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Thanks, Naomi, and good morning, everyone. Thank you for joining us today as we review our progress over the second quarter of 2019. At Syros, our vision is to build a great and enduring company that delivers transformative medicines for patients with severe diseases that have largely alluded other approaches. The foundation for achieving that vision is our leading gene control platform, which allows us to elucidate regulatory regions of the genome to home in on which genes to control, in which cells, for which patients and how best to modulate the expression of those genes to maximize the chances of providing a profound benefit for patients.

Because gene expression is fundamental to the function of all cells, our platform has the potential to create medicines across a range of diseases, fueling a sustainable pipeline over the long term to support our evolution into a fully integrated biopharmaceutical company. We continue to make significant progress toward that vision. Today, we have two clinical stage programs and ongoing clinical trials in six cancer population, multiple programs in preclinical and discovery research for cancer and monogenic diseases and an experienced leadership team that has collectively brought more than a dozen drugs to market. We are focused on three strategic priorities: advancing our clinical stage programs to key data readouts this year; and next, building on our leadership in CDK7 Inhibition; and growing our pipeline through ongoing investment in our discovery stage efforts.

Over the past quarter, we made progress on our ongoing clinical trials for 1425 and 1365 with the aim of announcing proof-of-concept data in 2020 that could support fast-to-market strategies in three distinct AML and ovarian cancer patient populations. Once a graveyard for drug development, the AML landscape is now rapidly evolving. Despite these advances, AML and MDS patients continue to face significant unmet medical needs. Having evaluated the current and evolving treatment landscape, we believe the highest unmet need exists in the relapsed or refractory AML study, and this population provides the most efficient path to bring 1425 to market for patients.

While patients are starting to benefit from new treatments in the front line unfit setting, we are not curing the disease. Patients continue to progress, and overall survival remains particularly poor for relapsed or refractory patients. Overall, in this heterogeneous disease of the elderly, there continues to be a significant need for well-tolerated novel therapies that provide clinical benefit. We are excited to announce that we have started enrolling patients in a new cohort in our Phase 2 trial evaluating 1425 in combination with azacitidine in relapsed or refractory AML patients, who are positive for our biomarkers of RARA pathway activation.

Based on the data we reported last year at ASH, we believe 1425 plus azacitidine is an active combination with a favorable tolerability profile, and we look forward to reporting potential proof-of-concept data from the relapsed or refractory cohort in 2020. Turning to the cohorts in newly diagnosed unfit AML patients, who are not suitable candidates for standard chemotherapy. As of this week, we have enrolled 20 of the planned 25 patients in the biomarker-positive cohort and expect to complete enrollment in the second half of the year. We plan to report updated data in the fourth quarter from both the biomarker-positive and biomarker-negative cohorts in newly diagnosed unfit patients.

These updated data should provide additional insights into the safety, clinical activity and tolerability of the 1425 azacitidine combination to support our overall development strategy in biomarker-positive patients. Turning now to our CDK7 franchise. Since the inception of the company, we have been focused on selective CDK7 inhibition, which we believe represents a potentially transformative targeted approach for difficult-to-treat cancers. Today, our CDK7 franchise includes two distinct molecules: 1365, our first-in-class selective CDK7 inhibitor currently in a Phase 1 trial; and 5609, our highly selective and potent oral CDK7 inhibitor that is expected to enter clinical development early next year.

As we have discussed before, we expect initial data from the expansion portion of the Phase 1 trial for 1365 in the fourth quarter, followed next year by potential proof-of-concept data from our single agent cohorts in ovarian clear cell cancer patients and in heavily pretreated, high-grade serous ovarian cancer patients. Specifically in the fourth quarter, we expect initial safety and efficacy assessments from the cohort evaluating 1365 as a single agent in heavily pretreated, high-grade serous ovarian cancer patients, who have had three or more prior lines of therapy. Initial safety and PK data from the cohort evaluating 1365 in combination with carboplatinum in high-grade serous ovarian cancer patients, who have had one or more prior lines of therapy, and initial safety, efficacy and mechanistic data from the cohort evaluating 1365 as a single agent in patients with advanced solid tumors that are accessible for biopsy. In 2020, we expect to have updated data from these cohorts, as well as initial data from the cohort of 1365 in combination with fulvestrant in metastatic HR-positive breast cancer patients, who are resistant to CDK4/6 inhibitors.

