Bio Green Med Solution, Inc. (BGMS) Q1 2021 Earnings Report, Transcript and Summary

Good afternoon, and welcome to the Cyclacel Pharmaceuticals First Quarter 2021 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. The company will also be accepting a limited number of questions submitted via e-mail to the address ir@cyclacel.com. Please note that today's call is being recorded. I would now like to turn the conference over to the Company.

Good afternoon, everyone and thank you for joining today's conference call to discuss Cyclacel's financial results and business highlights for the first quarter ending March 31, 2021.

Thank you, Arena, and thank you, everyone, for joining us today for our first quarter and business update call. On our last call in February, we provided an overview of the clinical development strategy for fadraciclib and CYC140. Our main objective remains to advance these targeted orally administered candidates into registration directed outcomes for multiple indications. We are pleased to report that we have achieved the initial key milestone delivering on this strategy with FDA clearance over IND for oral fadraciclib, or fadra for short in a streamlined Phase Ib/II clinical study in patients with advanced solid tumors. We expect to open the study in the next few weeks once contract discussions with the sides are concluded. The study design includes a Phase Ib part with patients receiving continuous escalating dosing of oral fadra with the objective of defining a recommended dose for Phase II. Although we will initially evaluate fadra as monotherapy, the design includes the possibility of combination treatments in relevant histologies as required with available or emerging standard-of-care. It is worth noting that before entering this Phase Ib study with the oral formulation Cyclacel has generated a significant amount of clinical data with the IV formulation in solid tumors as monotherapy and in liquid cancers as combination. In addition, we presented oral bioavailability data in October 2020, which demonstrated comparable dosing characteristics between the oral and IV forms with respect to Half-life maximum concentration an area and the curve.

Thank you, Spiro. As of March 31, 2021, cash and cash equivalents amounted to $47.8 million compared to $33.4 million as of December 31, 2020. The increase of $14.4 million was primarily due to $18 million of net cash provided by financing activities offset by net cash using operating activities of $3.6 million. There were no revenues each of the three months ended March 31 2021 and 2020. Research and development expenses were $2.6 million for the three months ended March 31, 2021 as compared to $1.1 million for the same period in 2020. R&D expenses relating to us CDK inhibitor program increased by almost $0.8 million for the three months ended March 31, 2021, as we continue to progress the clinical evaluation of fadra.

Please stand-by while we compile the Q&A roster. Your first question comes from the line of Jonathan Aschoff with ROTH Capital.

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Jonathan thank you for your question. I will ask Mark Kirschbaum to address that but just remind everybody that the study is starting with monotherapy. He then provides in the event that we don't see sufficient activity as a single agent to enroll combination cohorts. Perhaps Mark, you could share your insights on the trial design.

Well, thank you, Spiro. Yes, I mean, essentially agree. The trial is designed primarily to ascertain single agent activity. We believe there are a number of tumor indications where single agent activity may actually produce meaningful responses. So that's the primary focus of the cell tumor trial, given the landscape of leukaemia that’s a little different than that well known drugs will be combined that a standard in the leukaemia world. But I think our primary goal for the cell tumor trial is to go push the single agent activity and add combinations as we see activity.

Thanks. The last question is, what percent of your solid tumor patients that you expect to enroll will have KRAS patient, maybe you want some sort of threshold or are you just going to take what comes?

I think this is again, a question for Mark.

Sure. I assume you're speaking specifically about colon cancer. So again, the way this is designed is that there's a Phase I component of this trial, which is pretty much open to all tumor types that are relevant. And then there's an individual kind of two stage design cohort, specifically designed for colorectal cancer. And KRAS is a pretty significant percentage of those patients. We didn't formally exclude non KRAS patients since we haven't seen yet the clinical activity overall. But my presumption is that the percentage of those sessions will be high.

Okay. Thank you very much guys.

Thank you, Jonathan.

Your next question is from Kevin DeGeeter with Oppenheimer.

Thanks for taking my questions. Maybe, two from me there may evolve as well. With regard to the oral fadra study, can you just comment on how you're thinking about the starting dose and dose escalation given that you do have some prior exposure there with the IV? What I'm really driving it here is, how quickly might we hope to see this compound move through per dose escalation? And then thanks for the update with regard to KRAS CRC for fadra? Can you just comment on the treatment landscape for targeted agents for KRAS CRC and kind of how you see both fadra and CYC140 fitting into that landscape?

Great. Let's have Mark, answer your first question, Kevin about the dosing strategy based on existing IV data. And I'll take on the landscape question on KRAS colorectal cancer. Mark.

Yes, thank you. So the good news here is that based on the previous data that we had with the IV drug, we were able to model the dosing schedule based on pharmacokinetics that we already had. So I can tell you that we are already in the active dosing range from our very first dose level. So this is, we believe that we will be hitting the target already from the start. So depending on how well tolerated we'll be increasing the number of days and then dose but we believe that all of our doses from the start are within an active range.

Got it. And I'm sorry, Spiro I think you actually were going to take second part of that.

