Oncomed Pharmaceuticals Inc. (NASDAQ:OMED)
Q2 2016 Earnings Conference Call
August 9, 2016 4:30 PM ET
Michelle Corral – Senior Director-Investor Relations and Corporate Communications
Paul Hastings – Chairman and Chief Executive Officer
Jakob Dupont – Chief Medical Officer and Senior Vice President
Sunil Patel – Chief Financial Officer and Senior Vice President-Corporate Development and Finance
John Lewicki – Executive Vice President-Research and Development
Maury Raycroft – Jefferies
Michael Schmidt – Leerink Partners
Ted Tenthoff – Piper Jaffray
Nick Abbott – Wells Fargo Securities
Good afternoon, everyone, and welcome to the OncoMed Pharmaceuticals’ Second Quarter Investor Conference Call. This call is being recorded.
And this time, for opening remarks and introductions, I would like to turn the call over to Michelle Corral, Head of OncoMed Investor Relations and Corporate Communications. Ms. Corral, please go ahead.
Thank you, Shenan. Hello, everyone, and welcome to OncoMed Pharmaceuticals financial results call for the second quarter of 2016. I’m Michelle Corral, Senior Director of Investor Relations and Corporate Communications for OncoMed.
Leading the call today is Paul Hastings, our Chairman and Chief Executive Officer. Paul is joined by Sunil Patel, our Chief Financial Officer and Senior Vice President of Corporate Development and Finance; John Lewicki, our Executive Vice President of Research and Development; and Jakob Dupont, our Chief Medical Officer and Senior Vice President.
Before we begin, I would like to remind you that during the course of this conference call, management will make a number of forward-looking statements, including the future financial performance of the Company. These forward-looking statements reflect our current views with respect to future events are based on assumptions and are subject to risks and uncertainties that could cause actual results to differ from those projected. Given these risks and uncertainties, you should not place undue reliance on these forward-looking statements.
Please refer to our Annual Report on Form 10-K for the fiscal year ended December 31, 2015, and our other filings with the SEC, which discuss some of the important risk factors that may affect our business, results of operations and financial condition and that could cause actual results to differ materially from the forward-looking statements made on this call.
Except as required by law, OncoMed disclaims any obligation to publicly update or revise any forward-looking statements to reflect events or circumstances that occur after this call. Although this call may be replayed as of a later date, its continued availability does not indicate that we are reaffirming or confirming any of the information contained in the live conference call today.
And with that, I’d like to now turn the call over to Paul Hastings.
Thanks, Michelle, and thank you all for joining us for our second quarter 2016 financial results and corporate update. We’ve had a busy quarter since our last update, with four posters at the ASCO annual meeting oversight of 14 ongoing clinical trials for our seven OncoMed discovered clinical candidates. Ongoing preparation of two new immuno-oncology IND filings and continued focus on discovery innovation. All with the goal of providing improved treatment alternatives for patients for cancer. The upcoming months promise to be equally productive with a number of important catalysts fast approaching.
Most notably, we will report on randomized Phase 2 data, earliest at the end of this year or likely in the first half of next year 2017 for tarextumab in first-line small cell lung cancer and demcizumab in first-line pancreatic cancer first half of next year. Both trials present opt-in opportunities for our partners at GSK and Celgene. What’s important about this that a potential opt-in by Celgene for demcizumab or GSK for tarextumab, what propel these programs into randomized Phase 3 pivotal trials and would represent the first of a total of a $172 million in potential partner payments that we are eligible for in 2017.
Given of course, all the caveats the trials are successful and the partners choose to opt in. Demcizumab will then become a co-development and co-commercialization option program for Celgene where OncoMed could contribute one-third world-wide development expense Celgene would contribute two-thirds and with a fifty-fifty profit split in the U.S. and a double-digit royalty ex-U.S. for OncoMed.
Tarextumab would move to randomized Phase III trials performed by GSK and OncoMed would be eligible for double-digit royalties world-wide following approval and commercialization by GSK with OncoMed being on the Joint Steering Committee. In addition, we will report Phase 1b data for vantictumab and ipafricept, in combination with standard-of-care in pancreatic cancer and Phase 1a/1b data for anti-RSPO3 this year.
The final data from these ongoing Phase 1b trials will inform potential opt-in decisions in the first half of 2017 from our partners Bayer and Celgene, that again would contribute to the potential $172 million in potential 2017 opt-in payments that I mentioned earlier.
