Bio Green Med Solution, Inc. (BGMS) Q2 2020 Earnings Report, Transcript and Summary

Good afternoon, and welcome to the Cyclacel Pharmaceuticals Second Quarter 2020 Results Conference Call and Webcast. At this time, all participants are in a listen-only mode. After today's call, members of the financial community will have an opportunity to ask questions. [Operator Instructions] The Company will also be accepting a limited number of questions submitted via email to the address IR@cyclacel.com. [Operator Instructions] Please note that today's call is being recorded. I would now like to turn the conference over to the Company.

Thanks, Erica, and good afternoon to everyone. Thank you for joining today's conference call to discuss Cyclacel's financial results in business highlights for the second quarter ending June 30, 2020. Before turning the call over to management, I would like to remind everyone that during this conference call, forward-looking statements made by management are intended to fall within the Safe Harbor provisions of the Private Securities Litigation Reform Act of 1995 and section 21E of the Securities Exchange Act of 1934, as amended. As set forth in our press release, forward-looking statements involve risks and uncertainties that may affect the Company's business and prospects, including those discussed in our filings with the SEC, which include, among other things, our Forms 10-Q and 10-K. These filings are available from the SEC or our website. All of our projections and other forward-looking statements represent our judgment as of today, and Cyclacel does not take any responsibility to update such information. With us today are Spiro Rombotis, President and Chief Executive Officer; Paul McBarron, Executive Vice President, Finance and Chief Operating Officer; and Dr. Judy Chiao, Vice President of Clinical Development and Regulatory Affairs. Spiro will begin with an overview of our business strategy and accomplishments on Cyclacel's multiple clinical programs, and Paul provide financial highlights for the second quarter of 2020, which will be followed by a Q&A session. At this time, I would like to turn the call over to Spiro.