Given the high unmet need in the ovarian cancer patient population, where we are pursuing single agent development, we believe there are opportunities for accelerated development for 1365. We are proud of the work we have done to advance our CDK7 franchise to where it is today. In May, our work was highlighted in AACR's journal, Cancer Research, which detailed our discovery of 1365 and highlighted its promise as a potentially transformative targeted approach for a range of difficult-to-treat cancers. This external validation underscores our leadership in CDK7 inhibition as a novel approach for treating patients, whose needs are not adequately addressed by existing therapies.

It is this unrelenting commitment to delivering on our promise of CDK7 inhibition that fuels our ongoing efforts from 5609, which builds on our leadership from 1365. 5609 is a distinct chemical entity from 1365. It is an orally available, highly selective and potent non-covalent inhibitor of CDK7 with robust antitumor activity in multiple preclinical cancer models. We expect to present new preclinical data on 5609 in the fourth quarter, which we believe will provide further insight into the PK, PD and antitumor activity of 5609 in preclinical PDX models of several solid tumors.

We remain on track to complete IND-enabling studies in 2019 and expect to initiate a Phase 1 oncology trial in early 2020. In addition to these important clinical developments, we were happy to welcome Dr. Alice Shaw to our board of directors this quarter. Dr.

Shaw is the director of the center for thoracic cancers at the Massachusetts General Hospital and a professor of medicine at Harvard Medical School. She is a highly respected oncologist and a leader in translational medicine and the development of targeted cancer therapies. Her expertise will be invaluable as we continue to advance our pipeline and we look forward to her contributions. In closing, this is an exciting time for Syros.

We are approaching important data readouts that we believe has the potential to validate our fundamental approach to drug development and, more broadly, catalyze change in the treatment landscape for cancer patients with high unmet medical needs. By 2020, it is our hope that we will be one step closer to achieving our ultimate goal of delivering targeted therapies that provide a benefit for patients in dire need of better treatment options. We look forward to keeping you updated on our progress. With that, I'll turn it over to Joe Ferra to review our financial results for the quarter.

Joe Ferra -- Chief Financial Officer

Thank you, Nancy. Over the past quarter, Syros has maintained a strong financial position, reinforced by the $70 million financing we closed in April. Based on our current plans, we believe that our existing cash, cash equivalents and marketable securities will support our operating expenses and capital requirements to the end of the first quarter of 2021 beyond multiple expected data milestones for our clinical programs while also continuing to invest in our gene control platform. We ended the second quarter with $121.7 million in cash, cash equivalents and marketable securities, compared with $99.7 million on December 31, 2018.

We recognized $0.5 million of revenue in the second quarter of 2019, compared to $0.4 million for the second quarter in 2018. Revenue in both periods was earned entirely from our collaboration with Incyte. R&D expenses were $15.5 million for the second quarter of 2019, compared to $11.1 million for the same period in 2018. This increase was primarily a result of the progress of our existing clinical trials and our preclinical programs, including the advancement of 5609 into IND-enabling studies.

G&A expenses were $5.2 million for the second quarter of 2019, compared to $3.8 million for the same period in 2018. This increase was primarily due to an increase in employee-related expenses. Finally, we reported a net loss for the second quarter of $19.5 million or $0.47 per share, compared to a net loss of $14 million or $0.43 per share for the same period in 2018. With that, I will turn the call over to the operator for questions.

Thank you.

Questions & Answers:

Operator

Thank you. [Operator instructions] And our first question comes from Phil Nadeau with Cowen and Company. Your line is open.

Phil Nadeau -- Cowen and Company -- Analyst

Good morning. Congrats on the progress and thanks for taking my questions. Just a couple on the upcoming data releases. First, on 1365, I was curious if you'd help set expectations for that data.

What would you think would be encouraging to see from 1365 as a single agent and in combination in Phase 1?

Nancy Simonian -- Chief Executive Officer

Hi, Phil, thanks for the question. As we said, we're going to be presenting initial data from some of the cohorts in the fourth quarter, and then expect to have more robust data across all of the cohorts, including potential proof-of-concepts in the single agent relapsed ovarian cancer cohorts in 2020. I think for -- ultimately, for the proof-of-concept readouts, we, as you know, in the relapsed ovarian cancer populations, both the clear cell and the high-grade serous ovarian cancer populations, the current standard of care in terms of activity are really poor, very low response rates. So we think that really seeing something better than what standard of care would be in those settings has the opportunity in this patient population that is very sick. In terms of the early data on the combination, I mean, one of the important questions there is, can we safely combine 1365 with other agents in those studies.

