Bio-Path Holdings Inc

Good morning, ladies and gentlemen. Welcome to the BioPath Holdings Third Quarter 2023 Earnings Conference Call. At this time, all participants are in a listen-only mode. Should you need assistance, please signal for a conference operator by pressing star and zero. Following the formal remarks, we will open the call up for your questions. Please note, the call is being recorded. I would now like to turn the call over to Will O'Connor of Stern Investor Relations. Please proceed.

Thank you, Operator. Welcome to the Biopass Holdings conference call and webcast to review the company's third quarter 2023 financial results and to provide an update on recent pipeline and corporate developments. Earlier, we issued a press release which outlines the topics that we'll plan to discuss on today's call. The release is available at biopassholdings.com. With me today from Biopath are President and CEO, Peter Nielsen, and Senior Vice President of Finance, Accounting, and Administration, Anthony Price. Before we begin the call, I'd like to remind you that today's discussion will contain forward-looking statements that involve risks and uncertainties. These risks and uncertainties are outlined in today's press release and in the company's recent filings with the Securities and Exchange Commission, which we urge you to read. Our actual results may differ materially from what is discussed on today's call. With that, I'll now turn the call over to BioPath CEO, Peter Nielsen. Peter Nielsen Thanks, Will.

Good morning, everyone, and thank you for joining us. We enter the tail end of 2023 in a stronger position than ever. We have exceptionally promising data with Prexygebrus and AML and expect to generate even more data in 2024. Beyond Prexidiviricin, we continue to advance a robust clinical development program across a number of important programs that leverage our innovative DNA-valized platform technology to deliver RNAi nanoparticle therapeutics directly to cancer cells. We are forging a new path in DNA-powered medicine that we believe will give patients a fighting chance to beat these difficult-to-treat cancers. I'll begin with progress we have made with our lead product candidate, prexyzobrosin. As you know, we continue to be encouraged by the positive interim results from stage two of our phase two clinical trial of prexyzobrosin for the treatment of acute myeloid leukemia, or AML. In combination, with frontline therapy, disidabin, and venetoclax. This is meaningful because these patients are at the end of the line of treatment options. Note, most have already relapsed, or essentially everything in the treatment armamentarium currently available. So, a drug like Plexizaburicin can give hope to these patients. The call to study is an amended stage two of our Phase II trial in AML. It is an open-label, two-stage, multicellular study of flexor tuberosum in combination with the cytamin and venoclax in two cohorts of patients with previously untreated AML and relapsed-resistant AML. The third cohort includes treating relapsed-resistant AML patients who are venetoclax-resistant or intolerant with the two-drug combination of Prexidibirucin and Decidamin. The primary endpoint of this study will be the number of patients who achieve complete remission, which includes complete remission with incomplete hematologic recovery and complete remission with partial hematologic recovery. As a recap, of these very promising results we achieved, There were 14 newly diagnosed patients, evaluable in cohort one, and treated with at least one cycle of the Prexidibircin to Cytamin and Venetoclax combination therapy. All patients in this cohort were adverse risk by 2017 European Leukemia Net or EON guidelines or secondary AML. Frexatubiracin was well-tolerated, and adverse events were generally consistent with the Cytamin and Venetoclax treatment and or for AML. Twelve of the 14 evaluable patients, or 86%, achieved complete remission, and two, or 14%, achieved partial remission. In total, 100% of the evaluable patients had a response to treatment. The complete remission rate of 86% for the evaluable patients in cohort one is significantly higher than completion rates of 62% for newly diagnosed patients treated with the frontline combination treatment of Decidivine and Venetoclax. This result is further highlighted by the high risk rating of our cohort one evaluable patients and the inclusion of secondary AML patients, both of which are classes of patients with very difficult-to-treat disease. Fourteen refractory relapsed evaluable AML patients in cohort two were treated with at least one cycle of Prexin-Gerbericin, Decidivin, and Venetoclax combination therapy. All patients in this cohort were adverse risk by 2017 ELN guidelines or secondary AML. Prexin-Gerbericin was well-tolerated and AEs were generally consistent with the Cytamin and Venetoclax treatment and or for AML. Eight of the 14 evaluable patients, or 57%, achieved complete remission, two patients, or 14%, achieved partial remission, and three patients, or 22%, achieved stable disease. In total, 93% of the evaluable patients had a response to treatment. The remission rate of 57% of the evaluable refractory and relapse patients in cohort two is significantly higher than complete remission rate of 21% for refractory relapse patients treated with combination treatment of the cytamin and venetoclax. As with newly diagnosed patients in cohort one, this result is further highlighted by the high risk rating