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The data showed a significant association between CXCL12 expression and clinical benefit, including high levels of activity in both expansion cohorts: patients with angioimmunoblastic T-cell lymphoma, an aggressive form of T-cell lymphoma, often characterized by high levels of CXCL12 expression and patients with PTCL who lack a single nucleotide variation in the three prime untranslated region of the CXCL12 gene. We believe these data are strong enough to support potential registration of tipifarnib in both patient populations, and we intend to have discussions with regulatory authorities and key opinion leaders around next steps for the program.

In addition, based on the extraordinary activity observed thus far, we plan to continue enrolling patients in the AITL cohort of our Phase 2 trial in order to acquire more experience regarding safety and tolerability in this population, and we expect to provide additional data from this cohort at a medical meeting later this year. We believe that based upon the revised 2017 WHO classification of T-cell lymphomas, AITL and related lymphomas represent approximately one-third of all PTCL cases.

Our approach in CXCL12-driven PTCL has been consistent with the development strategy in HRAS mutant head and neck squamous cell carcinoma. We're primarily focused on indications where we can potentially drive single agent activity with durable objective responses. Further, we seek to identify the subsets of patients who are most likely to respond to treatment. Such indications ideally can be pursued with smaller single-arm registration-directed studies. Once we establish a foothold in a given indication, we can work toward broadening to earlier lines of therapy and expanding to larger patient populations, either as a single agent or in combination approaches.

In addition to establishing clear clinical proof-of-concept in T-cell lymphomas, we believe we've made significant progress toward broadening tipifarnib's potential to treat other CXCL12-driven indications of high unmet need. For example, we recently reported retrospective data from a Phase 2 trial of tipifarnib in patients with relapsed or refractory lymphomas. Our analysis identified pre-treatment tumor, CXCL12 expression, and CXCL12 reference sequences as potential biomarkers of clinical benefit in patients with diffuse large B-cell lymphoma and mycosis fungoides, the most common form of cutaneous T-cell lymphoma.

Further, recall earlier this year, we reported the identification of a potential association between CXCL12 expression and clinical benefit from tipifarnib in patients with pancreatic cancer. We continue to do additional preclinical work to validate tipifarnib in a CXCL12 high sub-population of pancreatic cancer patients, and we expect to initiate a proof-of-concept study early next year. Over time, we believe CXCL12 pathway biomarkers could enable registrational strategies for tipifarnib in multiple hematologic and solid tumor indications.

Now, let's turn our attention to our most advanced program, HRAS mutant head and neck squamous cell carcinoma, or HNSCC. The primary focus of the company continues to be the execution of our initial registration-directed trial of tipifarnib. To recap, the treatment cohort of our registration-directed study, which we call AMHN, is designed to enroll at least 59 evaluable patients with HRAS mutant HNSCC who have received prior platinum-based therapy. AMHN initiated in November 2018, and it is expected to take approximately two years to fully enroll.

Meanwhile, we've enrolled additional patients in our ongoing Phase 2 trial of tipifarnib in HRAS mutant HNSCC, which we call RUN-HN. We plan to provide an update from RUN-HN at a medical meeting later this year. The update's expected to include follow-up from ongoing patients as well as preliminary data on newly enrolled patients in both the HNSCC and other SCC cohorts. We remain enthusiastic about the potential for tipifarnib to treat patients with HRAS mutant tumors. Although our initial registration will focus on relapsed and/or refractory HRAS mutant HNSCC patients having HRAS variant allele frequency measurements greater than or equal to 20%, we see a broader opportunity set that includes combination therapies with immune therapies, cetuximab, and potentially chemotherapy. We intend to pursue these expanded indications as our resources permit.

Consistent with our perspective on a larger set of development opportunities for tipifarnib, I'm pleased to report we've also expanded the patent protection for tipifarnib in both the U.S. and Europe. Last month, we announced the U.S. Patent and Trademark Office issued two new patents, a method of treating patients with HRAS mutant HNSCC with any farnesyl transferase inhibitor and a method of treating patients with HRAS mutant non-small-cell lung carcinoma with tipifarnib. In addition, the European Patent Office granted a patent directed to the use of tipifarnib as a method of treating patients with HRAS mutant HNSCC. Each of these patents has an expiration date of August 2036, excluding any possible patent term extension. These new patents strengthen our competitive advantage as we continue to advance the development of tipifarnib. We now own a number of independent issued patents covering tipifarnib in HRAS mutant HNSCC, and we will continue to aggressively pursue additional intellectual property protection in the U.S. and abroad.

