Cyclacel Pharmaceuticals Inc (CYCC) 2020 Q2 法說會逐字稿

Good afternoon, and welcome to the Cyclacel Pharmaceuticals Second Quarter 2020 Results Conference Call and Webcast. (Operator Instructions) The company will also be accepting a limited number of questions submitted via e-mail 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 and 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 and/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 will 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.

At 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 combinations with other drugs to improve anticancer effectiveness and treatment outcomes. We are pleased to report continued progress and will briefly describe on today's call our plan for advancing our lead drug, fadraciclib.

Based on current spending plans, we estimate that 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 CDK9 isoforms, which act as key components of the p53 pathway. Activity against CDK2 results in reduction of cyclin E and against 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 strengthened the mechanistic rationale for fadraciclib's potential as an anticancer therapy including the benefits of inhibiting both CDK2 and CDK9 and elucidate the roles of cyclin E, MCL1 and MYC over expression. 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 I study in gynecological cancers. We will provide details on the progress of these studies later on, but would first like to review the relevance of fadraciclib's mechanism in

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Overexpression of cancer resistance proteins, such as MCL1, or amplification of oncoproteins, such as cyclin E, are associated with escape of cancer cells. MCL1 is one of the 10 most frequently over-expressed cancer genes and is 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 over expressed in several gynecological cancers, including breast, endometrial/uterine and ovarian. Addiction to cyclin E enables cancer cells to escape death after anticancer therapy. Suppressing these proteins forces aberrant cells into apoptosis, or program 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 resulted 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 desirable suppression of the protein in peripheral blood mononuclear cells and anticancer activity as monotherapy in heavily pretreated patients with solid tumors.

MCL1 suppression was observed in the majority of patients enrolled at the recommended Phase II dose, or RP2D, in Part I of our O65-1 dose escalation study using a sparsely administered schedule. We enrolled 26 patients who received fadraciclib as a single 4-hour infusion every 3 weeks. Nearly all patients who achieves stable disease with tumor shrinkage had molecular markers relevant to the drug's mechanism, including MCL1, cyclin E and/or MYC amplification.

We have enrolled a further 23 patients in the ongoing part 2 of the study with a more frequent dosing schedule of 1-hour infusion on days 1, 2, 8 and 9 every 3 weeks. Escalation in part 2 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 1.5 months 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 4 months of fadraciclib monotherapy.

We have submitted data from Part II of the study for publication at an upcoming oncology conference in late fall. On our last quarterly call, we described plans to further explore our 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/uterine or ovarian cancer patients, respectively. Patients will receive fadraciclib monotherapy and subsequently combination therapy depending on available options. Preparation for the study are 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 over expression. 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 4 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 2 dose escalation studies to test the hypothesis that suppressing MCL1 and BCL2 can result in anticancer activity against relapsed or refractory leukemias. MCL1 plays a dominant role in AML and is supported by a 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 06502. The primary endpoint of each study is the determination of RP2D and safety.

In our 065-03 AML study, antileukemic activity, consistent with the drug's mechanism, has been reported in 4 out of 11 patients dosed. These heavily pretreated patients received the combination of oral venetoclax and escalating doses of fadraciclib on a 4-hour infusion schedule once every 2 weeks. Based on the observed activity and previously reported reductions of leukemic blasts in the peripheral blood of patients, treated on lower doses with a combination, we plan to evaluate additional more frequent dosing schedules. In CLL, BCL2 over expression 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. 5 patients have been treated so far up to the fourth dose level or 150 milligrams per meter square. The first 2 patients failed ibrutinib therapy and one of the 2 also failed CAR-T. They were dosed once every 2 weeks with 64 milligrams per meter squared of fadraciclib and venetoclax as per label post ramp for 5 and 6 cycles, respectively, which was well tolerated. Both patients has continued shrinkage of their lymph nodes and one was MRD negative after 5 cycles on the combination.

A third patient now, dosed at 85 milligrams per meter squared of fadraciclib, also achieved MRD negativity after 6 cycles on the combination. Both of these studies are a 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 2 other programs, sapacitabine and CYC140.

In our DNA damage response program, 632-11, we're evaluating the safety and effectiveness of an oral combination of Cyclacel's nucleoside analog sapacitabine with venetoclax in patients with their last or refractory AML or MDS. This is a dose escalation study with 12 patients enrolled to date. 2 patients previously treated with combination therapy, including hypomethylating, agents have achieved 5 and 6 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 a veliparib, AstraZeneca's Lynparza in patients with BRCA-mutant breast cancer. 7 patients have been enrolled with 1 partial response and prolonged stable diseases observed.

In our antimitotic program, we're evaluating CYC140, a polo-like kinase, or PLK-1 inhibitor, which like fadraciclib, was discovered in-house. 6 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 PLK-1 inhibitor that has 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 corporate group to evaluate fadraciclib in histologies where MYC over expression is prevalent, and we will 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 preclinical studies in plasma donated by patients with COVID-19 disease. We will report the findings of these studies at Edinburgh once reported by the investigators.

