Binimetinib

KIRKLAND, QC , May 26, 2026 /CNW/ - Pfizer Canada announces that BRAFTOVI® (encorafenib) will be funded under Ontario's Funding Accelerated for Specific Treatments (FAST) program. Following positive reimbursement recommendation from the Canadian Drug Agency (CDA‑AMC), Ontario is the first province to fund Braftovi® for the treatment of patients with metastatic colorectal cancer (mCRC) with a BRAF V600E mutation, as detected by a validated test. This announcement is a significant step forward in accelerating access to innovative cancer therapies in Canada. "At Pfizer, we are driven to address priority areas of unmet need for patients," said Cynthia Di Lullo, Oncology Lead, Pfizer Canada. "However, innovation is most impactful when it reaches patients as quickly as possible. The development of BRAFTOVI® is a testament to our commitment in advancing cancer care, and its inclusion in the FAST program is a validation of what's possible when industry, government, and other healthcare stakeholders collaborate to put patients first." Ontario has set an important example with the FAST program, in recognizing the urgency to create a faster and more direct path from regulatory approval to public coverage and improving timely access for cancer patients. "For every Ontarian facing a cancer diagnosis, timely access to high-quality treatment can make all the difference. Through the FAST program, our government is accelerating access to life-saving therapies, including BRAFTOVI®, bringing hope, peace of mind, and transformative care to those who need it most," said Hon. Sylvia Jones, Ontario Deputy Premier and Minister of Health. The announcement also highlights the importance of continued collaboration across leaders in Canada's oncology communities, from governments to healthcare partners to industry to patient advocacy organizations. Ontario's FAST program demonstrates what is possible when shared commitment to patient care turns into action. "Colorectal cancer remains one of the leading causes of cancer-related deaths in Canada. 1 As a colorectal cancer survivor myself, I know the diagnosis can be devastating, and for patients with a BRAF V600E mutation, the prognosis can be particularly challenging," adds Barry Stein, President, Colorectal Cancer Canada. "Accelerated access for cancer therapies in Ontario represents a victory for precision medicine and for the Ontarians who stand to benefit. I look forward to seeing all our other provinces and territories initiate similar programs to accelerate patient access to new cancer therapies with a view to improving patient outcomes" Colorectal cancer is a significant health issue in Canada. In 2025 alone, it was estimated that 26,400 people would be diagnosed and 9,100 would die from the disease, representing 10 per cent of all cancer cases and deaths. 2 "The average wait time for oncology drugs in Canada is approximately 18.9 months, which is simply too long for those navigating a difficult diagnosis," said An Van Gerven, President of Pfizer Canada. "We commend the Government of Ontario and Minister Jones for their strong leadership and commitment to accelerating access to innovative cancer treatments through initiatives like the FAST program. Pfizer is proud to support these efforts and remains committed to working collaboratively to help ensure equitable access for patients in Ontario and across Canada." "For patients diagnosed with metastatic colorectal cancer, every single day counts. The waiting period to receive new treatments can be one of the most stressful parts of the cancer journey," shares Filomena Servidio-Italiano, President and CEO, Colorectal Cancer Resource & Action Network (CCRAN). "This announcement is a step forward for cancer care in Ontario, and perhaps most importantly it delivers tangible progress for patients and their loved ones by easing the burden of unnecessary wait times." Timely access benefits everyone. Faster access to treatment means healthier patients, reduced strain on hospitals and health systems, and can result in stronger health outcomes across the country. Governments nationwide can look to the Government of Ontario as a leading example of how bold, patient-focused reform delivers meaningful improvements in access to care. About BRAFTOVI® BRAFTOVI® (encorafenib) is indicated, in combination with binimetinib, for the treatment of patients with unresectable or metastatic melanoma with a BRAF V600 mutation, as detected by a validated test. Clinical data supporting the use of BRAFTOVI ® in the treatment of patients with BRAF V600 mutations are limited to patients with V600E or V600K mutations. BRAFTOVI ® (encorafenib) is indicated, in combination with cetuximab, for the treatment of patients with metastatic colorectal cancer (mCRC) with a BRAF V600E mutation, as detected by a validated test, after prior therapy. BRAFTOVI ® (encorafenib) is indicated, in combination with cetuximab and mFOLFOX6, for the treatment of patients with metastatic colorectal cancer (mCRC) with a BRAF V600E mutation, as detected by a validated test. BRAFTOVI ® (encorafenib) has been issued market authorization with conditions for this indication, pending the results of trials to verify its clinical benefit. Patients should be advised of the nature of the authorization. About Pfizer Canada Pfizer Canada ULC is the Canadian operation of Pfizer Inc., one of the world's leading biopharmaceutical companies. At Pfizer, we apply science and our global resources to bring therapies to people that help extend and improve their lives. We strive to set the standard for quality, safety, and value in the discovery, development, and manufacture of health care products. Every day, Pfizer colleagues work to advance wellness, prevention, treatments, and cures that challenge the most feared diseases of our time. To learn more about Pfizer Canada, visit pfizer.ca or follow us on LinkedIn , Facebook , Instagram or YouTube . _________________________ 1 2 SOURCE Pfizer Canada Inc.