Now, let's spend a moment on each of our emerging pipeline programs, beginning with our ERK inhibitor, KO-947. KO-947 is a potent and selective small molecule inhibitor of ERK, which we are advancing as a potential treatment for patients with tumors that have dysregulated activity in the MAPK pathway. Our preclinical data suggests that KO-947 has anti-tumor activity in KRAS- or BRAF-mutant adenocarcinomas as well as certain subsets of squamous cell carcinomas. We continue to evaluate dosing regimens for KO-947 with a goal of reaching a recommended Phase 2 dose or maximum tolerated dose. We anticipate completing the dose escalation portion of our Phase 1 trial by the end of this year.

In conducting the dose escalation trial for KO-947, our goals are to establish a go-forward dosing schedule, an understanding of the safety and tolerability profile, pharmacokinetic and pharmacodynamic data, some ERK inhibition or other biomarker data, and any early signs of anti-tumor activity. Although most of the patients in the dose escalation portion of our study will be in difficult to treat populations, such as pancreatic and colorectal cancer, we believe our Phase 1 strategy will provide a solid foundation to make data-driven decisions for KO-947's best path forward.

Our other emerging pipeline program is KO-539, a potent and selective small molecule inhibitor of the menin mixed lineage leukemia, or menin-MLL protein-protein interaction. We've generated preclinical data that support the potential anti-tumor activity of KO-539 in genetically defined subsets of acute leukemia, including those with rearrangements or partial tandem duplications in the MLL gene as well as those with oncogenic driver mutations in genes such as NPM1. Last week, we announced the FDA has granted orphan drug designation to KO-539 for the treatment of acute myeloid leukemia. This decision by FDA follows the clearance of our investigational new drug application in March, and it recognizes the potential for KO-539 to address the population of patients with high unmet need. Regulatory and clinical reviews have now been completed, and we're in the final stages of study start-up for our Phase 1 clinical trial of KO-539 in relapsed or refractory AML.

With that, I'll turn the call over to Marc Grasso for a discussion of our financial results for the second quarter of 2019.

Marc Grasso -- Chief Financial Officer and Chief Business Officer

Thank you, Troy, and good afternoon, everyone. I'll provide a brief overview of our financial results here on the call and invite you to review our 10-Q filed today for more detailed discussion.

Research and development expenses for the second quarter 2019 were $11.4 million, compared to $11.5 million for the second quarter of 2018. The slight decrease in R&D expenses for the quarter was primarily due to a decrease in clinical development activities related to our Phase 2 trials of tipifarnib, offset by an increase in clinical development activities related to our registration-directed trial for tipifarnib.

General and administrative expenses for the second quarter of 2019 were $4.5 million, compared to $3.8 million for the second quarter 2018. The increase in G&A expenses was primarily due to increases in personnel cost and non-cash share-based compensation. Net loss for the second quarter 2019 was $14.9 million, or $0.38 per share, compared to a net loss of $14.7 million, or $0.45 per share, for the second quarter 2018.

As of June 30th, 2019, we had cash, cash equivalents, and short-term investments of $261.4 million compared with $179 million as of December 31st, 2018. This includes net proceeds of approximately $108 million from the public offering we completed in June 2019. By way of updated guidance post the offering, we expected our current cash, cash equivalents, and short-term investments will be sufficient upon current operations into the second half of 2021.

We believe we remain in the strong position to execute on our ongoing registration-directed trial for tipifarnib and HRAS mutant HNSCC. In addition, we have the opportunity to capitalize on our positive Phase 2 data in PPCL, explore additional indications for tipifarnib, accelerate pre-NDA efforts, hand advance the next generation farnesyl transferase inhibitor program, as well as devote additional resources toward our emerging pipeline programs.

With that, I will now turn the call back over to Troy.

Troy Wilson -- President and Chief Executive Officer

Thank you, Mark. We enter the latter half of this year in a strong position, armed with two distinct clinically validated biomarkers for tipifarnib, two emerging pipeline programs, and the financial resources to better realize the potential value of these assets. Before we jump into the Q&A session, let me quickly lay out our anticipated milestones for the remainder of this year and early next year. For tipifarnib, additional data from our Phase 2 trial in HRAS mutant HNSCC and other HRAS mutant SCCs in the fourth quarter of 2019, additional data from the AITL expansion cohort and our ongoing Phase 2 trial in the fourth quarter of 2019, additional data from our Phase 2 trial in chronic myelomonocytic leukemia in the first half of 2020, and initiation of a proof-of-concept study in pancreatic cancer in the first half of 2020. For KO-947, completion of the dose escalation portion of our Phase 1 trial by the end of 2019, and for KO-539, initiation of our Phase 1 trial in the second half of 2019.