Thank you, Jan, and thank you, everyone, for joining us today for our second quarter 2020 business update call. First and foremost, we hope that all of you listening to our webcast are safe and well. The global pandemic continues to affect nearly all human activity and create uncertainty in every business sector. It is becoming clear to society that in order to emerge from the COVID-19 crisis, we need to create novel science-based solutions, and that pharmaceutical innovation will play a central role in this fight. And Cyclacel, we take our corporate social responsibility very seriously, including protecting the health and safety of our employees, the patients we serve, and the communities in which we live and work. We have maintained relevant protective measures and are following government orders, with our employees mostly working from home. To date, we have worked closely with clinical trial sites to ensure adequacy of clinical supplies and compliance with relevant FDA guidance. We have been advised by clinical investigators that they continue to screen and register patients in our studies and remain on track with enrollment. As an illustration, we have enrolled a total of 86 patients in company-sponsored studies, with fadraciclib, sapacitabine, and CYC140 as monotherapy and in combinations thus far. At the same time, we cannot assume that circumstances, such as localized spikes, or a second surge, will not make it more difficult for patients to remain on or join our studies. Cancer patients faced increased risks in this environment, such as frequency of visits and translational research requirements. Like other sponsors, we are working with our collaborating investigators to address such matters in our trial design. Cyclacel's business strategy is to build an innovative pipeline, addressing the rising problem of cancer resistance. We are studying the ability of our agents alone and in combination with other drugs to improve anti-cancer effectiveness and treatment outcomes. We are pleased to report continued progress, and will briefly describe on today's call our program for advancing our lead drug, fadraciclib. Based on current spending plans, we estimate our cash and equivalents of $25.3 million as of June 30, 2020 will provide a cash runway to the end of 2022. We will next review our lead development program. Fadraciclib, our novel CDK inhibitor, targets the CDK and nine isoforms, which act as key components of the p53 pathway. Activity against CDK2 results in reduction of cyclin E, and again, CDK9 in reduced expression levels of MCL1. We were pleased to announce the publication in PLOS One of a peer reviewed study of fadraciclib by scientists from Cyclacel and the Institute of Cancer Research in London. The findings from the study strengthen the mechanistic rationale for fadraciclib's potential as an anti-cancer therapy, including the benefits of inhibiting both CDK2 and CDK9, and elucidate the roles of cyclin E, MCL1, and MYC overexpression. Furthermore, independent findings from Duke University reported at the ASCO 2020 Virtual Scientific Program corroborate the attractiveness of this dual targeting approach against CDK2 and CDK9. Cyclacel is evaluating fadraciclib as a single agent in patients with solid tumors, and in combination with other drugs in patients with hematological malignancies. We are also preparing our planned Phase 1 study in genealogical cancers. We will provide details on the progress of these studies later on, but we'd first like to review the relevance of fadraciclib's mechanism in [Technical Difficulty]. Overexpression of cancer resistance proteins, such as MCL1, or amplification of oncoproteins, such as cyclin E, are associated with the escape of cancer cells. MCL1 is one of the 10 most frequently overexpressed cancer genes, and as a member of the BCL2 protein family, including BCL2, BFL1, and BCL-XL. These proteins act as pro-survival mechanisms for cancer. Cyclin e, a protein encoded by the CCNE gene, is overexpressed in several gynecological cancers, including breast, endometrial slash uterine, and ovarian. Addiction to cyclin E enables cancer cells to escape death after anti-cancer therapy. Suppressing these proteins forces aberrant cells into apoptosis, or programmed cell death. Cyclacel's therapeutic strategy is to suppress the expression of such proteins and reactivate the apoptotic machinery, leading to cancer cell death. Recent discoveries of the importance of MCL1 have resolved in a race to bring to market medicines suppressing this protein. We believe that fadraciclib is a leader in this race, based on demonstration of durable suppression of the protein in peripheral blood mononuclear cells and anti-cancer activity as monotherapy in heavily pre-treated patients with solid tumors. MCL1 suppression was observed in the majority of patients enrolled at the Recommended Phase 2 Dose, or RP2D, in part one of our 065-01 dose escalation study, using a sparsely administered schedule. We enrolled 26 patients who received fadraciclib as a single four-hour infusion every three weeks. Nearly all patients who achieved stable disease with tumor shrinkage had molecular markers relevant to the drugs mechanism, including MCL1, cyclin E, and/or MYC amplification. We have enrolled a further 23 patients in the ongoing part two of the study with a more frequent dosing schedule of one hour infusion on days one, two, eight, and nine every three weeks. Escalation in part two has reached the fourth dose level, and additional patients have been enrolled to establish RP2D. As previously reported, a patient at the fourth dose level with heavily pretreated MCL1 amplified endometrial cancer achieved radiographically confirmed partial response or PR after a month and a half on fadraciclib. This patient is continuing on study after over a year on the same dose of fadraciclib. After the last restaging, shrinkage in her target tumor lesions has improved to 83%. Other patients achieved stable disease, including a patient with cyclin E amplified ovarian cancer with tumor shrinkage of 29% after four months of fadraciclib monotherapy. We have submitted data from part two of this study for publication at an upcoming oncology conference in late fall. On our last quarterly call, we described plans to further explore fadraciclib in a tissue agnostic precision medicine driven study, evaluating patients with gynecological cancers. The concept behind the study broadly follows the precedent setting approval of pembrolizumab in microsatellite instability high or mismatch repair cancers. This study is planned as an open label, parallel cohort study design, with an initial sample size of 60 patients, with each cohort enrolling 20 breast, endometrial slash uterine, or ovarian cancer patients respectively. Patients will receive fadraciclib monotherapy, and subsequently, combination therapy, depending on available options. Preparations for the are study advancing in consultations with experts, along with development of the study design. In parallel, we are selecting a vendor to provide genomic analysis for the biomarkers of interest, MCL1, cyclin E, and or MYC overexpression. Once the study has started in early 2021, we expect enrollment to take approximately a year, notwithstanding pandemic delays. In addition to intravenous administration of fadraciclib, we're evaluating an oral capsule formulation. We have dosed four patients to date and reached the second dose level. Initial pharmacokinetic or PK data demonstrated a PK profile closely overlapping that of the IV administration, with encouraging exposure levels at the equivalent dose. In our hematological malignancies program, we have opened two dose escalation studies to test the hypothesis that suppressing MCL1 and BCL2 can result in anti-cancer activity against relapsed or refractory leukemias. MCL1 plays a dominant role in AML, and is supported by preclinical evidence of synergy of fadraciclib and venetoclax in inducing apoptosis. We're evaluating a fadraciclib and venetoclax combination in patients with relapsed or refractory AML or MDS in the 065-03 study, and relapsed or refractory chronic lymphocytic leukemia or CLL in 065-02. The primary endpoint of each study is the determination of RP2D and safety. In our 065-03 AML study, anti-leukemic activity consistent with the drug's mechanism has been reported in four out of 11 patients dosed. These heavily pre-treated patients receive the combination of oral venetoclax and escalating doses of fadraciclib on a four-hour infusion schedule once every two weeks. Based on the observed activity and previously reported reductions of leukemic blasts in the peripheral blood of patients treated from lower doses with a combination, we plan to evaluate additional, more frequent dosing schedules. In CLL, BCL2 overexpression is the main feature, and MCL1 is an escape mechanism. Leukemia cells, especially in the lymph nodes, may stop responding to venetoclax, followed by relapse, often associated with MCL1 over expression. Eradicating CLL in the lymph nodes, and achieving minimal residual disease or MRD negativity is an important treatment objective. In 065-02, enrollment has been slow, reflecting the long relapse free survival after frontline CLL therapies. Given that eventually, a large number of patients will relapse, investigators have advised Cyclacel to persist as an unmet medical need is emerging. Five patients have been treated so far up to the fourth dose level, or 150 milligrams per meter squared. The first two patients failed ibrutinib therapy, and one of the two also failed CAR-T. They were those two once every two weeks with 64 milligrams per meter squared of fadraciclib and venetoclax as per label post ramp for five and six cycle respectively, which was well tolerated. Both patients had continued shrinkage of their lymph nodes, and one was MRD-negative after five cycles on the combination. A third patient now, dosed at 85 milligrams per meter squared of fadraciclib also achieved MRD negativity after six cycles on the combination. Both of these studies are part of our Risk Sharing Alliance with the University of Texas MD Anderson Cancer Center, whereby MD Anderson assumes patient costs for all studies, and we provide investigational drugs and other limited support. The MD Anderson Alliance also includes clinical trials with our two other programs, sapacitabine and CYC140. In our DNA Damage Response Program, 682-11, we're evaluating the safety and effectiveness of an oral combination of Cyclacel's nucleoside analog sapacitabine with venetoclax in patients with relapsed or refractory AML or MDS. This is a dose escalation study, with 12 patients enrolled to date. Two patients previously treated with combination therapy, including hypomethylating agents, have achieved five and six cycles of treatment, respectively. In addition, an investigator sponsored trial, or IST, is enrolling at the Dana Farber Cancer Institute, evaluating a combination of sapacitabine with olaparib AstraZeneca Lynparza in patients with BRCA-mutant breast cancer. Seven patients have been enrolled, with one partial response and prolonged stable diseases observed. In our antimitotic program, we're evaluating CYC140 a polo-like kinase, or PLK1 inhibitor, which like fadraciclib, we discovered in house. Six patients with advanced leukemias have been recruited to 140-01, our first in-human single agent dose escalation study. No dose limiting toxicities have been observed thus far. CYC140 is a small molecule selective PLK1 inhibitor that demonstrated potent and selective target inhibition and high activity in xenograft models of human cancers. We have received interest from investigators to study CYC140 in patients with solid tumors, which we are now evaluating. Turning to our other ISTs, we are collaborating with an international cooperative group to evaluate fadraciclib in histologies where MYC overexpression is prevalent, and we'll provide updates once the study is open for enrollment. The University of Edinburgh continues to evaluate the comparative potential of our CDK inhibitors, fadraciclib and seliciclib, for reducing runaway inflammation and subsequent lung injury in pre-clinical studies and plasma donated by patients with COVID-19 disease. We will report the findings of the studies at Edinburgh, once reported by the investigators. In addition to other ISTs, at Cedars Sinai Medical Center, and the University of Newcastle are evaluating seliciclib, our first generation CDK inhibitor, in patients with Cushing's disease and rheumatoid arthritis, respectively. During the quarter, we continued to move our programs forward to multiple data outcomes over the next two years. Our upcoming key milestones include report updated fadraciclib Phase 1 safety and efficacy data with frequent IV dosing schedule in patients with advanced solid cancers; report initial safety and PK data from Phase 1 study of fadraciclib or formulation; treat first patient in fadraciclib Phase 1/2 precision medicine driven study; report initial data from fadraciclib venetoclax Phase 1 study in relapsed or refractory AML and CLL; report initial data from CYC140 Phase 1 first in-human study in relapsed or refractory leukemias; report initial data from sapacitabine venetoclax Phase 1 study in relapsed or refractory AML or MDS; and report data from Phase 1B/2 sapacitabine olaparib IST in BRCA-mutant metastatic breast cancer when reported by the investigators. With capital on hand estimated through the end of 2022, we have the resources to deliver key milestones in our clinical studies. I would now like to turn the call over to Paul to review our second quarter 2020 financials. Paul?