Relay Therapeutics (Nasdaq: RLAY), based in Cambridge, Massachusetts, has opened a first-in-human study of RLY-8161, a small molecule the company describes as a potential first NRAS-selective inhibitor, in patients with advanced NRAS-mutant melanoma and other solid tumors — entering a target space where no approved direct inhibitor currently exists. The Phase I trial (NCT07584226) enrolled its first participants in March 2026 across four US sites, including Massachusetts General Hospital and Memorial Sloan Kettering Cancer Center. The study is structured in two sequential parts: dose escalation in any NRAS-mutant solid tumor, followed by expansion at the recommended Phase II dose in a population enriched for NRAS-mutant disease. Enrollment is planned for approximately 35 participants. The primary completion date is set for December 2027, according to the trial record. Eligibility is restricted to adults with unresectable Stage III or IV melanoma or other solid tumors bearing a documented primary oncogenic NRAS mutation, an ECOG performance status of 0 or 1, and measurable disease by RECIST v1.1. Notably, the protocol excludes patients with known activating KRAS, HRAS, or BRAF mutations and anyone who has received prior therapy targeting the RAS-MAPK pathway — including MEK, ERK, RAF, or RAS inhibitors. That exclusion criterion defines the intended treatment population as RAS-MAPK pathway-naïve, which has implications both for the scientific interpretation of early efficacy signals and for the eventual commercial positioning of the asset. The science behind NRAS selectivity NRAS mutations drive oncogenesis primarily through constitutive activation of the MAPK and PI3K signaling cascades. In melanoma, NRAS mutations — most commonly at codon 61 (Q61R, Q61K, Q61L, Q61H) — are present in approximately 15%–20% of cases and have historically been associated with aggressive disease and limited targeted therapy options. BRAF-mutant melanoma has been addressed by a well-established class of BRAF and MEK inhibitors, but NRAS-mutant melanoma has remained without a direct targeted agent. Attempts to inhibit the pathway downstream through MEK inhibition alone have produced limited and transient responses in clinical trials. RLY-8161 is designed to inhibit NRAS selectively, sparing KRAS and HRAS. Relay Therapeutics has stated publicly that this isoform selectivity is intended to address a core liability of pan-RAS inhibitors: on-target toxicity arising from inhibition of wild-type KRAS, which plays essential roles in normal tissue homeostasis. The precise binding mechanism of RLY-8161 — including whether it engages the GDP-bound or GTP-bound state of NRAS, and whether it acts covalently or non-covalently — has not been disclosed in public sources to date. NRAS Q61 mutations impair intrinsic GTPase activity, leaving the protein constitutively loaded with GTP and active; how RLY-8161 engages this state remains a key mechanistic question that early pharmacodynamic data from the trial may begin to address. The trial includes serial measurement of NRAS mutant allele fraction in circulating tumor DNA as a secondary endpoint, providing a pharmacodynamic readout of target engagement over time. This design element reflects an intent to correlate drug exposure with on-target biological effect before efficacy conclusions are drawn. Competitive context for the RLY-8161 program The most directly relevant competitive program is daraxonrasib (RMC-6236), developed by Revolution Medicines (Nasdaq: RVMD), which is a RAS(ON) multi-selective inhibitor currently in Phase I/II development across multiple RAS-mutant tumor types, including NRAS-mutant disease. Daraxonrasib targets the active, GTP-bound state of RAS across multiple isoforms and has generated highly promising early clinical data in KRAS-mutant cancers; its NRAS cohort data remain limited in public disclosures. The mechanistic distinction Relay is drawing is explicit: RLY-8161 is designed to inhibit only NRAS, while daraxonrasib engages KRAS, NRAS, and HRAS in their active states. Whether isoform selectivity translates into a differentiated clinical or tolerability profile is a question the RLY-8161 Phase 1 data will be positioned to begin answering. MEK inhibitors such as binimetinib, developed by Pfizer (NYSE: PFE) and previously studied in NRAS-mutant melanoma, have demonstrated modest single-agent activity in this population but have not produced durable responses sufficient to establish a standard of care. Their clinical history in NRAS-mutant melanoma provides a reference point against which any direct NRAS inhibitor will be measured, though the mechanistic differences between upstream NRAS inhibition and downstream MEK inhibition make direct comparisons difficult to interpret without head-to-head data. This article was generated with AI assistance and reviewed and edited by the AllSci editorial team Explore more at AllSci News: https://allsci.com/news/ Your email address will not be published. Required fields are marked * Comment * Name * Email * Website Copyright © 2026. AllSci Corp. All rights reserved.