RSPO3 opt-in would trigger a co-development, co-commercialization opportunity with Celgene and Oncomed and the Bayer opt-ins would trigger Bayer’s Phase II and beyond development of vantictumab and ipafricept and future high single-digit to double-digit royalties on the two molecules to Oncomed with participation on the Joint Steering Committee.
Also we intend to report Phase 1a first-in-human data for our DLL4/VEGF bispecific antibody at a medical meeting later in 2016. So by this time next year our earlier stage drugs the anti-DLL4/VEGF bispecific and brontictuzumab our anti-Notch1 antibody, we’ll be enrolling Phase 1b clinical trials and we will have began clinical trials for our two new immuno oncology programs bringing the total number of clinical stage OncoMed discovered novel therapeutics to nine.
Turning our focus to the quarter that’s just completed, Jakob Dupont, our Chief Medical Officer will now give us some highlights from our recent ASCO presentations on demcizumab, tarextumab, vantictumab and ipafricept. Following that Sunil Patel, our Chief Financial Officer, will walk us through the financial highlights of the quarter. Jakob?
Thanks Paul and hello to everyone joining us today. On the heels of a highly productive AACR meeting where we presented data for GITR ligand FC vantictumab, anti-RSPO3 and demcizumab programs, we had four clinical data presentations at the ASCO Annual Meeting. A real highlight of Oncomed’s ASCo was a presentation of data of our two Wnt pathway inhibitors in Phase 1b, which were featured in a poster discussion session. These were the first presentations of combination data vantictumab and ipafricept with standard-of-care chemotherapy.
As Phase 1b study’s, safety is the primary endpoint in both combinations trials and we’re we're pleased to report that we are seeing very good signs here. As you may recall early on in our studies of vantictumab and ipafricept, we saw some bone toxicity in the form of mild to moderate agility fractures following a brief partial clinical hold we implemented a bone safety plan that includes a dosing strategy, a monitoring of bone markers and bone density along with the occasional administration of zoledronic acid and upon the implementation no such subsequent fractures have been observed in either trial.
Vantictumab is being studied in combination with paclitaxel in patients with HER2-negative breast cancer. In addition to safety we’re looking at preliminary efficacy and biomarkers. What we saw with the vantictumab did not appear to exacerbate paclitaxel’s side effects. And the most common toxicities reported were fatigue, constipation, diarrhea and nausea. We’ve also seen early signs of efficacy particularly in the difficult to treat breast cancer cohorts overall of the 27 patients valuable for response, the overall response rate was 33% in the study. Some of the most encouraging anti-tumor responses were observed in patient subgroups with high unmet medical need, such as third-line metastatic patients where four out of 11 or 36% achieved partial response and patients with triple-negative breast cancer in which six of 15 patients or 40% achieved partial response with the combination. These subgroups would be expected to be among the very least responsive to treatment.
Additionally OncoMed's breast tumor six-gene signature biomarker appeared to successfully identify HER2-negative breast cancer patients who achieved better progression-free and overall survival outcomes with vantictumab and paclitaxel treatment. The six-gene Wnt pathway signature does not appear to be prognostic in the HER2-negative breast cancer setting thus we feel this could be a predicted biomarker for vantictumab and breast cancer in later stage development of the drug candidate.
The ipafricept ovarian cancer trial also presented at ASCO is designed as a dose escalation study to assess the safety and tolerability of the ipafricept in combination with paclitaxel and carboplatin in patients with recurrent platinum-sensitive ovarian cancer. The most common toxicities reported were nausea and fatigue, and higher grade ipafricept-related adverse events included neutropenia and hypophosphatemia. Early encouraging evidence of anti-tumor effects was also observed in this study.
Of the 19 patients valuable for response, the overall response rate was 84% with eight patients or 42% achieving a complete response and eight patients or 42% once again with partial response. An exploratory biomarker analysis described patient tumors with high Wnt activation to be more likely to achieve a complete response to ipafricept and carboplatin/paclitaxel treatment, once again suggesting a possible predicted biomarker for this drug.