Thank you, Spiro. As outlined in today's press release for the quarter ended June 30, 2020, cash and cash equivalents totaled $25.3 million, compared to $11.9 million as of December 31, 2019. The increase of $13.4 million was primarily due to net proceeds of $18.3 million from an equity financing in April 2020 and net cash used in operating activities of $4.7 million. We estimate that cash resources as of June 30 will fund currently planned programs through the end of 2022. Research and development expenses were $1.2 million for each of the three months ended June 30, 2020 and 2019. R&D expenses relating to the transcriptional regulation program of fadraciclib increased by approximately $0.2 million for the three months ended June 30, 2020, as we continued to grow progress with clinical evaluation. General and administrative expenses for the three months ended June 30, 2020 were $1.3 million, compared to $1.2 million for the same period of the previous year. Total other income net for the three months ended June 30, 2020 was $20,000, compared to $0.2 million for the same period of the previous year. The decrease in approximately $0.2 million for the three months ended June 30, 2020 is primarily related to income received on an asset purchase agreement with Thermo Fisher Scientific Inc. United Kingdom R&D tax credits were $0.3 million for each of the three months ended June 30, 2020 and in 2019. Net loss for the three months ended June 30, 2020 was $2.2 million compared to $1.8 million for the same period in 2019. And following the April equity financing, our common stock outstanding is 4.9 million shares. Operator, we are now ready to take questions.

