Deciphera Pharmaceuticals, Inc.

Good afternoon, everyone, and welcome to Decipher Pharmaceutical's fourth quarter full year 2021 financial results conference call. Today's call is being recorded. At this time, I would like to turn the call over to Megan Myers, Senior Vice President at Argo Partners. Megan?

Thank you, Operator. Welcome, and thank you for joining us today to discuss Deciphera's fourth quarter and full year 2021 financial results. I'm Megan Myers with Argo Partners. With me this afternoon to discuss the financial results and provide a general corporate update are Steve Herter, President and Chief Executive Officer, Dan Martin, Chief Commercial Officer, and Tucker Kelly, Chief Financial Officer. Before we begin, I would like to remind you that any statements we make on this call that are not historical facts are forward-looking statements reflecting the current beliefs and expectations of management made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Examples of forward-looking statements made during this conference call include our expectations for our preclinical and clinical programs, our commercialization of Kinloch, and 2022 guidance. Forward-looking statements made on this call involve substantial risks and uncertainties that could cause actual results to differ materially from those expressed or implied by the forward-looking statements, and we cannot assure you that our expectations will be achieved. Such risks and uncertainties include those set forth in our most recent annual report on Form 10-K, as well as our other SEC filings. We assume no obligation to update or revise any forward-looking statements. Following this call, a replay will be available on the company's website, www.deciphera.com. With that, I will now turn the call over to Steve Herter, President and Chief Executive Officer of Deciphera. Steve?