In addition to the data, we presented for our Wnt inhibitors, we noted with interest an oral presentation by Dr. Jason Luke from the University of Chicago to discuss the potential role of the Wnt pathway in tumors that are resistant to immune checkpoint inhibitors. The Wnt pathway has long been associated with beta-catenin signaling, which is known to present T-cell invasion and undermine immune system attacks of tumors and consequently prevent immune oncology therapeutics for being effective. Thus Dr. Luke and Dr. Gayeski’s research conclude that the testing of Wnt pathway inhibitors in combination with immuno-oncology agents could be an important priority, since it’s believed that disrupting the Wnt/beta-catenin signal could turn these so called non-inflamed tumors into inflamed ones and thus make these tumors vulnerable to immune system attack.
We believe we maybe the first in the clinic with targeted large molecule Wnt pathway inhibitors and are well-positioned to answer these important clinical questions. We’ve been approached by academic investigators and others interested in developing studies to test these combinations. This is a scenario of interest for us and for Bayer and an opportunity that we will be monitoring closely.
Additionally, at ASCO two presentations occurred that represented updated data. In particular, the Phase 1b results of tarextumab in small cell lung cancer and demcizumab in first-line non-small cell lung cancer these data were highly consistent with what we reported previously from Phase 1b studies, so just a few key points from each presentation.
Starting with tarextumab, 15 patients treated at higher does of the antibody above 10 milligrams per kilogram with chemotherapy appeared to have greater reduction of target tumor lesions on CT scan, and resulted in an important survival, in improved survival outcome with a median overall survival of 16 months. In contrast 12 patients treated with lower dose tarextumab of 10 milligrams per kilogram or less and chemotherapy had a median survival of seven months of no published survival rates for chemotherapy and this setting is about 9.4 months.
Also new data was presented indicating the patients with tumors were high in the Notch pathway genes of Hes1, Hes6, Hey1 and Hey2, achieved improved survival compared to those tumors that did not show elevated expression of these Notch genes. Results were particularly pronounced in the patients who received higher doses of tarextumab, taken together these data support our selection of 15 milligrams per kilogram of tarextumab as the Phase 2 dose in combination with chemotherapy and the potential of Hes/Hey expression on these tumors as a predictive gene signature, as a secondary endpoint of the Phase 2 PINNACLE trial.
Turning to the demcizumab data, the most important takeaway was that we continue to see a tail on the Kaplan-Meier survival curve, meaning prolonged survival in the subset of first-line non-small cell lung cancer patients. These subjects receive combination of demcizumab with carboplatin and pemetrexed chemotherapy with another five months of follow-up since our last look in December. We had no new deaths occur on study. 35% of patients or eight out of twenty three remain alive between 18 and 37 months since initiating treatment.
The rest of our clinical development efforts continue to advance notably we’ve moved our Phase 1b clinical trial of demcizumab plus Keytruda into the expansion cohorts. Additional we will present two abstracts of Phase 1b trials of vantictumab and ipafricept in combination with chemotherapy and the first-line metastatic pancreatic cancer at the European Society for Medical Oncology or ESMO annual meeting in Copenhagen, in Denmark in October.
Additionally, pending abstract acceptance as Paul mentioned, we hope to present first-in-human clinical data of our novel anti-DLL4/VEGF bispecific and our novel anti-RSPO3 candidate later this year. And our efforts to file an IND on either GITR ligand FC or immuno-oncology agent number two before year-end remain on track. We look forward to keeping you updated on our progress for all of the above.
I’d now like to turn the call over to Sunil. Sunil?
Thank you Jakob. As a reminder more details on our financial results can be found in our Form 10-Q which was filed today with the SEC. For the second quarter, as of June 30, 2016, we had cash, cash equivalents and short-term investments of $171.5 million, compared to cash of $193.5 million as of March 31, 2016.
Revenues in the second quarter 2016 were $6.7 million, as compared to $4.7 million in the second quarter of 2015. The $2 million increase in revenue over the same period in 2015 was primarily due to the $70 million safety milestone achieved in the fourth quarter of 2015, which was recorded as deferred revenue and amortized over the estimated performance period of the collaboration.
Research and development expenses for the second quarter of 2016 were $29.7 million, compared with $22 million for the same period in 2015. Higher R&D expenditures during the second quarter 2016 were attributable to increased manufacturing and clinical costs for the Phase 2 demcizumab program, and the Phase 1a/b trial of anti-RSPO3, as well as IND-enabling manufacturing and toxicology costs for the GITR ligand FC and the IO#2 programs.