...

With that, operator, we're now ready for questions.

Questions and Answers:

Operator

Ladies and gentlemen, at this time, if you have a question, please press *1 on your touch-tone telephone. If your question has been answered or you wish to remove yourself from the queue, please press #. To prevent any background noise, we ask that you please place your line on mute once your question has been stated.

And our first question is from Konstantinos Aprilakis from Deutsche Bank. Your line is now open.

Konstantinos Aprilakis -- Deutsche Bank -- Senior Biotechnology Research Analyst

Good afternoon, guys. Thanks for taking my questions and congrats on all the progress this quarter. So, with regard to AMHN, I was wondering if you could provide some color on the proportion of patients who screened for enrollment that meet the relevant cutoffs that you've set for HRAS mutant allele frequency and serum albumin?

Troy Wilson -- President and Chief Executive Officer

Konstantine, thanks for the question. Antonio, do you wanna address Konstantine's question?

Antonio Gualberto -- Head of Development and Chief Medical Officer

Yes, Konstantine, it's 5%. So, the actual data actually confirmed this [inaudible] that we did.

Konstantinos Aprilakis -- Deutsche Bank -- Senior Biotechnology Research Analyst

So, you're actually seeing 5% of the world?

Antonio Gualberto -- Head of Development and Chief Medical Officer

One out of 20 patients. Yeah, 5%.

Konstantinos Aprilakis -- Deutsche Bank -- Senior Biotechnology Research Analyst

That's great. And then, is the goal still to involve 100 clinical centers in enrolling patients, and then how many of those sites are open if that's the case?

Antonio Gualberto -- Head of Development and Chief Medical Officer

It's approximately that's the number. We're obviously not releasing numbers on the percentage of sites that are open.

Konstantinos Aprilakis -- Deutsche Bank -- Senior Biotechnology Research Analyst

And then just switching gears a little bit to KO-539, I was wondering can you share some detail on that trial besides the design and maybe the latest sort of biomarker selection strategy? Are you still planning to look at partial tandem duplication and all that as well as NPM1 and DNMT3A driver mutations?

Troy Wilson -- President and Chief Executive Officer

Antonio, you wanna go ahead and take that?

Antonio Gualberto -- Head of Development and Chief Medical Officer

So, this will be an AML relapsed or refractory population. In principle, those escalation is gonna have an accelerated portion. It's not gonna have initial selection of patients, but the intent is once we are getting close to recommend a Phase 2, they'll make the switch to the rearrangement on the NPM1 mutant population in their rotations.

Konstantinos Aprilakis -- Deutsche Bank -- Senior Biotechnology Research Analyst

Great. Thanks, guys.

Troy Wilson -- President and Chief Executive Officer

Thanks, Konstantine.

Operator

Thank you. Our next question is from Tyler Van Buren from Piper Jaffray. Your line is now open.

Tyler Van Buren -- Piper Jaffray -- Senior Biotech Equity Research Analyst

Hey, guys. Good afternoon. Thanks for taking the questions. I had a question on the ERK data update by year end. You gave us some additional color there and spoke about pancreatic and colorectal, and you seem pretty confident in having the dose ranging done by year end, but the trial, my understanding is that it's been going on for a while, so could you just discuss kind of the time frame that you've been evaluating this program for, the number of patients enrolled, and also a little bit more of specificity around the challenges with respect to dosing and dosing regimen, and whether you think it could drive monotherapy responses or is more likely to be a combination partner?

Troy Wilson -- President and Chief Executive Officer

Thanks for the question. I'll share my thoughts and then invite Antonio to comment. So, the opportunity with the KO-947 is that you're inhibiting ERK, which we know is a central actor in tumor cells. It's also a very important protein in normal cells. And consistent with other inhibitors of the MAP kinase pathway, including MEK inhibitors and even other ERK inhibitors, you know that along with clinical activity is gonna come toxicities. And those toxicities are pretty well understood. They include rash, and diarrhea, and GI. Those are the pretty common toxicities. Our approach KO-947, because we could see prolonged pathway inhibition with intermittent dosing and we could dose with an IV formulation, we thought perhaps we could get to higher exposures in patients and in the tumors with intermittent IV dosing. So, that's been the approach that we've taken.