In addition to other ISTs, at Cedar 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 2 years. Our upcoming key milestones includes: report updated fadraciclib Phase I safety and efficacy data with frequent IV dosing schedule in patients with advance solid cancers; report initial safety and PK data from a Phase I study of fadraciclib or formulation; treat first patient in fadraciclib Phase I/II precision medicine-driven study; report initial data from fadraciclib venetoclax Phase I study in relapsed or refractory AML and CLL; report initial data from CYC140 Phase I first-in-human study in relapsed or refractory leukemias; report an initial data from sapacitabine venetoclax Phase I study in relapsed or refractory AML or MDS; and report data from Phase Ib/II 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 3 months ended June 30, 2020, and 2019. R&D expenses relating to the transcriptional regulation program, fadraciclib, increased by approximately $0.2 million for the 3 months ended June 30, 2020, as we continue to progress the clinical evaluation.

General and administrative expenses for the 3 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 3 months ended June 30, 2020, was $20,000 compared to $0.2 million for the same period of the previous year. The decrease of approximately $0.2 million for the 3 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 3 months ended June 30, 2020 and in 2019. Net loss for the 3 months ended June 30, 2020, was $2.2 million compared to $1.8 million for the same period in 2019.

In Following the April equity financing, our common stock outstanding is 4.9 million shares. Operator, we are now ready to take questions.

(Operator Instructions) We do have a question in queue from Jonathan Aschoff with ROTH Capital Partners.

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 when could that trial potentially start?

Thank you for your question, Jonathan. First of all, we're not experts in either virology or inflammation. We are obviously an oncology company, but we are learning from our collaborators in the University of Edinburgh fast 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 have 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 over expressed, the same thing occurs in COVID-19 related viral pneumonia. The patients eventually after having a high level of over acting neutrophils go on to develop acute lung injury, which is oftentimes not reversible. The goal of the University of Edinburgh study is to compare fadraciclib, our newest higher potency second-generation CDK inhibitor, with the first generation seliciclib molecule. They have already tested and published several publications over the last decade with seliciclib showing 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 as we know, have recently discovered the utility of dexamethasone in COVID-19 disease. I think at this point, we will wait for them to come back with initially the ex vivo data from plasma of 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 or demonstrated study.

My last question is -- in the sapacitabine and venetoclax trial went from about 6 when I updated it last to 12 in enrollment, and you added 0, 6 with a 1, 4. But what kind of unifies the fadraciclib trial, AML, MDS as well as the CLL, they stayed at 11 and 5, respectively, over the last several months.

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

Yes. Can you hear me?

Yes. We can hear you. There you go.

Okay. Well, I think the unify theme is that all 3 drugs, sapacitabine, fadraciclib, and CYC140 are expected to have antileukemic activity based on the mechanism of actions. And I think 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 could move the drug, either single agent or in combination upfront.

Your next question is from Kumar Raja with Brookline Capital Markets.

With regard to the precision medicine study, we talked about the study design developing. Maybe you can talk a little bit about what needs to be done before you can start the trial in the first quarter of '21.

Thank you for your question, Kumar. This is quite simply to interrogate a number of key opinion leaders in 3 relevant types of women's cancers. This is to ensure that we can visibly 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 single agent or possibly a combination with 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. And many patients do not get offered PARP inhibitors, most likely because they don't have sensitivity to platinum in the first place. A large number of these patients, we understand from clinician discussions, have second amplification. So this is a population we'd like to focus on. In breast cancer, [a certain population beholds] that progress after treatment with hormonotherapy for their hormone receptor-positive breast cancer, together with CDK 4/6 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 static difference in terms of predicting from both resistance and sensitivity to palbociclib therapy, the main CDK 4/6 inhibitor, were cyclin E amplification, which we know can be targeted by fadraciclib. So we will have this discussion with KOLs, which are now underway.

Simultaneously, as we briefly mentioned in the prepared 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. It's 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 did this on 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 or should we fall possibly more conservatively into a combination program with available standards of care, so we can demonstrate doublet or triplet activity as 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 will expand the maximum effort to achieve that goal over the rest of 2020.

And in terms of interactions with the regulators, what are your expectations in terms of timing? And also you talked about parallel enrollment and taking about 1 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 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 3 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 2 reasons to suggest that. One is the sheer size of patients. Hormone receptor-positive breast cancer is almost 3/4 of all breast cancers observed in the United States. Approximately 80% of these patients will be offered, at some point, CDK4/6 inhibitor therapy in combination with hormonotherapy, and the vast majority of those who are still alive will relapse. At the time that they all progress to disease or sensitivity to the CDK4/6 drug, they could be tested for second amplification. If they're found to be secondly amplified, they will be possible candidates for the study. So given the tens of thousands of patients that could be available with this type of eligibility criteria, we feel that breast is the likely one to go faster. Let me ask Judy to step in and speak about interaction with FDA in such a program.