[Operator Instructions] You do have a question in queue from Jonathan Aschoff with ROTH Capital Partners.

Thank you. Hello, guys. I was curious, what needs to be seen in the plasma test for the COVID-19 program in order to enter a clinical trial and could that trial potentially stun?

Thank you for your question, Jonathan. First of all, we're not experts in either biology or inflammation. We are obviously an oncology company but we're learning from our collaborators and the University of Edinburgh first in the face of the pandemic. It appears that there are several patient groups that could benefit to your question from an intervention that would perhaps dampen the overactive inflammatory response. The primary biomarker for this would be activated neutrophils. This is a disease where the patients do not have cancer, but just like in cancer, when cells become upregulated and become overexpressed, the same thing occurs in COVID-19 related viral pneumonia. The patient's eventually after having a high level of overactive neutrophils go on to develop acute lung injury, which is oftentimes not reversible. The goal of the University of Edinburgh studies is to compare fadraciclib on U.S. higher potency second-generation CDK inhibitor with the first generation seliciclib molecule. They have already tested and published several publications over the last decades, with seliciclib showing it can dampen the overactive inflammatory response. But of course, we're quite keen to seek to reproduce that data with a more potent newer drug. Once that is done, they have proposed to us to run an exploratory medicine study, which would look at a modest number of patients to demonstrate clinical benefit. Thereafter they belong to a U.K. wide consortium of hospitals, which have recently discovered the utility of dexamethasone in COVID-19 disease. I think at this point, we'll wait for them to come back with initially the ex-vivo data from plasma donor patients, and then discuss in this forum or subsequently when they will decide and if they will decide to go into a clinical program in a small number of patients that demonstrate a study.

Thanks for that, Spiro. My last question is the sapacitabine and venetoclax trial went from about six when I updated it last to 12 in enrollment and you added zero to six with a 140. But what kind of unifies the fadraciclib trials AMLMDS as well as the CLL. They stayed at 11 and five respectively, over the last several months.