Phil Nadeau -- Cowen and Company -- Analyst

Great. OK. That's helpful. And then second, on 1425, you mentioned some data from the newly diagnosed cohort in the fourth quarter.

Given that 20 or 25 patients are enrolled today, approximately how many would be evaluable for that Q4 data release?

Nancy Simonian -- Chief Executive Officer

We haven't been explicit about the number of patients that we have, but we're -- the fact that we have 20 patients enrolled already, I think you can expect, compared to the data we presented before, to have many more patients, greater durability and ideally being able to present further data to help to validate the combination of 1425 with azacitidine, which the early data really supported a highly active combination. And I think the other really important thing will be the tolerability profile because the early data suggested that we were not seeing increased oral toxicity and no increased neutropenia. So that combination is really validating this as an active combination in the study.

Operator

Thank you. Our next question comes from Ted Tenthoff with Piper Jaffray. Your line is open.

Ted Tenthoff -- Piper Jaffray -- Analyst

Great. Thank you very much. Thanks for the update. Quick question, if I may, on the CDK7.

So -- and then it may be a little early to sort of get into detail, but maybe you can provide some preliminary thoughts. Tell us sort of how you intend to develop these compounds together? I mean, I can imagine or envision the short-route indications where IV may combine or play better, and there's others where oral may make more sense. I really like that you guys are doubling down on this target. Can you kind of give us some preliminary thoughts on how you see the two being developed and where one might be better than the other? Thank you.

Nancy Simonian -- Chief Executive Officer

Ted, thanks for the question. As you know, we -- 'as Joe said, we are really excited about the potential for CDK7 inhibition. And therefore, we've been moving the oral molecule along. I'm really excited about that program.

We're in the process of really evaluating based on the preclinical data where we think the optimal places develop 5609 and also as we are developing 1365. So that's all kind of in the process of really evaluating. The 5609 is a distinct molecule. Well, they're both selective CDK7 inhibitors.

So we're really analyzing the data and where we think both commercially unmet need, but also biologically makes the most sense to develop it.

Ted Tenthoff -- Piper Jaffray -- Analyst

OK. Yes. I'm just thinking of a visit of IV and oral. So thank you very much.

Operator

Thank you. [Operator instructions] Our next question comes from Jason Butler with JMP Securities. Your line is open.

Jason Butler -- JMP Securities -- Analyst

Thanks for taking the questions, and congrats on the progress. Just one on the relapsed/refractory AML cohort. Is there a 100% overlap of the sites versus the frontline cohort? Are you looking to add additional sites for this new cohort?

David Roth -- Chief Medical Officer

Thanks for the question. Yes, this is David. Yes. So the relapsed/refractory AML cohort, obviously, is focused on combining SY-1425 plus azacitidine, and we're currently operating in the same backdrop of clinical investigation sites.

And the study is ongoing, actively enrolling, both in the United States, as well as in Europe.

Jason Butler -- JMP Securities -- Analyst

Great. And then for 5609, can you just point us to how we should think about the preclinical PK/PD data and how that might translate -- that profile might translate into human?

Eric Olson -- Chief Scientific Officer

Yes. This is Eric Olson. Yes, we've been profiling, well, 1365 and 5609 extensively in preclinical models, evaluating the PK/PD efficacy relationship. As you know, for 1365, a covalent molecule.

There's a disconnect between PK and PD, given the covalent nature. So 5609 being noncovalent is a more standard analysis of PK/PD and efficacy. So we look at things like semen, AUC, CMaX, all the different potential parameters that could be driving efficacy in the preclinical models and then translate that into the clinical paradigm. Of course, understanding PD effects of the molecule, we were using our platform and understanding the regulation of genes to also make a translation of what we see in the tumors and the animals, and then we'll be measuring those in the clinic.

Jason Butler -- JMP Securities -- Analyst

Great. Thanks for taking questions.

Operator

Our next question comes from Mark Breidenbach with Oppenheimer.

Matt Biegler -- Oppenheimer and Company -- Analyst

Hey, guys, this is Matt, on for Mark. Congrats on the progress. I just had a quick question on the anticipated data from 1365 in 4Q. So in the past, you guys have talked about the possibility of using like a biomarker-focused strategy based on RB status, and I'm just wondering if you're planning on parsing out the data from the expansion cohort by RB status or maybe some other biomarker that might be used going forward?

Nancy Simonian -- Chief Executive Officer

Thanks, Matt. I'm going to ask David to answer that question.