Well, in deals that we have already safety data on fadraciclib in the current Phase I studies, I think that such a program as a Phase I/II study in solid tumors will 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, we need to be submitted to the FDA, but there's no requirement for us to wait for FDA approval and before we move forward. I hope that answers your question.

And maybe one question based on the PLOS paper, where you see -- you have tested the TNBC and it seems to have a very high inhibitor 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 in 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 Dinaciclib, an early generation CDK9 inhibitor with broad promiscuous target profile, together with pembrolizumab which, of course, the most successful IO drug, anti-PD-1 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 markets of interest to Cyclacel. So we are, obviously, a month later from this announcement, intensively studying these findings, and trying to understand what this portent 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 with the drug as a single agent.

And maybe finally, in terms of COVID-19, maybe in terms of timing, when can we get the next update on that?

You're welcome, Kumar. This is a great question. We wish we knew the answer. This is a program run by collaborating group. It is not our program. We agreed to provide 3 drug and share our data. So we can facilitate their work, but they are the experts. They have a very large group in the center for inflammation research at the university. They have been active with 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 and Scotland continued under lockdown, even though the southern part of the U.K. was allowed to go back to some level of normality, Scotland remain under lockdown. They have since been able to go into the lab, but things have taken longer than they plan. And we hope that towards the end of the year, we'll have a better sense of when they would do a clinical trial. But the first report we might have in the second half of this year will be the outcome of the 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, with -- because of its higher potency more efficiently. And that clearly, it is not something that is in our control, but we are very keen to find out. Thank you again for all your questions.

Your final question is from Wangzhi Li with Ladenburg.

Do you hear me?

Yes, we can hear you now.

We can hear you now, Wangzhi.

Okay. Good. First question is regarding the AML study. You mentioned the 4 of the 11 patients show (inaudible) activity. Maybe I missed your description. Could you provide a further color on what (inaudible) activity for the patients?

Sorry, the line was a bit crafty. Would you mind repeating the last part of your question?

(inaudible)

We can't hear you very well, but I think the question you asked, Wangzhi, was of the 4 out of 11 patients in the AML study that had a reduction in blasts, and then we couldn't hear the second part.

Unfortunately, the sound quality didn't last. 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 would, to explain what we have seen and given the population of heavily pretreated relapsed/refractory patients, what it portends for the future of fadraciclib and AML. Over to you, Judy.

Well, thank you, Spiro. I think it's encouraging to see that we have a decrease in peripheral blast. But I think that once the drug -- right now, it's dose every 2 weeks. So I think that once the drug is removed, that the blast do return. So therefore, our take is that we need to intensify the dosing schedule. And for example, instead of giving it every 2 weeks, there may be too far apart that we intend to pursue it every week. And hopefully, that will lead to more sustainable reduction in the 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. These are not the first relapsed patients. We've seen patients who went through 5 therapies and even more. So these are really very tough patients. But of course, it's encouraging to see a decrease in peripheral blast. And I think our next plan is to try to intensify the dosing schedules. And to see if we can have a more sustainable decrease in the peripheral blast as well as bone marrows.

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

Yes. And then I think you mentioned you're evaluating CYC140 in solid tumors. Just wondering, do you have any color to share in terms of what's picking the support or what [things] you see from the Phase I study to draw your decision to expansion into solid tumor now?

Thank you for that question. Let me clarify that, first of all, the drug continues in a 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'd consider developing the drug also in solid tumors. And as we mentioned in prepared remarks, this is under consideration. We have not yet given any detail what type of solid tumor, what are the relevant markets, what is the clinical setting in which we think that PLK1 inhibition could be 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's an extensive pharmacological literature in this field but very little evidence that PLK inhibitor 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 speed of patients across your trials or what impact from COVID-19 -- related impact and what your outlook for patient enrollments later this year and related data reports?

That's a great question that every sponsor has asked nowadays or at least the last several months. And of course, we're 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 I studies, very heavily to 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 that pandemic is moving to other locations, including Houston where MD Anderson is, but no longer in Boston. So it's a bit of an evolving picture, but one can say, broadly speaking, that we have not seen a slowdown for the reasons I described. We mentioned before on the patient in the Dana-Farber study, the second part of our Phase I program, who 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 4 times every 3 weeks. She sits in the chair at Dana-Farber for a 1-hour infusion. But it's clear that this single-agent treatment has stabilized her disease and giving her a chance to hope for a better future once she was referred for terminal care. So one can say that COVID-19 and risk of exposure is the least of her concerns and stopping therapy would be extremely an attractive option if it had to be considered at all. So for these reason, so long as we are in this environment where patient survival is relatively short, I don't think that we will experience a significant decline in enrollment.

Now once 2021 comes in and we begin our Phase I/II 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 an 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. Although we have spoken to international investigators, we've tried to focus on the United States for all these 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, we have been spared the worst and have not had to either suspend any programs or slow them down.

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.