G&A expenses for the quarter ended June 30, 2016 were $4.8 million, compared to $4.3 million for the same period in 2015. The increased cost during the second quarter of 2016 were due to higher employee-related costs, including stock based compensation expenses.
Net loss for the second quarter of 2016 was $27.7million or $0.91 a share, compared to $21.6 million or $0.72 a share for the same period of 2015. The change in net loss was due to the increases mentioned above in research and development expenses.
Overall, our spending remains in line with 2016 projections at approximately $10 millions per month and we expect to end the year with the cash balance of more than $100 million.
Without any partner revenues from milestones or opt-in payments, we have sufficient run-way to the first quarter of 2018. Between now and the end of 2018, we may be eligible to receive more than $270 million in opt-in and milestone payments from our partners at Bayer, Celgene and GSK. And as Paul mentioned, we estimate that more than $172 million of that could be achieved in 2017.
I will not turn the call back over to Paul.
So thanks Sunil. And in closing I’d like to briefly review some upcoming milestones and catalysts. So before year-end, we look forward to submit more data presentations for our Phase 1 pipeline candidates. Additional 2016 milestones include the IND filing for the first of our two new immuno-oncology candidates, prior to year-end.
As Jakob mentioned we will file on either our wholly-owned novel GITRL fusion or our Celgene partnered IO#2 candidate with the second IND to follow shortly thereafter.
Now as mentioned at the top of this call, 2017 promises to be an even busier year with data from multiple Phase 1b and randomized Phase 2 clinical trials for tarextumab, demcizumab, vantictumab, ipafricept and anti-RSPO3, that could trigger optons from each of our partners totaling more than $172 million in 2017. These optons as well as other collaboration revenues can result in $270 million in payments between now and the end of 2018. We will continue to keep you informed of more specific timing. Our diversified and deep pipeline, our discovery and development capabilities and our partnerships with Celgene, Bayer and GSK provide us with numerous opportunities to build value and we are highly optimistic about what the future holds for our company, our shareholders and for the patients who may ultimately benefit from our drugs.
So right now, like to open the call for Q&A. As a reminder, Jakob, Sunil and John are with me and available to answer your questions. Operator questions and answers please.
[Operator Instructions] Our first question comes from the line of Brian Abrahams of Jefferies. Your line is now open.
Hi, thanks for your question. This is Maury on for Brian. Congratulations on the progress. I guess to start, can you remind what the expansion cohorts will look like for the Demcizumab plus Keytruda combo trial? And a comment on the types of cancers you're anticipating in the PD1 refractory solid tumor cohort?
Sure. So we have three expansion cohorts in that study, which are initiating enrollment now. The first is second-line, non-small cell lung cancer, non-squamous histology. The second cohort is anti-PD-1 progressor patients. And to your second question, I think, we would expect patients to come on to study that have been through other PD-1 inhibitors for approved indications, such as lung cancer, renal cell, bladder cancer, melanoma. I think those are the likely indications that we would see. And in terms of the third expansion cohort that is castrate-resistant prostate cancer. Those were the three expansion cohorts.
Okay, and then for the PD1 refractory patients, any ideas in if these will be weighted more towards Pembrolizumab, or Nivolumab, or some other PD1?
We are open to any of the above. I think we just have to see how the enrollment comes. I suspect we’re going to see patients who received either nivolumab or pembrolizumab or for that matter vedolizumab [ph] as well.
Okay, and kind of a big picture question, I guess based on the recent update from Bristol Meyers last week, just wondering if PDL1 cut off, if that has any impact on your view on biomarkers in general, and any impact on the current trials that you're running in future trial design?
Yes so I think this is very interesting we’ve obviously been following the story of the frontline lung cancer space very carefully because we have the on-going DENALI randomized Phase 2 where we’re combining demcizumab with carboplatin and pemetrexed. So we certainly are developing this phase with one of our anti-cancer stem cell agents that also incidentally does have immune effects we believe through the modulation of myeloid-derived suppressor cells in the tumor of these lung cancer patients.
Our biomarker data has suggested that PDL1 status of non-small cell lung cancer tumors does not matter, so the efficacy of demcizumab is based on our Phase 1b data that we presented on numerous occasions, including recently at the ASCO meeting. So we think that we are in a very good place in terms of not being tied to PDL1 expression, we think our drug can work in – either in the presence of PDL1 overexpression or in the absence of PDL1 overexpression.