David Roth -- Chief Medical Officer

Yes. Thanks. So we had previously described associations between RB pathway abnormalities and associated abnormalities in the cell cycle regulation as we relate to sensitivity to our drug in preclinical models. And we are evaluating all of that in our clinical trial, both by targeting tissue and looking at things like circulating tumor DNA.

And obviously, we're going to make some efforts to understand the impact of that in patients and how the drug performs. We haven't yet specifically indicated with that specificity what would be available in the fourth quarter for reporting however.

Matt Biegler -- Oppenheimer and Company -- Analyst

Great. Thanks.

Operator

Thank you. And our next question comes from Zegbeh Jallah with Roth Capital Partners. Your line is open.

Zegbeh Jallah -- Roth Capital Partners -- Analyst

Good morning. Thanks for taking my question. I'm kind of glad to see that enrollment for 1425 in units. I know AML patients is on track.

I'm sure that's the feed in itself. But Nancy or David, I was just wondering, from the readout in 4Q '19, would you be able to provide some guidance on the regulatory pathway part? Or will you wait for initial results in the relapsed/refractory AML cohort before going south? And I have a follow-up.

Nancy Simonian -- Chief Executive Officer

Thanks, Zegbeh. Thanks so much for your question. As you know, earlier this year, we announced that, and as we were thinking about the development of 1425 in combination with azacitidine and reviewing the overall competitive landscape and thinking about what would be the most efficient path to bring that combination to market, we have decided to kind of focus on the relapsed/refractory or basically, second line and beyond AML, where despite multiple new therapies available, both in the front line and the relapsed, the overall survival there remains very poor or less than six months. So we believe that there's a very high unmet medical need.

There's a need for new therapies with the different mechanism of action also that can -- are very well tolerated. I mean, so we think the 1425 azacitidine combination data really supports a focus there. We also know that there's a precedence for a more -- an efficient path from the regulatory standpoint to bring drugs in that setting to market. We think that 1425 has the opportunity in really all lines of therapy, including in the newly diagnosed.

So we continue to pursue the cohorts in the newly diagnosed. And as we get further data here and we look at the broader landscape, we'll determine kind of the best path forward in the newly diagnosed. But the key for us right now is to generate proof-of-concept data, which we expect to have in 2020 in the relapsed/refractory cohort, and then that data from there would serve as the basis for considering an accelerated path.

Zegbeh Jallah -- Roth Capital Partners -- Analyst

Thanks, Nancy. And then just a quick follow-up here. Without any data for azacitidine, I'm looking at biomarker-positive patients, what are your thoughts there regarding, do you expect to see azacitidine perform like it has in the past with a broader patient population? Or do you expect the responses to be slightly different in this biomarker-positive patient just in terms of looking forward as a control arm.

Nancy Simonian -- Chief Executive Officer

I'm going to ask David to answer that question.

David Roth -- Chief Medical Officer

Yes. And just with respect to biomarker-positive versus biomarker-negative, we have reported last year at ASH that we had observed a high response rate with the majority of patients all responding quite swiftly right after just 28 days of treatment. And when benchmarking those results to the biomarker-negative enrolled patients, we saw that the results are pretty distinct in the sense that it has a known response rate in the mid-teens to mid-20% range, and the majority or at least half the patients should be responding by about four months. So we think that there's a consistency of responses, even in our own hands, to single-agent aza, we've demonstrated a distinction from with our biomarker-positive cohort.

And then in terms of the relapsed population, aza as a single agent has an approximate 15% response rate with relatively short duration. And so we're anticipating that we'll be able to differentiate a combination effect in that population.

Zegbeh Jallah -- Roth Capital Partners -- Analyst

Thank you David. That's it for me.

Operator

Thank you. And I'm showing no further questions. At this time, I would like to turn the call back to Ms. Nancy Simonian for any closing remarks.

Nancy Simonian -- Chief Executive Officer

Thank you, operator, and thank you all for joining us today and for your continued support of Syros. Have a great day.

Operator

[Operator signoff]

Duration: 28 minutes

Call participants:

Naomi Aoki -- Vice President of Corporate Communications and Investor Relations

Nancy Simonian -- Chief Executive Officer

Joe Ferra -- Chief Financial Officer

Phil Nadeau -- Cowen and Company -- Analyst

Ted Tenthoff -- Piper Jaffray -- Analyst

Jason Butler -- JMP Securities -- Analyst

David Roth -- Chief Medical Officer

Eric Olson -- Chief Scientific Officer

Matt Biegler -- Oppenheimer and Company -- Analyst

Zegbeh Jallah -- Roth Capital Partners -- Analyst

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