Yes, you asked the question about landscape for KRAS mutant colorectal cancer of course, most investors are aware that there are two drugs that are targeting a one of the many mutations characterizing the KRAS genotype which is G12c. These two drugs are sotorasib and Degrasib from Amgen and respectively have shown promising activity in non small cell lung cancer. But the data in Poland was less exciting, although still promising probably would require a combination. This has given rise to a number of new agents positioning for potential convenience once these two drugs reach the market, but I will draw your attention to two facts. First of all, G12c only addresses about 10% of the KRAS population. There are at least five other mutations possibly more responsible for treatment failure and disease progression in this cancer. We know that the other CDK9 drugs are given primarily intravenously, which means that given them to solid tumor patients could be a challenge, as we discovered with fibrocyte have given intravenously as daily pressure on the target it will be hard to achieve as patients even before the pandemic, especially now would be resisting daily therapy with an intravenous drug. And finally, there is the question of what about PLK1, as we know PLK1 has produced PRs in a group of five patients out of 14 treated with KRAS mutant colon cancer. This was as part of a triplet with angiogenesis agent of Aston as well as for chemotherapy. So it remains to be seen whether PLK1 by itself as a single agent can have activity in the setting. So we intend to answer both of these questions. CDK9 inhibition in our case together with CDK2, as well as PLK1 inhibition as single agent in the setting of KRAS colon cancer, this could be a higher priority for the company, but not necessarily derailing us from the already announced clinical development plan is just giving us the chance to perhaps -- we see activity. Hope this gives you some perspective.

Its super helpful then. My follow up actually pertains to the dose escalation for the oral fadraciclib study. And specifically, given that you’re starting at what’s penetrating therapeutic dose, these patients have an opportunity to transition to a higher dose as you escalate and to the extent that's permitted in the protocol, kind of how long would a patient typically needs to be able to stay on drugs before having an opportunity to dose escalate. Thanks.

Mark.

Yes, it's a very specific question about the trial function. We don't have intubation dose escalation is built into the study at this point in time, again, because we believe that all our doses are active. The dosing schedule again is primarily increasing the number of days and weeks. But yes, there's no plan for intubation dose escalation at this point in time.

Great, thanks for taking my questions.

Thank you, Kevin. And let me say for the benefit of those of you listening the webcast that more detail on Mark's comments is available on our presentation in the corporate presentation section of our website. Operator back to you.

Thank you. Your next question is from Wangzhi Li with Ladenburg.

Hi, thanks for taking my question. First question on the KRAS discovery, so since you have both the CDK9 inhibitor and PLK1 inhibitor and both issuing to kind of inhibitor KRAS mutant cancer, you have any insight or these two mechanisms overlap or can they be synergistic or what's the potential to command and have any picnic experience or does it make sense to test in the trial?

That's a great question. Wangzhi. Thank you for asking that. I think there are two ways to address such a question from a portfolio management point of view. It seems to us that there is some biological rationale, but has not been fully studied because these are relatively recent discoveries. As a more practical matter though, two unapproved drugs on the same protocol is a challenge for many sponsors. And that's one of the reasons where people are looking to guess about the emerging standard-of-care and KRAS mutant colon cancer for example and then seek to combine with an approved drug which we know is a tested strategy that could lead to rapid FDA approval, and I suspect the faculty will follow the same path. Ultimately, though, until we understand the translational consequences of each of these drugs as single agents and understand at what stage of the KRAS mutation or spectrum do they work is really hard to speculate on combinatorial possibilities, but it's something that has said to me crossed our mind and we'll look at it at a later time.

That makes sense. One more question on the investigator sponsored trial -- being with the I mean, it's a small number looks quite encouraging. Do you have any further background or the pacing kind of baseline condition? How does it compare to monitor the trial, historically if you compare this response rate and outcome?

Yes, that's a great question. Thank again for asking that. When this question refers to the investigator response for trial, combining our third drug sapacitabine and oral nucleoside analog with oral olaparib, which is the standard-of-care in the setting of metastatic breast cancer, which is mutant for BRCA. In that setting, the reference study is called Olympiad. It's an AstraZeneca study was olaparib. That study showed about 50% PR. But I don't believe that this is the right metric to compare this small data set, as you pointed out Wangzhi. Our view is that small numbers and one could easily get seduced by the attractiveness of small numbers. But we need to see a bigger population to draw conclusions. There is one point about this data which is intriguing. The olaparib and for that matter, all PARP inhibitors, duration of effect is modest is usually around a year, and most patients discontinue therapy due to more suppression. We know from our studies in leukaemia, that sapacitabine can be taken for multiple years, I believe the longest patient on sapacitabine has been on for more than five years, which suggests that if we can stretch the therapeutic benefits with an olaparib combination in the setting of PR or durable stable disease much beyond the olaparib single agent benefit, then we could create a continuum of care which would be very exciting, population of patients who have nothing once PARP inhibitors fail. So that I think is the main interest of the investigators who are paying for the course of the study. But we're going to keenly watch and of course, we are in frequent dialogue with them as this data unfolds.

Got it. Thanks for taking my questions.

Thank you, Wangzhi.

And there are no further questions in the queue at this time. I will turn it back over to management for closing remarks.

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

This concludes today's conference call. Thank you for participating. You may now disconnect.