Deciphera Pharmaceuticals, Inc. Presents Initial Phase 1 Single Agent Dose Escalation Data for First-in-Class ULK Inhibitor of Autophagy, DCC-3116, at the European Society for Medical Oncology (ESMO) Congress 2022

On September 10, 2022 Deciphera Pharmaceuticals, Inc. (NASDAQ: DCPH), a biopharmaceutical company focused on discovering, developing, and commercializing important new medicines to improve the lives of people with cancer, reported positive initial data from the single agent dose escalation portion of the Phase 1 study of DCC-3116, the Company’s first-in-class, potent, and selective small molecule switch-control kinase inhibitor of ULK1/2, in patients with advanced or metastatic tumors with a mutant RAS or RAF gene (Press release, Deciphera Pharmaceuticals, SEP 10, 2022, View Source [SID1234619350]). Results from the study were presented in an oral presentation as a Proffered Paper titled "Initial monotherapy results of a phase 1 first‑in‑human study of ULK1/2 inhibitor DCC‑3116 alone and in combination with MAPK pathway inhibition" at the ESMO (Free ESMO Whitepaper) Congress 2022.

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"We are excited to report first-in-human DCC-3116 clinical data demonstrating a favorable tolerability profile and pharmacokinetics, and strong target inhibition across all dose levels tested," said Matthew L. Sherman, M.D., Chief Medical Officer of Deciphera. "As the first ULK1/2 inhibitor to enter clinical development, these positive initial results represent a significant milestone as we prepare to initiate combination dose escalation later this year. With a novel mechanism of action and strong preclinical data demonstrating compelling anti-tumor activity in combination with a broad array of RTK, RAS, and other MAP kinase pathway inhibitors, we believe DCC-3116 has the potential to open a new frontier in the treatment of cancer."

Anthony Tolcher, M.D., FRCPC, Co-Founder and Director of Clinical Research, NEXT Oncology said, "The initial DCC-3116 monotherapy results reported today are very encouraging and strongly support the advancement of DCC-3116 into the combination setting. The preliminary data show DCC-3116 to be a very well-tolerated agent that has demonstrated strong target inhibition of ULK 1/2 from even the lowest tested dose. I look forward to the selection of the combination starting dose and advancing the program into the first combination studies with MEK and KRASG12C inhibitors."

Summary of Data and Findings

As of June 9, 2022, 18 patients with locally advanced or metastatic cancer with a RAF or RAS mutation were enrolled across four cohorts dosed with DCC-3116 twice daily (BID): 50 mg BID (n=3); 100 mg BID (n=4); 200 mg BID (n=7); and 300 mg BID (n=4). The median number of prior anti-cancer regimens was three (range 1-10). The most common cancer types were colorectal (56%) and pancreatic (28%) and patients had KRAS (83%) and BRAF (17%) mutations.

The results of the primary objectives of safety and tolerability as well as the additional objectives of pharmacokinetics, pharmacodynamics, and anti-tumor activity are summarized below:

Safety and Tolerability:

Treatment with DCC-3116 was well tolerated and most treatment-emergent adverse events (TEAEs) were Grade 1/2; the most common (≥15%) TEAEs regardless of relatedness reported (all grades) were: fatigue (39%), dehydration (22%), alanine transaminase (ALT) increases (17%), anemia (17%), aspartate transaminase (AST) increases (17%), decreased appetite (17%), hyponatremia (17%), nausea (17%), and vomiting (17%).
No dose-limiting toxicities or treatment-related serious adverse events were observed with DCC-3116; two asymptomatic, reversible Grade 3 alanine transaminase increases that led to dose interruption and reduction were reported as treatment-related.
Pharmacokinetics, Pharmacodynamics and Anti-Tumor Activity:

DCC-3116 exposure appeared to increase dose-proportionally across the four dose levels tested from 50 mg BID to 300 mg BID; at all doses levels, the area under the curve (AUC) of DCC-3116 was at or above the AUC of the lowest tested dose that was effective in preclinical studies.
DCC-3116 demonstrated target inhibition with significant decreases in phosphorylation of ATG14, a direct ULK1/2 substrate, in peripheral blood mononuclear cells; at all dose levels, reductions in phosphorylated ATG14 were observed that were associated with anti-tumor activity in preclinical studies combining DCC-3116 and a MEK inhibitor as measured by reductions in phosphorylated ATG13 in tumors.
Fourteen patients were evaluable for response per Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 as of the cutoff date; best overall response was stable disease and the disease control rate at week 16 was 29%.
Dose cohorts 100 to 300 mg BID are being expanded to further characterize the safety, pharmacokinetics, and pharmacodynamics of DCC-3116. In the fourth quarter of 2022, we expect to select the starting dose of DCC-3116 for, and initiate, dose escalation cohorts in combination with MEK and KRASG12C inhibitors.

Conference Call and Webcast
Deciphera will host a conference call and webcast to discuss data presentations from the Company’s DCC-3116 and vimseltinib clinical programs at the ESMO (Free ESMO Whitepaper) Congress 2022 on Sunday, September 11, 2022, at 7:30 AM ET/ 1:30 PM CEST. The event may be accessed by registering at View Source A webcast of the event will be available in the "Events and Presentations" page in the "Investors" section of the Company’s website at View Source The archived webcast will be available on the Company’s website within 24 hours after the event and will be available for 30 days following the event.

About DCC-3116
DCC-3116 is an investigational, orally administered, potent, and highly selective switch-control inhibitor designed to inhibit cancer autophagy, a key tumor survival mechanism in cancer cells, by inhibiting the ULK1/2 kinases, which have been shown to be the enzymes responsible for initiating autophagy. DCC-3116 is currently being studied in a Phase 1/2, multicenter, open-label, first-in-human study as a single agent and in combination with RAS/MAPK pathway inhibitors in patients with advanced or metastatic solid tumors with a RAS/MAPK pathway mutation (NCT04892017).