And I think the other point I’d like make is and you brought up the Keytruda Study that we have ongoing. We have set our drug up for hopefully success in a variety of different ways. Obviously our long-term development strategy has been to combine demcizumab and lung cancer with a platinum bevelled in front line metastatic disease we still think that’s a very viable strategy currently.
But then with the emergence of the checkpoint inhibitors, we’ve also obviously initiated the combination trial with demcizumab plus Keytruda. And as you heard one of the cohorts that we’re looking at is non-small cell lung cancer. So I think we hopefully are going to be set up for success with our progress in Celgene in lung cancer either in combination with chemo or in combination with a checkpoint inhibitor.
So we’re prepared for whatever standard-of-care emerges whether it’s current or future standard-of-care, we’re ready for both. Bryan.
Thanks very much. Thank you very much.
Thank you. And our next question comes from the line of Michael Schmidt of Leerink Partners. Your line is now open.
Hi, thanks for taking my questions. I had one regarding the upcoming update at ESMO on the Wnt pathway inhibitors. Just wondering what invest in ex some cases [ph] should be going into this update? Maybe could you comment sort of number of patients treated, and sort of duration of follow-up, and sort of what you're trying to – I guess what are some of the outcomes that are being assessed, there?
Absolutely, so thanks for the question, Michael. I think the ESMO update is going to have a very similar appearance to the Wnt combination trials that we personated at ASCO in breast and ovarian cancer. So for the two pancreatic presentations at ESMO, you’re going to see similar types of data here at ipafricept with gemcitabine Abraxane, vantictumab. With gemcitabine Abraxane you are going to see safety data, you are going to see if there are any bone concerns. After we amended these protocols, you are going to biomarker data, including data on predictive biomarkers, and you are going to see early efficacy of the sort that you saw in the breast cancer and the ovarian cancer study, namely response rates, waterfall plots. And we will certainly give some information on the duration of patients on study.
And in terms of the amount of information you will see, it’s roughly going to be the same magnitude that you saw for the breast and ovarian study because all of these trials were essentially started around the same times, a couple of years ago. And you are going to see similar numbers of patients with about the same if not a little bit more follow-up on these patients because we’re doing a very recent data – data now in preparation for ESMO.
Great, and then to sort of thinking about the patient type that's being enrolled in these pancreatic cohorts, would the impact trial be the correct comparator for assessing a standard of care efficacy relative to the patients that are enrolled in your study?
Yes, I think that's very appropriate. With these two trials we really did use impact as the reference study for that new standard-of-care of gemcitabine and Abraxane. So when you think about how we dosed the patients the scheduling of gemcitabine and Abraxane and the doses that we used, and the way we – the eligibility criteria and so forth, they're very similar to impact, where obviously we made a few modifications in terms of the eligibility criteria after we came about the bone adverse event early on in the clinical development of ipafricept and vantictumab. But I think by and large these are very similar populations to impact.
Great, thanks. And so, post-ESMO, will there be another data readout, or will that package then go to Bayer for the opt-in decision right away?
Well, so what you'll see from the ESMO, the two presentations at ESMO, the pancreatic studies and what you saw at ASCO in the breast and ovarian trials that these were ongoing studies. So we are still, as we described, continuing to enroll patients. The timing of completion of these four studies from an enrollment perspective is toward the end of this year, beginning of next, so our timelines for presenting an opt-in packaged to Bayer remains in that first half of next year. But these – so we are getting towards the end of the studies, I’m sure that we’re going to present once the studies are completed enrollment with our partners. Bayer will present the final results from these trials. We should be at some point next year at the maximum [ph].
And we are in discussions with them on an ongoing basis relative to the data as it emerges. So between now and when we present the opt-in package to them, which could be early next year, they get updates regularly on where we are.
I see, thanks. And then one more, if I may, regarding the anti-RSPO3 program. I'm just wondering, similar question going into this data update at year-end. The source data look rather – will that already include patients with selected genetic alterations?
Yes, so as you’ve heard in our updates and also the recent update from Gordon Health, we believe the anti-RSPO3 program is one that has the strong connection to predictive biomarker hypotheses, one of which being RSPO3, overexpression by tumors and certainly another being these trans-locations that we see in colorectal cancer are the RSPO3 gene which has been reported on an nature publications, and so forth. So we certainly do intend, pending the acceptance of the abstract at the medical meaning at the end of the year, that we will present for the RSPO3 program, the safeties and preliminary efficacy, as well some biomarker data, including information on those predictive biomarkers.
