Bio-Path Holdings Inc

Good morning, ladies and gentlemen. Welcome to the Biopath Holdings full year 2022 earnings conference call. At this time, all participants are in a listen-only mode. Following the formal remarks, we will open the call for your questions. At this time, I'd like to turn the floor over to Will O'Connor of Stern Investor Relations. Sir, please proceed.

Thank you, Operator. Welcome to the Biopath Holdings conference call and webcast to review the company's full year 2022 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 plan to discuss on today's call. The release is available at biopathholdings.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, 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.

Thank you, Will. Good morning, everyone, and thank you for joining us. 2022 was a year in which we made great progress executing on our mission to bringing new medicines to the battle against cancer. With a disease as evasive and resistant to treatments as cancer, we need to bring bold new approaches to fight this deadly disease. At Biopath, we are bringing true innovation to the fight against cancer with our de-enablized platform across a number of hard-to-treat cancers. We are proud of the progress we've made and inspired by the hope we can bring to patients with limited or no treatment options. In December, we were delighted to report the initiation of an important Phase 1B clinical trial in BP1001-A 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 Prexagiviracin sharing the same drug substance with enhanced nanoparticle properties. This trial is being conducted at several leading cancer centers and will initially evaluate the safety of 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 around mid-year. Next, let's turn to the progress we have made with our lead product candidate, Prexigyboricin. We continue to make significant progress advancing stage two of our phase two clinical trials of Prexigyboricin for the treatment of acute myeloid leukemia, or AML, in combination with frontline therapy, Decidivine and Venetoclax. The amended stage two of this phase two trial in AML is an open-label, two-stage, multi-center study of Prexagiviricin in combination with Decidivine and Venetoclax in two cohorts of patients with previously untreated AML and relapsed resistant AML. A third cohort includes treating relapsed resistant AML patients who are venetoclax-resistant or intolerant with the two-drug combination of Prexagiviricin and Decidivin. The primary endpoint for 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 hematology recovery. An interim analysis will be performed on each cohort to assess the safety and efficacy of the treatments. In the coming weeks, we will assess the initial safety and efficacy of this combination therapy with the potential to qualify for expanded program status. Turning now to our BP1002 program, which targets BCL2. As you know, BCL2 is responsible for driving cell survival in up to 60% of all cancers. High expression of BCL2 has been correlated with poor prognosis for patients diagnosed with AML. Medical acts have shown activity against anti-apoptotic protein BCL2 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 the 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 treatments. A total of six available patients will be treated with BP1002 monotherapy and a standard 3 plus 3 design with a starting dose of 20 milligrams per square meter. The approved treatment cycle There's 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 cytobin and refractory relapse AML patients. We expect cohort completion completion and initial data readout from this study around mid-year. 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, metastases, and drug resistance. It's overexpression. and aberrant activation characterize many cancers, including breast, lung, ovarian, liver, and colon cancer. Activation of the STAT3 pathway in breast and ovarian cancer cells promotes tumor initiation, migration, and taxol resistance. STAT3 also promotes 5-FU resistance in colorectal cancer cells. Its role in numerous malignancies made STAT3 a potential cancer therapeutic agent. 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 taxel and 5-FU. These results are in line with previous work in which BP1003 plus gemcitabine displayed enhanced antitumor activity to 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. We look forward to filing an IND application for this very promising product candidate later this year. With that, I'll now turn the program over to Anthony Price for a brief review of our financials along with balance sheet highlights. Anthony?