I think this is probably a question for Judy Chiao but let me say as a preamble that we're talking about very different disease settings. In AML, the fadraciclib we enrolled very fast. In fact, we run out of slots with 11 patients enrolled in the record time. The venetoclax study took longer but eventually got to the same level. In the case of 140, this is the first-in-human study, where we're asking the patient who is probably close to the end of life to altruistically offer their participation into a study with a regimen never before tested in humans is very different challenges for these patients to make a decision. So by that explanation, let me ask Judy to comment with her views. Do we have Judy on the line still?

Yes, can you hear me?

We can hear you.

Okay. Well, I think the unifying theme is that all three drugs sapacitabine, fadraciclib and CYC140 are expected to have anti-leukemic activity based on the mechanism of actions. I think that the current trial is really trying to define a safety dose in the relapsed refractory setting and hopefully, that once that's done that we can move the drug either a single agent or in combination upfront.

Okay, thank you very much, guys.

Thank you, Jonathan.

Your next question is from tomorrow Kumar Raja with Brooklyn Capital Market.

Thanks for taking my questions. With regard to the physician medicine study, we talked about study design developing. Maybe you can talk a little bit about what needs to be done before you can start the trial in first quarter of 2021.

Thank you for your question, Kumar. This is quite simply to interrogate a number of key opinion leaders into three relevant types of women's cancers. This is to ensure that we can feasibly enroll in these populations. These will be patients that will be relapsed or refractory presumably to current disease standard of care. They will be offered the clinical protocol with either a single agent or possibly combination or standard of care and therefore, we need to understand what the current and more importantly, emerging landscape is in each of these tumor types. These are not necessarily overlapping universes. For example, in ovarian cancer, the current standard of care would be most likely chemotherapy, platinum for example, or a PARP inhibitor. But many patients don't get offered PARP inhibitors, most likely because they don't have sensitivity to platinum in the first place. A large number of these cases we understand from donation discussions have stagnated amplification. So this is the population we'd like to focus on. In breast cancer, as soon as the population progress as the different with hormonal therapy for the hormone receptor-positive breast cancer together with CDK4/6 inhibitor. Why? Because as we know in a large study published at ASCO last year, the PALOMA-3 trial, the only biological marker that showed stats same difference in terms of predicting for both resistance and sensitivity to fadraciclib therapy, the main CDK4/6 inhibitor was second amplification, which we know can be targeted by fadraciclib. [Technical Difficulty] remarks we are exploring different vendors to provide central laboratory testing for the biomarkers of interest. This type of genomic profiling initially at baseline possibly also later is critical to understand the translational side of this clinical study. Is one thing about being able to say that a patient achieved tumor shrinkage, ideally partial response or even better, a very different thing to say that it is a mechanism. So we feel this is a very important part of our program. Ultimately, it all depends whether we see sufficient single-agent activity to move forward in a precision medicine study, once we involve possibly more conservatively into combination program with available standards of care, so we can demonstrate double or triple activity. Hence we have seen in many refractory cancers in recent months. So we think that this is an eminently doable program between now and the beginning of next year, the first quarter of 2021 and we'll expand the maximum effort to achieve that goal over the rest of 2020.

And in terms of interactions with the regulator, what are your expectations in terms of timing? Also, you talked about the parallel enrollment and taking about one year for the enrollment given that these are going to be different indications maybe you can provide your thoughts on what are your expectations in terms of which one of these trials might enroll comparatively faster than others?

Thank you, Kumar. Let me take the last part of your question and then Judy can discuss about interactions with regulatory authorities. So as far as timing and which of the three cohorts would enroll fastest, it seems to us and of course, that's our current judgment, it may change tomorrow, that the breast cancer program will go faster. There are two reasons to suggest that. One is the sheer size of patients. Hormone receptor-positive breast cancer is almost three-quarters of all breast cancers observed in the United States. Approximately 80% of this patient will be offered at some point CDK4/6 inhibitor therapy, in combination with hormonal therapy, and the vast majority of those who are still alive will relapse. At the time that they show progressive disease or lose sensitivity to the CDK4/6 drug, they could be tested for secondary amplification. If they are found to be secondary amplified, they will be possibly candidates for this study. So given the tens of thousands of patients that will be available with this type of eligibility for FDA, we feel that breast is the likely one to go faster. Let me ask Judy to step in and speak about interaction with the FDA in such a program.