of Biopass Cohort 2 evaluable patients and the inclusion of secondary AML patients. Efficacy data from the initial interim analysis of Cohort 1 and Cohort 2 are compelling and show that frexetraburacin-based combination therapy was not only safely administered in Cohort 1 and Cohort 2 to high risk risk newly diagnosed and refractory relapse AML patients considered unsuitable for standard chemotherapy, but also demonstrated efficacy signals significantly better than current therapies. This is particularly encouraging as relapse refractory patients are a challenging population in which current treatment options are suboptimal. On the strength of these data, We currently plan to pursue US Food and Drug Administration, or FDA, expedited programs for fast track and breakthrough therapy designations. We look forward to keeping you apprised of our progress on the regulatory front. In October, we hosted a key opinion leader event to discuss the evolving treatment landscape in AML. We were privileged to have Dr. Jorge Cortes and Dr. Meryl O'Hanlon, true luminaries in the hematologic and oncology space as our guest speakers. The discussion was illuminating and engaging, bolstering our conviction in the Prexager Burris and Clinical Development Program as both physician experts were deeply encouraged by our interim results and further underscored the great unmet medical need for these relapsed patients. It was heartwarming to have these AML specialists highlight the fact that results of this magnitude are simply not seen in this patient population. Having this independent and expert point of view that supports Biopass' mission was inspiring. I encourage you all to listen to the archive of this event, which is available on our website. Turning now to our BP1002 program. which targets BCL-2. As you know, BCL-2 is responsible for driving cell survival in up to 60% of all cancers. The high expression of BCL-2 has been correlated with poor prognosis for patients diagnosed with AML. Venetoclax has shown activity against anti-apoptotic protein BCL-2 and works by neutralizing the protein's BH3 domain. It is an approved treatment for chronic lymphocytic leukemia or CLL patients and untreated AML patients. However, with the exception of some patients treated with allogenetic hematopoietic cell transplantation, disease relapse invariably occurs oftentimes due to BH3 domain mutation over time. BP1002 also targets BCL2 protein. However, BP1002 activity is based on blocking the BCL2 messenger RNA and not the BH3 domain. As a result, we believe that BP1002 could provide an alternative for venetoclax patients who have relapsed, including AML patients who previously received venetoclax treatment. A total of six evaluable patients will be treated with BP1002 monotherapy in a standard 3 plus 3 design with a starting dose of 20 milligrams per square meter. The approved treatment cycle is two doses per week over four weeks, resulting in eight doses administered over 28 days. The Phase 1b portion of the study will commence after completion of BP1002 monotherapy cohorts, and will assess the safety and efficacy of BP1002 in combination with the cytamine and refractory relapsed AML patients. We expect cohort completion and initial data readout from this study in the coming months. Next, let's turn to our Phase I-1B study, clinical trial of BP100A in patients with solid tumors, including ovarian endometrial pancreatic and triple-negative breast cancer, some of the most challenging cancers to treat with today's therapeutic toolkit. BP1001-A is a modified product from Prexacobrosin, sharing the same drug substance with enhanced nanoparticle properties. The clinical trial is in the second dose cohort. This trial is being conducted at several leading cancer centers and will initially evaluate the safety in solid tumor patients. Patients diagnosed with recurrent ovarian and endometrial cancer often have poor outcomes, and it is our hope that we may provide clinical benefit for such patients. We look forward to cohort completion and data readout from this study in early 2024. Finally, let's review the progress we've made with BP1003, which targets the STAT3 protein. STAT3 is a transcription factor that regulates various tumorigenic processes, such as tumor proliferation, metastasis, and drug resistance. Its overexpression and aberrant activation characterize many cancers, including breast, lung, ovarian, liver, and colon cancers. Activation of the STAT3 pathway in breast and ovarian cancer cells promotes tumor initiation, migration, and taxol resistance. STAT3 also contributes to 5-FU resistance in colorectal cancer cells. Its role in numerous malignancies made STAT3 a potential cancer therapy target. BP1003. is a novel liposome-incorporated STAT3 antisense oligodeoxynucleotide that efficiently reduces STAT3 expression and enhances the sensitivity of breast and ovarian cancer cells to Taxol and 5-FU. These results are in line with previous work in which BP1003 plus gemcitamin displayed enhanced antitumor activity and pancreatic ductal adenocarcinoma. Together, these results strongly suggest that BP1003 combination therapy is a novel strategy for patients with advanced solid tumors. We are particularly excited to launch our first in-human validation of this cutting-edge therapy in an especially challenging cancer indication that has limited treatment options. With that, I'll now turn the program over to Anthony Price for a brief review of our financials along with balance sheet highlights.