Okay, great, thank you so much.
Thank you, Michael.
Thank you and our next question comes from the line of Ian Somaiya of BMO Capital Markets. Your line is now open.
Hi, this is Nate [ph] on for Ian. Congrats on the progress, and thanks for taking my questions. My first is about the upcoming Phase 2 data for Demcizumab in pancreatic cancer. So, based on your discussions internally and with Celgene, what are you looking for in terms of a response outcome that you would consider positive and could really move the program forward? And is there any way you could see data that would support filing based on the Phase 2 data?
So let me start with our partners. All are looking for trends in the Phase 2 studies and in the studies before that that we’ve conducted with them to make opt-in decisions. But Jakob you might want to expand further on, what we might expect to see?
Certainly, so the Yosemite trial, which you’re referring to, which is that global randomized Phase 2 study of about 200 patients, we haven’t reported that we are coming towards the end of enrollment of that study, which is obviously very exciting, it’s a three-arm trial, with two experimental arms, one control arm and that is the opt-in study for Celgene, as Paul mentioned. We and our partner Celgene are looking to make a decision of whether or not to take the program into Phase 3.
The study is designed as the progression-free survival trial, obviously to try to get an early read out, but we acknowledge that for registration and so forth that overall survival will likely be the desired end-point from the FDA perspective. So we will certainly look at the totality of the data with Celgene, we’ll look at response rates, we’ll look at PFS that primary end point, we’ll certainly get a strong read of overall survival on the trial and obviously safety. And we believe the safety of this program has been going very well after we switched the truncated dosing. And we will certainly seek to get a statistically significant result on PFS. And we set the study up to show about a two-month improvement in PFS.
But again, as Paul mentioned, the goal here is to show trends and directions that really make the program worthy of taking to Phase 3. Now to your question about whether or not this would be a registration-enabling trial. We haven’t designed the study in that regard, but obviously, if the data are very strong and if we feel that this would be to the benefit of patients out there to have a discussion with the FDA and other regulatory authorities based on the safety and the efficacy that we see, we would certainly be open to that possibility.
Great, and then with the Keytruda combo study, do you have any data pre-clinically that would support efficacy in PD1-resistant tumors? And then I guess, following up from that, when should we anticipate data from this trial, given the fact that some of these patients have a very high on the E to end [ph] are likely, or prognosis? Do you think that we could see data sooner than later?
Yes, so this is John. We presented data at the ACR meetings for the past two years and in reality that Keytruda plus DEM study is really founded on a strong preclinical foundation. In those studies, we’ve demonstrated synergistic active, we look at a range of different tumors in immunocompetent mice, we've demonstrated synergistic activity between the Keytruda and DEM, we’ve even demonstrated activity of DEM and in synergy with PD1 in tumors that are not that responsive to anti-PD1. So I think that speaks to the issue of potentially refractory states.
I think what really underlies our enthusiasm here is a quite prominent memory T-cell response that occurs with demcizumab and is particularly amplified in combination with anti-PD1. In those studies, we've treated animals with either agent alone or in combination. In animal what we've done is we've taken animals that have basically been cured and weeks and months later we've re-challenged them with tumor cells we’ve done this multiple times and tumors fail to do recur. So really in entering into this study like I said was really based on very strong preclinical data that provided the rational.
And this is Jakob to your second question about data availability and we certainly agree with the statement about high unmet medical need for these patients. So we are targeting some point next year for data presentation as you heard on today's call, we have completed dose escalation, we're now moving into the expansion cohorts, we obviously would like to get those expansion that enrolled as quickly as possible, we have great and very engaged sights and hope to do that but my anticipation is that we would try to present something publicly on this data some point mid to later part of next year.
Great. Thanks for taking the question.
[Operator Instructions] Our next question comes from line of Ted Tenthoff of Piper Jaffray. Your line is open.
Great, thanks very much. Just want to get an update, I know there was some commentary on this earlier today, but with respect to progress towards a clinic with the novel immuno-oncology agents, always impressed by the breadth and depth of this pipeline. But, when can we actually see some of those advance in the clinic as well?