Well, in view that we have already safety data on fadraciclib in the current Phase 1 study, I think that such a program as a Phase 1/2 study in solid tumors would not be subjected to the scrutiny that the FDA typically require for the first-in-human study. Now what I mean by that is that the protocol obviously would need to be submitted to the FDA, but there's no requirement for us to wait for FDA approval before we move forward. I hope that answers your question.

And maybe one question based on the PLOS paper where you see your tested TNBC and it seems to have very high inhibitory content; it seems to be effective there. Any thoughts on potentially testing in TNBC?

That's an excellent question, again, Kumar, and perhaps a provocative one. We are interested in triple negative breast cancer, TNBC, as you suggest, however, at this point we have not included into our program. The reason is the rapid egress or recent approval of IO, immuno-oncology drugs in this space. There is however a relevant finding that was published a month ago during ASCO 2020, and that is a report from UCSF, University of California, San Francisco, combining [indiscernible], an early-generation CDK9 inhibitor with broad promiscuous target profile, together with pembrolizumab, which is of course, the most successful IO drug anti-PD1 drug we have today in our disposal. The study was done in TNBC patients but only those that have MYC amplification. You will recall that MYC is one of the markers of interest of Cyclacel. So, we are obviously a month later from this announcement, intensively studying these findings, and trying to understand what this portends pertains for fadraciclib. But we certainly intend to discuss TNBC with relevant investigators as the opportunity develops, but only as a second priority to what we have outlined, which is breast endometrial/uterine and ovarian where we have clinical signals for the drug as a single agent.

And maybe finally, in terms of COVID-19, maybe in terms of timing; when can we get a next update on that? Thank you.

You're welcome. Kumar, this is a great question. We wish we knew the answer. This is a program run by collaborating group, this is not our program. We agreed to provide the drug and share our data, so we can facilitate the work; but they are the experts, they have a very large group in the Center for Inflammation Research at the University; they've been active in this field for decades. And we're really waiting for them to come back with completion of their studies. They had initially difficulty accessing the lab, as Scotland continued under lockdown, even the southern part of the UK was allowed to go back to some level of normality, Scotland remain under lockdown. Since they've been able to go into the lab, but things have taken longer than we planned. We hope that towards the end of the year we'll have a better sense of whether there will be a clinical trial but the first report will might have in the second half of this year will be the outcome of a comparative study of fadraciclib versus seliciclib. So the first job here is to show that fadraciclib has reproducible lowering of the overactive inflammatory response as seliciclib does and hopefully [indiscernible] more efficiently. Now that clearly is not something that is in our control but we are very keen to find out. Thanks, again, for all your questions.

Your final question is from Wangzhi Li with Ladenburg. Mr. Li, your line is open. Mr. Li, your line may be on mute.

Hello, can you hear me?

Yes, we can hear you now. Thank you

We can hear you, Wangzhi.

Thanks for taking my question. First question is regarding the [indiscernible]. You mentioned four out of 11 patients of AML [ph]; evidence indicates activity, maybe I missed your description. I just wonder for the color on what kind of activity for the patients?

Sorry, the line was little bit crappy [ph]. Would you mind repeating the last part of your question?

[Technical Difficulty]

We can't hear you very well, but I think the question you asked Wangzhi, was of the four out of 11 patients the AML study that had reduction in blasts. And then, we couldn't hear the second part.

[Technical Difficulty]

Unfortunately, the sound quality is lost [ph]. But I will ask on the hope that I got the gist of your interest. I will ask Dr. Chiao Judy to come in, if you will, to explain what we have seen. And given the population of heavily pretreated relapsed refractory patients and what it portends for the future of fadraciclib and AML [ph]. Over to you, Judy.

Well, thank you, Phil. I think it's encouraging to see that we have a decrease in peripheral blasts. But I think that once the drugs -- right now it goes to every two weeks, so I think that once the drug is removed, that the blasts do return. So therefore, our take is that we need to intensify the dosing schedule. And for example, instead of giving it every two weeks that may be too far apart, that we intend to pursue it every week and hopefully, that will lead to more sustainable reduction in a blast, not only in the peripheral blood, but eventually in the bone marrow as well. And I think that one has to take into consideration that the patients currently enrolled in our studies are really very refractory, we would -- these are not the first relapse patient. We have seen patients who went through five therapies and even more; so these are really, very tough patients. But it's also encouraging to see a decrease in peripheral blasts, and I think our next plan is to try to intensify the dosing schedules and to see if we can have more sustainable decrease in peripheral blasts, as well as bone marrows.

