On January 11, 2026 Exelixis, Inc. (Nasdaq: EXEL) reported its preliminary unaudited financial results for the fiscal year 2025, provided financial guidance for fiscal year 2026 and delivered an update on its business. Exelixis anticipates 2026 will be a significant year of clinical, regulatory and commercial progress as the company grows its current cabozantinib business, works toward building a potential second commercial franchise with zanzalintinib and moves its earlier stage pipeline forward. As outlined at its December 2025 R&D Day, the company seeks to leverage its diverse pipeline and key clinical collaborations to build next-generation oncology franchises that can improve standards of care for patients with cancer.

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Preliminary Fiscal Year 2025 Financial Results & 2026 Financial Guidance

Exelixis is providing the following preliminary unaudited 2025 financial results and financial guidance for 2026. Net product and total revenues guidance do not currently reflect any revenues resulting from a potential U.S. regulatory approval and commercial launch of zanzalintinib for the treatment of patients with previously treated metastatic colorectal cancer (CRC). The U.S. Food and Drug Administration (FDA) is currently reviewing Exelixis’ New Drug Application (NDA) for this proposed indication, when used in combination with atezolizumab (Tecentriq).

Fiscal Year 2025

Fiscal Year 2026 Guidance

Total revenues

~ $2.320 billion

$2.525 billion – $2.625 billion

Net product revenues

~ $2.123 billion

$2.325 billion – $2.425 billion(1)

Cost of goods sold, % of net product revenues

~ 3.7%

3.5% – 4.5%

Research and development expenses

~ $825 million(2)

$875 million – $925 million(3)

Selling, general and administrative expenses

~ $520 million(4)

$575 million – $625 million(5)

Effective tax rate

n/a(6)

21% – 23%

Ending cash and marketable securities(7)

~ $1.65 billion

n/p

(1)

Exelixis’ 2026 net product revenues guidance range includes the impact of a U.S. wholesale acquisition cost increase of 3.0% for both CABOMETYX and COMETRIQ effective on January 1, 2026.

(2)

Includes $40.8 million of non-cash stock-based compensation expense.

(3)

Includes $50.0 million of non-cash stock-based compensation expense.

(4)

Includes $72.2 million of non-cash stock-based compensation expense.

(5)

Includes $75.0 million of non-cash stock-based compensation expense.

(6)

Preliminary results not yet available.

(7)

Cash and marketable securities are composed of cash, cash equivalents and marketable securities. Fiscal year 2026 guidance not provided (n/p).

The preliminary 2025 financial information presented in this press release has not been audited and is subject to change. The complete Exelixis Fourth Quarter and Fiscal Year 2025 Financial Results are planned for release after market on Tuesday, February 10, 2026.

"Exelixis enters 2026 with a strong and growing commercial business, the opportunity to bring a potential second oncology franchise to market and an exciting pipeline of novel small molecules and biotherapeutics," said Michael M. Morrissey, Ph.D., President & CEO, Exelixis. "Our momentum accelerated throughout 2025, driven by the continued strong commercial performance of CABOMETYX in renal cell carcinoma and advanced neuroendocrine tumors. We also achieved major milestones with the first positive pivotal data readout and subsequent U.S. regulatory filing for zanzalintinib, our next potential franchise molecule, and drove meaningful pipeline progress."

Dr. Morrissey continued: "To achieve our goal of becoming a top-5 solid tumor oncology company, Exelixis is pursuing a multi-franchise approach that fosters innovation, manages risk and maximizes the value of our portfolio for all our stakeholders. Building on the cabozantinib experience, we aim to establish lasting franchises in renal cell carcinoma, neuroendocrine tumors and colorectal cancer where our products can be successful as monotherapies or in combination, including with other Exelixis pipeline assets. Through careful prioritization and disciplined investments in high-value opportunities, we are confident we can drive sustained near- to mid-term growth while returning capital to shareholders and improving the standards of care for patients with cancer."

Anticipated Cabozantinib Milestones

Growth and Acceleration of Cabozantinib Commercial Franchise. Exelixis expects cabozantinib franchise growth to continue in 2026, building on the product’s position as the leading tyrosine kinase inhibitor (TKI) and oral therapy in renal cell carcinoma (RCC) and neuroendocrine tumors (NET). As of the third quarter 2025, in RCC, CABOMETYX (cabozantinib) was the market leader as the number one TKI monotherapy and the most prescribed TKI in combination with immunotherapy (IO). The accelerating uptake in NET builds on the March 2025 U.S. regulatory approval of CABOMETYX for two new NET indications, advanced pancreatic and extra-pancreatic NET (pNET and epNET), based on results from the CABINET study. As of the third quarter 2025, CABOMETYX was the leading oral therapy in the second-or-later line (2L+) NET market, with broad uptake across 2L+ patient types and practice settings. Based on this success and with additional gastrointestinal (GI) cancer opportunities ahead, Exelixis is expediting the full buildout of its GI sales team to accelerate growth in NET and prepare for potential future indications for zanzalintinib in GI cancers.