The team has been prosecuting a couple of different doses and schedules, and this is unfortunately something that can only really be done empirically. There isn't a computer program or anything that's gonna allow you to model it. You give the patients as much drug as they can take, and then you have to introduce a holiday, and those holidays are empirically defined. So, to draw an analogy to tipifarnib, we give tipifarnib, 600 milligrams, twice a day, one week on and one week off. The one week off, it's the holiday needed to sustain that high dosing. We are working toward a dosing schedule for ERK that we think will put us in a position to pursue either an approach as a monotherapy or in combination.

As long as we keep going, I think we continue to be encouraged. It is just something that one has to do slowly in Phase 1. If you see something, you have to expand and then keep going, and that's really where we are. We get the question frequently are we looking in selected populations, which is why we're giving people the color that as would be expected in a Phase 1 unit. Most of the patients are end-stage pancreatic or colorectal, where particularly at lower sub-therapeutic doses, you're just not expecting to see very much. We do have clear biomarker-defined populations that we can go into, both as a monotherapy and combination, but we need a recommended Phase 2 dose and schedule to get there, and I think the team is making good progress. It's never over until it's over. We expect that it may take the rest of this year to finalize the Phase 1, and so that's why we're guiding that the earliest we could present the data would be early next year, and we're trying to give some color on the data that people might expect.

Let me pause there and just invite Antonio if he wants to add anything to my comments.

Antonio Gualberto -- Head of Development and Chief Medical Officer

Just to mention that, obviously, there have been multiple failure target in this pathway. There have been successes. In BRAF melanoma, for example, we know that the pathway is [inaudible] pancreatic cancer, and we have our data in those squamous tumors, and we know how to select those patients. So, by using an IV, we can get higher exposures that you could ever get with an oral compound. Many of the oral compounds have issues of bio-viability and is [inaudible]. So, we can get high exposures with the IV. And of course, if you give a daily IV, you're gonna reach [inaudible] very quickly, but that's really not feasible in the long term, so you need to be working those regimens. Do I give an IV every three days or give it every seven days? When we see maculopapular rash, how many days you have to use [inaudible]?

So, that's what Troy's referring to that all these things have to be done empirically, so you get the best possible recommended phase to those before you do the real testing in the most susceptible population in a Phase 1 extension or in the Phase 2. We have done extensive work in animals in PDX model, more than 250 PDX model, so we know what are the potential most sensible tumors, so we now need to get a good recommended phase to those to test the hypothesis.

Tyler Van Buren -- Piper Jaffray -- Senior Biotech Equity Research Analyst

Great. Thanks very much for the details and comments.

Troy Wilson -- President and Chief Executive Officer

Pleasure. Thank you, Tyler.

Operator

Thank you. Our next question's from Jonathan Chang from SVB Leerink. Your line is now open.

Jonathan Chang -- SVP Leerink Partners -- Managing Director

Hi. Thanks for taking my questions and congrats on the progress. First question, can you help set investor expectations ahead of the fourth-quarter RUN-HN update? How much data should investors expect versus the last update?

Troy Wilson -- President and Chief Executive Officer

Antonio, would you like to take Jonathan's question?

Antonio Gualberto -- Head of Development and Chief Medical Officer

I mean, typically, we will present every single patient that have been involved in the trial until the data presentation that will include every patient enrolled in the head or neck cohort as well as any of the squamous patients. We need to provide a balance between enrolling in the pivotal and enrolling in the Phase 2, so yes, we will have some patients, but if you can imagine, our focus is to enroll the people [inaudible]. We only enroll in the Phase 2 if a patient has identified in a site in which the pivotal study is still not yet open. So, I cannot give you a number at the present time. Again, we'll present every single patient enrolled, but you cannot expect very high numbers because we're trying to accelerate the pivotal as much as we can.

Jonathan Chang -- SVP Leerink Partners -- Managing Director

Got it. Appreciate the color. Second question, how are you thinking about KO-947 from a potential clinical collaboration or partnership standpoint?