So as we've said Ted and Jakob and John might want to add to this or maybe not, but we expect to follow one of the INDs later this year, the second one early next year. So pending the filing of the IND and the acceptance of the IND and first patient and it’s usually between 30 days and 60 days after we file. So that’s when we would expect to be in the clinical, the first one and then the second one in the next half of the following year, with the same sort of scheduled of events.
Those will just be the first two and there’s others behind those, as we move things along, right Ted.
Excellent. Well, I'm looking forward to data in the back half, and for some of the filings on those new INDs, too.
Thank you. And our next question comes from the line of Jim Birchenough of Wells Fargo Securities. Your line is now open.
Hi, good afternoon. It's Nick, in for Jim. Good afternoon, ladies and gentlemen, thanks for taking my questions, and as always, a very data-rich report. It makes taking notes a bit of a challenge. But so just going back to the Dem plus Pembro, so is it too early for you to be able to comment on any biomarker data that perhaps suggests an increase in the inflammatory tumor microenvironment, or some positive biomarker changes that you've observed from the preclinical studies?
Yes, so I cannot comment on I’m sure John, might want to add to that as well. We obviously have extensive biomarker programs in that clinical trial of demcizumab plus pembrolizumab and we are collecting those samples, we’re obviously looking at cellular things related to the immune system, also cytokines and other gene aspects that we’re looking at, as well. We haven’t analyzed that data yet. But as John, articulated early articularly the girl we think that the really nuanced aspect of the mechanism of action of adding demcizumab to pembrolizumab is around these myeloid-derived suppressor cells, where we see – in our pre-clinical models, we see reductions of MDSCs after treatment.
So while we’re catching our net somewhat broadly looking at the immune effects of adding demcizumab to pembrolizumab, we are focusing to a significant degree on those MDSCs and working with our investigators like Johann de Bono at The Royal Marsden and really trying to understand more about these MDSCs and what happens, when you add on the demcizumab treatment. I don’t know John if you want to…
No, I don’t really have very much to add. I think Jakob summarized it well. I mean the one thing to add is we undertake the clinical studies with Keytruda and DEM. We do have – once again, we’ve done extensive biomarker work pre-clinically. So we have enough number of different methods, assays and things established that will allow us to evaluate various markers whether they would be save times, whether they would be circulating blood cells, whether they would be potential alterations in tumor and we’re well positioned to investigate those things as the data rolls out.
Thank you. And then so, following-up on that if Celgene elects not to opt in after Yosemite, do they get a second bite with the combo data?
They do and they get a second bite with DENALI and then they get another – third bite if you will and then another bite with the bispecific because the bispecific is the DLL4 containing antibody as well. So, Celgene has partnered a number of our compounds and there will be five of six will be co-development, co-commercialization opportunities including demcizumab and bispecific. But the demcizumab and bispecific molecules both contain anti-DLL4 component of demcizumab and they get multiple bites at that apple.
And we would expect them Nick to bite at the first one particularly since this is going to be pancreatic cancer right in their suite spot, nothing else has worked so far. And we have high hopes in keeping our fingers crossed that is a molecule that's very material to them and to us and will create a lot of value for everybody.
Okay. It makes sense to me. A question on the predictive biomarkers, have you been able to look longitudinally, do these biomarkers appear to change their expression as patients’ progress through various lines of therapy or do they look like they remain quite stable?
It’s something we're looking at Nick, but I think the real important aspect here is that these are predictive biomarkers. So what's really important to us is the expression of these biomarkers at baseline and what we've basically shown for instance with the six-gene signature associated with vantictumab and breast cancer. We’ve shown that that are very strongly predicts outcomes. We did extensive preclinical studies to show that it’s strictly predicted whether or not a tumor in combination with chemotherapy was responsive. So while these markers may change longitudinal manner and while we’ve analyzed the number when genes that absolutely change in response to therapy, I think that few of these predictive markers has said they’re really predictive at baseline.
Okay, okay, that make sense. And my last question just on the GITR ligand program, so it was obviously becoming quite a crowded area. Can you comment on where investigator that you’re speaking with appreciate potential benefits of your approach first as an antibody approach for example, a standard antibody?
Are we talking about GITR ligand, Nick, is that what you’re saying?
Yes, sorry, yes.
Go ahead. Do you want to take a shot at that, Jakob.