Thank you, Megan, and good afternoon, everyone. Thank you for joining us today as we provide an update from the fourth quarter, review our financial results, and look to the year ahead. We begin 2022 with a successful commercial franchise, a portfolio of first-in-class and best-in-class product candidates, and a productive research engine that continues to fuel our future growth. Earlier this year, we outlined our key strategic priorities for the year, which include maximizing the value of Kenlock and GIS in the U.S., and successfully launching this important medicine and fourth-line gist in key European markets. Rapidly enrolling the phase three registration-enabling study of Vimseltinib in tenosynovial giant cell tumor, or TGCT, and presenting an update from the ongoing phase one-two study of Vimseltinib in this disease. For DCC3116, our first-in-class oak inhibitor, presenting initial monotherapy data from the phase one study and initiating the Tremetinib combination part of the study. And finally, declaring a development candidate from our ongoing pan-RAF inhibitor research program. We're excited about our milestones for 2022 as we continue to advance our mission and build long-term shareholder value. Let me begin today with an update on our pipeline. We have begun enrollment in the Phase III Registration Enabling Motion Study for Vimseltinib, a potential best-in-class CSF1 receptor inhibitor for the treatment of TGCT. Patients with TGCT experience a significant disease burden and often present with multiple symptoms, including significant pain, stiffness, and limitations in joint function. Benseltinib has demonstrated clear clinical proof of concept in an ongoing Phase I-II study in TGCT patients. At the European Society of Medical Oncology meeting last year, we presented data from the dose escalation cohorts from the phase one portion of the study, and initial results from the phase two expansion cohort, showing that treatment with Vimseltinib resulted in a 47% objective response rate, including a complete response in one patient. We believe these data reflect how potent and selective Vimseltinib is for the CSF1 receptor, and the potential for this product candidate to offer meaningful benefit to patients with TGCT. Patients in the more mature dose escalation portion of the study had impressive durability on treatment. And as of the data cutoff, the average time on therapy was 10.7 months. And 72% of patients remained active on treatment. Importantly, the initial safety and tolerability profile for Vimseltinib was promising. with the majority of treatment emergent adverse events being Grade 1 or 2. We look forward to building on and expanding these results with updated safety and efficacy data from the ongoing Phase 1-2 study later this year. Based on these compelling data, we designed the Phase 3 Registration Enabling Motion Study of Vimseltinib in TGCT and announced in January that enrollment was underway. The study is expected to enroll 120 patients at over 40 sites globally. Patients will be randomized two-to-one, Vimseltinib compared to placebo, with a primary endpoint of response rate at 25 weeks. We are leaders in exploring the role of autophagy as a broad resistance mechanism in cancer, and DCC3116, our first-in-class ALK inhibitor, has the potential to benefit a significant number of cancer patients by targeting ALK, the initiating factor in the autophagy pathway. There is a growing body of research demonstrating the key role autophagy plays in tumor growth, and we have built an industry-leading position in targeting this pathway. Autophagy is the catabolic process in which cells recycle their components as a source of energy, and cancer cells activate this pathway as an escape mechanism due to anticancer therapy. Receptor tyrosine kinase, or RTK, RAS, and MAP kinase pathway-driven cancers are known to have high basal levels of autophagy, which these cancers use to maintain nutrient supply and to regulate cancer cell metabolism and survival. Autophagy has been observed to be upregulated in mutant cancers and is also known to mediate resistance to inhibitors of RTK, RAS, and map kinase signaling pathways. The ALK kinase is the initiating factor in the pathway, and by inhibiting ALK with a potent and selective inhibitor, such as 3116, we have the potential to target this important mechanism of resistance. We have now generated preclinical data, both independently and with academic collaborators, showing the ability of DCC3116 to address autophagy induced by a variety of RTK, RAS and MAP kinase pathway inhibitors, such as EGFR inhibitors, KRAS G12C inhibitors, and MEK inhibitors. With the broad potential role of autophagy as a resistance pathway, there is a significant opportunity to benefit patients across a broad spectrum of solid tumors. Given the frequency of RAS, RAF, and RTK mutations in approximately 70% of human cancers, we believe the opportunity for DCC3116 as a first-in-class ALK inhibitor is significant. We're making good progress in the phase one study of DCC3116, and our near-term focus is to reach the recommended monotherapy phase two dose and then move into the first set of dose escalation combination cohorts with a MEK inhibitor in the second half of this year. We expect to present initial data from the monotherapy dose escalation portion of the study later in 2022. Based on the exciting new preclinical data we have generated, we are also planning to evaluate the combination of DCC3116 with the KRAS G12C inhibitor in non-small cell lung cancer, subject to regulatory feedback. Moving to our preclinical pipeline, we recently announced our plans to declare a development candidate from our PAN-RAF research program later this year. We are focused on our goal of developing a best-in-class dual inhibitor of BRAF and CRAF kinases which would address class 1, 2, and 3 BRAF mutations as well as BRAF fusions. By leveraging our switch control kinase inhibitor platform, we believe we can develop an inhibitor with superior pharmaceutical properties and a long residency time, adding another clinical development program to our portfolio of potentially best-in-class and first-in-class product candidates. Before I turn the call over to Dan, I'd like to share a brief update on recent developments with Kinloch. Last month, we presented more detailed results from the Intrigue Phase III clinical study of Kinloch in second-line GIST at the American Society of Clinical Oncology plenary series session. Although the study did not meet the primary endpoint of superiority compared to Sinitinib in second-line GIST patients, the results showed that the efficacy with Kinloch was comparable to Sinitinib. Kinloch was generally well-tolerated. and fewer patients in the Kinloch arm experienced grade 3-4 treatment emergent adverse events compared to sunitinib. Patient-reported outcome measures also showed a more favorable tolerability profile for patients treated with Kinloch compared to patients who received sunitinib. We intend to publish the full results of the INTRIG study in a peer-reviewed journal in the coming months. Finally, a few weeks ago, the National Comprehensive Cancer Network, or NCCN, published updated GIST clinical practice guidelines and added a recommendation for the use of Kinloch 150 milligrams twice daily dosing, or BID, upon disease progression on Kinloch 150 milligrams once daily dosing, or QD. An exploratory analysis of the Invictus phase three study of Kinloch in fourth line and fourth line plus GIST published in The Oncologist in November of last year showed that patients who received Kenlock dose escalation to 150 milligrams BID from 150 milligrams QD after disease progression experienced substantial additional clinical benefit as measured by further progression-free survival. I'll now turn the call over to Dan Martin, our Chief Commercial Officer, to provide an update on our commercial efforts. Dan?