Troy Wilson -- President and Chief Executive Officer

Jonathan, thanks for the question. I think it goes back to what we were saying earlier, which is a critical question in anyone's mind, looking at an agent, whether it's a monotherapy or in combination, is what's the recommended Phase 2 dosing schedule, what are the signals that you're on target, and then of course, what are the associated toxicities? What's the tolerability profile?

There is certainly interest, both as a monotherapy. Antonio mentioned squamous head and neck. We have insight into that population through our expanding network of head and neck sites, so we were keenly interested in the 11q13 amplified population, as you know from our preclinical data, but there's also interesting opportunities to combine with other agents on the MAP kinase pathway, the PI3 kinase pathway, potentially agents that are critical to the cell cycle control, and we'll be, I think, in a good position to determine the next steps forward. We keep all the options on the table as far as partnering is concerned across the pipeline.

Jonathan Chang -- SVP Leerink Partners -- Managing Director

Got it. Thanks for taking my questions.

Troy Wilson -- President and Chief Executive Officer

Sure. Thank you.

Operator

Thank you. Our next question is from Jay Olson from Oppenheimer. Your line is now open.

Jay Olson -- Oppenheimer & Co -- Research Analyst

Hey, guys. Congrats on the progress and thanks for taking my questions. I wanted to start with the recently issued patents. Congratulations on those. I'm curious about the broad method of use patent for the entire class of farnesyl transferase inhibitors. Would that block the freedom to operate for other molecules that you don't own to be studied in that space?

Troy Wilson -- President and Chief Executive Officer

So, Jay, thanks for the question. If you take a step back, what the field of farnesyl transferase inhibition was missing was an identification of the biomarkers that would allow for rational selection strategies. Janssen had treated 5,000 patients across 70 different trials, anecdotal reports of activity, but never enough activity to sort of drive a registrational program. It was the combination of the molecular and the clinical insights that we had an understanding of the biology and then a whole lot of both clinical and preclinical work that has gone into the disclosures that are supporting these patents.

And as much as we can, we've tried to kind of bring investors along and the market along with this because this is an unusual situation. You don't typically see a compound out there with such a demonstrated track record of clinical activity without an understanding of how it works. Probably the last example maybe was the IMiDs, right? The IMID Franchise with revlimid, and pomalidomide, and before that, thalidomide. And so, to your specific question, the patent that issued from the U.S. Patent and Trademark Office, the claim covers a method of treating patients with HRAS mutant head and neck squamous cell carcinoma using any farnesyl transferase inhibitor.

So, our read of that is, yes, if there is an FTI, even including a new molecule, one that's just been invented, that uses that biomarker method as a method of enrichment for patients, then you would be covered by that patent claim. And you can imagine that we are taking this same strategy across each of our biomarker initiatives, whether it's CXCL12, wherever it may be. And we'll have more to say about that in the months and years to come, but we were very, very pleased that the patent office recognized our pioneering position in the farnesyl transferase inhibitor space and in really providing the missing link that's allowed us to unlock the clinical and hopefully the commercial value.

Jay Olson -- Oppenheimer & Co -- Research Analyst

Great. Thanks for that additional color. That's very helpful. And then, I did wanna maybe just follow up on KO-947. Could you maybe outline your target product profile for that molecule and maybe map out the scope of the commercial potential?

Troy Wilson -- President and Chief Executive Officer

So, the target product profile, Antonio spoke to it in his comments. At least at this stage, we're expecting it's going to be an IV formulation. We are pursuing a weekly schedule. We're also pursuing an intermittent schedule that is more frequently than weekly. And then I think probably the next appropriate thing to talk about is the target population. And there, we've done an extensive survey preclinically to try to identify those tumors with specific characteristics that are responsive to inhibition by 947 as a monotherapy. And we've shown that preclinical data. We've published it at ACR. It includes examples of BRAF and KRAS mutant adenocarcinoma. It also, interestingly, includes head and neck squamous and esophageal squamous cell carcinomas that have 11q13 amplifications.

But that's preclinical. Obviously, there's work to be done clinically. And as Antonio mentioned, we're optimistic that we'll have an opportunity either as a Phase 1 extension or a Phase 2 trial to be able to evaluate 947 in some selected populations. We haven't said yet what those are, but obviously, we have a keen interest in head and neck. In terms of the potential, our understanding -- and this is all preliminary data -- is the 11q13 amplification is 20% to 25% of head and neck. It's perhaps even larger in esophageal. So, those are pretty significant populations, and of course, we're well acquainted with the high unmet need in the head and neck HNSCC population.