Sure, yes, so I think we’ve received quite a bit of interest. We’ve mentioned before that we did an immuno-oncology advisory board. We have a key group of eight academics expert immunology advisors both clinical and pre-clinical and we presented this program in addition to our own number two program and we have received very good feedback. And these investigators have shown great interest in participating in the Phase 1 clinical trial of that that program pending the IND acceptance and so forth.
So I think people will recognize the novelty of the try Merck GITR ligand Fc approach. And I think again that that efficacy that we’ve shown at AACR, as John mentioned, where we actually see robust single agent activity granted in the pre-clinical setting with this GITR targeting approaches is something that we’ve received very good feedback on that. And it is looks like a post molecule. So I think we’ve seen quite a bit of interest.
Just to add reiterate what Jakob said, I think people do see our approach very compelling and I think the key is that we – our approach is very differentiated for the crowd here. And we believe it’s a much more effective approach.
Right. And let me just say that between John Lewicki, Austin Gurney and Tim Hoey, these guys and Ann Kapoun works on the biomarker component in discovery. This strategy and Nick, you know, because you were there at that poster with us at AACR that GITR ligand poster got a lot of attention. It’s still early, but Austin has discovered something that’s very unique. We get a lot of comments about it, no matter where we go from whether it’s at scientific meetings or with investors, who really dig into the details.
And we look forward to generating more data on that. Presenting that and just a reminder that that is a wholly-owned OncoMed asset, that is not partnered. And that sort of transitions us from the 50:50 or the one-third, two-third cost and 50:50 profit split co-development and co-commercialization to a wholly-owned OncoMed asset. So that’s the next step for us and we look forward to moving that along as quickly and expeditiously and clinical relevant as possible.
Great. Thank you very much and I look forward to seeing you in cloudy, Copenhagen later in the year.
On Saturday, yes, we’ll see there. Okay, thanks, Nick. I think we have one more follow up question, is that right from Michael at Leerink.
Yes. Your line is now open.
Hey, guys. Thanks for taking those – yes, thanks for taking my follow up. It’s just on the biomarker aspect of some of your studies. So for the Wnt pathway inhibitors, is the gene expression signature the same in the pancreatic trial that compared to the other trials that were done before?
Yes. This is Jacob. They're not actually. So we in our efforts to define predictive biomarkers coming out of our xenograft models and really moving those into the clinic. We certainly looked and brought biomarkers when we looked at tumors specific ones as well. So when you look at the – and we presented this data at meetings like AACR, but our signature for vantictumab breast is distinct from ipafricept ovarian, which is distinct from vantictumab and pancreatic as well.
But in all instances reflective of the Wnt pathway – associated with the Wnt pathway.
Yes. And is it true that the biomarker analysis is that pre-specified going – before starting the study.
Well, in these Phase Is absolutely, so what we do actually is we require a baseline tumor samples to the mention for every patient enrolled in the Phase I trials. These are obviously open label studies. But we have locked in these signatures in some cases like the breast cancer, six gene signatures in RUO test that can be rapidly converted to a CLIA test. And then what we tend to do is collect a number of these tumors all at once and have saved them all at once to see how these the signature is pan out across different patients now. To your maybe another inference of your question has to do with how we might use this going forward with our partner Bayer, if Bayer were to opt-in to the vantictumab and ipafricept what would the possibilities be.
Certainly you could do what we've done in Phase I, which is collect based on tumors and take in all comer population and look for yours signatures and correlate that with PFS and OS and those types of efficacy end-points or you could consider doing a selection trial where you test patients at baseline. I think either possibility is open in Phase II and beyond, but we certainly feel good about the fact that as we moved these programs, run the pre-clinical arena into the clinic that we have some robust hypotheses that are really well setup for later stage testing.
Okay, great. Thanks so much for the follow-up.
Thank you, Michael.
And I’m showing no further questions at this time. I would now like to turn the call over to Mr. Paul Hastings for closing remarks.
Great and thanks everybody for joining us today and for your continued support. And as many of you have said, since 2004 this company has put seven OncoMed discovered drugs into the clinic and 14 different clinical trials. There will be two more INDs filed for total of nine. OncoMed discovered both cancer stem cell and immuno oncology therapeutics, hopefully by this time next year.
So, we look forward to updating you on the progress across this entire research and development pipeline in the months to come and the team is always accessible to answer your questions. So thank you very much for joining us today.
Ladies and gentlemen, thank you for participating in today’s conference. This concludes today’s program. You may all disconnect. Everyone, have a great day.
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