugs.

I would also like to thank all of the patients and their families who participated in our trials and make these studies and analysis possible. And lastly again, I would like to thank all of the hard work that Mike and Jay have done for the company to bringing us to this stage as well. Thank you..

Ladies and gentlemen, thank you for your participation in today's conference. This does conclude today's program. You may all disconnect, everyone have a great day..