So, the challenges of inhibiting ERK in terms of finding a dosing schedule and an acceptable tolerability are offset by the fact that these are some very significant populations that we're talking about, and we hope by the end of this year, as we've said, to be in a position where we've got a good working understanding of the drug, and then we can really start to explore it in some populations where we might expect to see some encouraging signs of clinical activity. Does that answer your question?

Jay Olson -- Oppenheimer & Co -- Research Analyst

Yes. That was perfect. Thank you for taking the questions.

Troy Wilson -- President and Chief Executive Officer

Sure.

Operator

Thank you. Our next question is from Joel Beatty from Citi. Your line is now open.

Joel Beatty -- Citi -- Biotechnology Equity Research Analyst

Hi. Thanks for taking the questions. Could you provide an overview of the opportunity for tipifarnib in HRAS positive squamous cell carcinoma beyond what's currently being focused on in the Phase 3 AMHN trial, either other head and neck patients or tumors other than head and neck?

Troy Wilson -- President and Chief Executive Officer

Thanks, Joel, for the question. So, to the earlier question that Antonio answered, we think that when you define the population as HRAS mutant HNSCC patients with a varying allele frequency greater than 20%, our best guess is that's about 5% of the head and neck population across all lines of therapy. We do think there's a significant population of head and neck patients who have HRAS mutant varying allele frequencies lower than 20%, and of course, we're excluding those from the registrational study because we don't see responses as a monotherapy.

We do think there's an opportunity to treat those patients either sequentially or in combination with other agents. And in my comments, I called out potentially combinations with immune therapy, with cetuximab, potentially with chemotherapy. Those are not clinical studies that we have even planned yet but certainly places for expansion. I think stepping even kinda one level higher, in our corporate presentation, we've guided to there may be as many as 7,500 HRAS mutant patients in the squamous cell carcinomas generally, and that would include not just head and neck but lung and other histologies as well. And to reach those patients, it may not be a response rate-driven trial. It may be a time-to-endpoint or survival trial.

We're gonna have to step our way through that, but I think what we're encouraged by is these HRAS mutant tumors are not responsive, to our knowledge, to any other therapy. They don't respond to immune therapy, they don't respond to cetuximab. They respond to varying degrees to tipifarnib, and then it becomes a matter of how you thoughtfully expand your label from our initial relapsed refractory head and neck to potentially be able to move to those other populations. So, hopefully our corporate presentation gives you some guidance on the HRAS population with the caveat that it's gonna take monotherapy in the initial instances, and then combination or sequential treatment as you look to broaden out the label.

Joel Beatty -- Citi -- Biotechnology Equity Research Analyst

Great. Thank you.

Troy Wilson -- President and Chief Executive Officer

Sure.

Operator

Thank you. As a reminder, ladies and gentlemen, if you have a question, please press *1 on your touch-tone telephone.

And our next question is from Chris Shibutani from Cowen. Your line is now open.

Chris Shibutani -- Cowen -- Senior Research Analyst

Great. Thanks very much. One specific question on the ERK inhibitor, and then maybe a bigger picture, broader one. On the ERK inhibitor, Troy, based upon what you guys know so far, when you contemplate potential combinations, can you describe any particular agents that you think would be logical candidates for combination work?

Troy Wilson -- President and Chief Executive Officer

Chris, thank you for the question. I mean, I wanna be a little bit guarded here, both from a development and an intellectual property perspective. I've kind of alluded to this in that there would be a logical rationale that combined with other inhibitors of the MAP kinase pathway, combinations with inhibitors of the PI3 kinase pathway might also make sense, and then certain instances of cell cycle agents that are disrupting the cell cycle. I think we're gonna be driven by what we see as a monotherapy, whether you're going forward in combination, you wanna ensure that you've got a good understanding in a robust level of monotherapy activity. That can be either responses or it can be disease stabilization, but I think we wanna understand that. But let me invite Antonio to comment if he wants to add anything. I'm just kind of giving you general comments until we get sort of toward the end of the year and into next year and have more clarity.

Antonio Gualberto -- Head of Development and Chief Medical Officer

I will only add that it's very attractive to consider the combination with other molecularly targeted therapies, but we also have to think in development, you have to consider the [inaudible] combining with [inaudible]. So, if you have activity in head and neck in a subset, you're probably gonna do the combinations with cetuximab, with [inaudible], with pembrolizumab in order to expand your label horizontally, similar to your comment before about tipifarnib. Yes, we can expand horizontally, but if there is a particular subset in which you have very high activity, you can move vertically treating [inaudible] setting. That's the basic [inaudible] for adjuvant treatment.