Thank you, Judy. I don't know if you've heard the answer, Wangzhi.

Yes, thank you. And then, I think you mentioned you're evaluating [indiscernible] in solid tumors. Just wondering, do you have any color if you can share in terms of what the preclinical support or what synchronous you speak [ph] from the Phase 1 study to draw your decision to expansion into the solid tumor now?

Thank you for the questions. Let me clarify that, first of all, the drug continues first in human study in MD Anderson Cancer Center as part of our alliance with MD Anderson in refractory leukemic patients, AML or MDS; that program is ongoing. The context of our interest in solid tumors arose from investigators approaching Cyclacel, asking us whether we would consider developing the drug also in solid tumors. And as we mentioned in our prepared remarks, this is under consideration. We have not yet given any detail; what type of solid tumor, what are the relevant markers, what is the clinical setting in which we think that PLK1 inhibitor is relevant. But there is certainly a lot of interest in the literature about the role of antimitotic agents without the liabilities of taxanes. And as you know, there is an extensive pharmacological literature in this field, but very little evidence that PLK inhibitors themselves could be active. So this is a field of current study, and we hope to give more color on that topic probably in early 2021.

Got it. And then, my last question is, maybe overall, you comment on the enrollment fee of patients across your trial or what the impacts from COVID-19 -- related impact and what's your outlook for [indiscernible] later this year and related data reports?

That's a great question that every sponsor is asked nowadays; so did the last several months, and of course, we are no exception. I think we can say that our experience of the pandemic over the last several months has been relatively light one. We're enrolling mostly in Phase 1 studies with very heavily pretreated patients, whose expectation of survival with the exception of CLL is not very good; we're talking about weeks and months, not years. CLL patients take a long time to relapse, that's a different setting as we explained earlier. So, I have to say that in the early days of the pandemic when we had primarily hotspots along the Atlantic and the Pacific Northwest Coast of the United States have not had much of an impact. Now, I think the pandemic is moving to other locations, including Houston or where MD Anderson is, but no longer in Boston; so it's a bit of evolving picture. But one can say, broadly speaking that we have not seen a slowdown, so the reasons are described. We mentioned before the patient in the Dana Farber study, the second part of our Phase 1 program, it has been on fadraciclib monotherapy for over a year for her endometrial cancer which is MCL1 amplified. For this patient, life is a very challenging proposition right now. She lives in the perimeter of Boston, has to commute into town to the southwest side of the center city to receive her therapy four times every three weeks; she sits in the chair at Dana Farber for one hour infusion. But it's clear that the single agent treatment has stabilized her disease, and given her a chance to hope for a better future when she was referred for terminal care. So one can say that COVID-19 and risk of exposure is the least of our concerns, and stopping therapy would be extremely unattractive option, if it had to be considered at all. So for this reason, so long as we are in this environment where a patient survival is relatively short, I don't think that we will experience significant decline [indiscernible]. Now once 2021 comes in, and we begin our Phase 1/2 study, we expect this to be in a lot more centers, it will most likely require a multicenter approach to enroll quickly, as we have said about a year; and this is unpredictable and somewhat unknowable at this point. We will certainly take into account emergence of hotspots or second surges across different parts of the country. Now that we have spoken to international investigators, we've tried to focus on the United States for obvious reasons; we have a better understanding of the evolving nature of the pandemic there. So every sponsor is facing those issues but we think so far, they have been spared the worst and have not had to either suspend any programs or slow them down.

Got it. Thanks for taking my questions.

Thank you, Wangzhi.

And there are no further questions in queue at this time.

Thank you, operator. And thank you all for participating in Cyclacel's second quarter 2020 earnings call. We appreciate your support of our efforts to fulfill our strategy and realize stockholder value by demonstrating safety, efficacy and cost effectiveness of our medicines. We look forward to updating you on our progress, and meeting some of you at upcoming conferences, either virtually or hopefully in person. Please stay safe and well. And operator, at this time, you may end the call.

Ladies and gentlemen, this concludes today's conference call. Thank you for participating. You may now disconnect.