Adjuvant treatment, it could be one or two years of treatments. So, there's a large opportunity once you identify the subset that is very sensitive to proceed vertically to larger populations, and also, as you indicated, horizontally with targeted therapy but obviously with a standard of care, and then you are being carried by the immunotherapy, you are being carried by the cetuximab chemotherapy combinations, but for both cases, for tipifarnib and for 947.

Chris Shibutani -- Cowen -- Senior Research Analyst

Great. And then, a question about tipifarnib, the lead asset which you guys have been working diligently on for a while now, is it reasonable to believe that your experience is changing as you continue to pursue the clinical development? By that, I'm trying to gauge is it getting easier to find the patients? And as you're continuing to enroll patients, is there some sort of transition that's occurring in terms of the type of patients that are coming forward so that as we think about the experience with the Phase 3 enrollment, should we think about the mix of patient backgrounds somehow altering, or shifting, or perhaps even improving that would maybe impact either the timing of completion or the probability of success or the outcome?

Troy Wilson -- President and Chief Executive Officer

Chris, I might answer the question the following way. So, first of all, nothing is easy, and it's a great credit to Antonio and the entire team for what they've been able to do to move tipifarnib to where it is today. One of the biggest challenges with any registrational trial is just the scope and complexity of up to 100 sites worldwide, however many different languages. This is not a continuation of the Phase 2. This is an entirely new study, and it's the little things that you have to pay attention to. It's the contracts, the IRB reviews. We are screening 1,500 patients to be able to find the 74 that will allow us to conduct aim, and the team is making great progress in executing on the study. I wouldn't say it's easier. I would say they understand the task, and fortunately, we've got a lot of experienced people who have done registrational trials and understand what you need to do to execute at this scale on a global basis. But again, let me invite Antonio if he wants to add anything to my comments.

Antonio Gualberto -- Head of Development and Chief Medical Officer

I will just mention that, obviously, the discovery of the biomarker interaction with CXCL12 opened an opportunity that is much larger than what we saw initially with HRAS in lymphoma, in myeloma, in solid tumors. Think about the potential CXCL12 target population in pancreatic cancer is a third of pancreatic cancers. So, obviously, some of the discoveries are because it can be translated from one tumor to another while leave those tumors in which CXCL12 is a negative prognostic made things in a way easier because we are reproducing interactions that we have [inaudible] previously. And then, there's another aspect of these technical aspects.

So, currently, we have NGS panels that determine the target for tipifarnib and the target for 947, so we mentioned before, the 11q13 amplification, so those genes that determine what patient population is susceptible to 947. We can already see when we do the screening for tipifarnib because it's the same platform. So, the more experience that we acquire with these tools, the better the relationship we have with the clinical sites, then we can move compounds in indications, in settings in clinical side, which we have already a good relationship. So, in a way, it's always difficult, but certainly, experience, it will help with development of subsequent drugs.

Chris Shibutani -- Cowen -- Senior Research Analyst

Great. Thank you for the comments, and it's great to see the portfolio and the pipeline continue to broaden. I think it's very positive. Thanks very much.

Troy Wilson -- President and Chief Executive Officer

Thank you, Chris. And thanks again for participating in our call today. We'll be at the Wedbush Healthcare Conference in New York in a couple of weeks. Look forward to seeing a number of you there. In the meantime, if you have any additional questions, please feel free to contact Pete, Marc, or myself. Thanks again and have a good evening, everyone.

...

Operator

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

Duration: 44 minutes

Call participants:

Pete De Spain -- Vice President, Investor Relations and Corporate Communications

Troy Wilson -- President and Chief Executive Officer

Marc Grasso -- Chief Financial Officer and Chief Business Officer

Antonio Gualberto -- Head of Development and Chief Medical Officer

Konstantinos Aprilakis -- Deutsche Bank -- Senior Biotechnology Research Analyst

Tyler Van Buren -- Piper Jaffray -- Senior Biotech Equity Research Analyst

Jonathan Chang -- SVP Leerink Partners -- Managing Director

Jay Olson -- Oppenheimer & Co -- Research Analyst

Joel Beatty -- Citi -- Biotechnology Equity Research Analyst

Chris Shibutani -- Cowen -- Senior Research Analyst

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