Anticipated Zanzalintinib Milestones

Ongoing U.S. Regulatory Review in CRC. Exelixis is preparing for the potential first commercial launch of zanzalintinib for the treatment of patients with previously treated CRC, when used in combination with atezolizumab. The regulatory filing was based on positive results from the phase 3 STELLAR-303 pivotal trial, which met one of its dual primary endpoints, with the combination of zanzalintinib and atezolizumab demonstrating a statistically significant reduction in the risk of death versus regorafenib in the intention-to-treat population at the final analysis. An overall survival (OS) benefit with the combination was consistently observed across pre-specified subgroups, including geographic region, RAS status, liver involvement and prior anti-VEGF therapy.

STELLAR-303 CRC Study Final Analysis of Second Dual Primary Endpoint of OS in Patients without Liver Metastases Expected Mid-2026. In 2025, a prespecified interim analysis of STELLAR-303’s other dual primary endpoint, OS in patients without liver metastases (non-liver metastases or NLM), showed a trend favoring the combination; however, these data were immature at the data cutoff. The trial is proceeding to the planned final analysis for this endpoint, which is expected in mid-2026, based on current event rates.

Topline Results for STELLAR-304 Anticipated Mid-2026. STELLAR-304 is a phase 3 pivotal trial evaluating zanzalintinib in combination with nivolumab versus sunitinib in previously untreated patients with advanced non-clear cell RCC. The primary endpoints in the trial are progression-free survival (PFS) and objective response rate (ORR). STELLAR-304 completed enrollment in May 2025. Topline results expected in mid-2026, based on current event rates.

Enrollment Progress for STELLAR-311 Trial of Zanzalintinib in Advanced NET. Exelixis is actively enrolling patients in the phase 2/3 STELLAR-311 pivotal trial, which is evaluating zanzalintinib versus everolimus as a first oral therapy in patients with advanced NET, regardless of site of origin, who have received up to one prior line of therapy. Initiated in June 2025, STELLAR-311 is the first study to randomize a small molecule against an active control in this setting, with the potential to broadly redefine oral treatment options for these patients. The primary endpoint of the trial is PFS per Response Evaluation Criteria in Solid Tumors (RECIST) 1.1 as assessed by Blinded Independent Central Review.

Additional Ongoing and Planned Pivotal Trials for Zanzalintinib. In addition to the ongoing Exelixis-sponsored STELLAR-303, -304, and -311 trials, additional zanzalintinib pivotal trials include:

LITESPARK-033, which is evaluating the combination of zanzalintinib and WELIREG (belzutifan) versus cabozantinib in first-line advanced RCC following IO administered in the adjuvant setting. LITESPARK-033 was initiated in December 2025 and is the first Merck-sponsored pivotal trial of zanzalintinib and belzutifan in RCC under the companies’ clinical development collaboration. A second Merck-sponsored pivotal trial of zanzalintinib and belzutifan in RCC is anticipated to begin in early 2026. Details of this anticipated study are forthcoming.
STELLAR-316, which will evaluate the potential of zanzalintinib, with and without an immune checkpoint inhibitor, to keep patients disease-free in the adjuvant CRC setting. As currently proposed, the study will enroll patients with resected stage II/III CRC who have completed definitive therapy and tested positive for molecular residual disease (MRD), but do not have radiographic evidence of disease. The primary endpoint of STELLAR-316 is disease-free survival, with secondary endpoints including circulating tumor DNA clearance. Exelixis recently announced a collaboration with Natera, a global leader in cell-free DNA and precision medicine, in which Natera will provide its Signatera assay to identify MRD-positive patients for enrollment in the trial. Exelixis expects to initiate STELLAR-316 in mid-2026.
STELLAR-201, which will evaluate zanzalintinib in recurrent meningioma, the most common primary intracranial neoplasm for which there are currently no approved systemic therapies. The study is planned to enroll patients with Grade I/II/III meningioma with relapse/progression following radiation/surgery or who are not candidates for radiation/surgery. The proposed primary endpoint of the trial is ORR, with secondary endpoints including duration of response, PFS and OS. Pending favorable results, the trial represents an opportunity for zanzalintinib to become the first and only systemic therapy approved for this form of cancer. Exelixis expects to initiate STELLAR-201 in mid-2026, and a confirmatory phase 3 study is also being planned.
Anticipated R&D Milestones

Progress of Phase 1 Clinical Programs for XL309, XB010, XB628 and XB371. Exelixis is advancing ongoing phase 1 clinical trials for XL309 (USP1 inhibitor), XB010 (5T4-targeting ADC), XB628 (PD-L1 + NKG2A bispecific) and XB371 (TF-targeting ADC). If phase 1 data are supportive, Exelixis plans to progress these molecules into full development as part of its strategy to build next-generation oncology franchises across tumor types and novel combination regimens, including with zanzalintinib and other therapeutic modalities. Combination opportunities of particular development interest highlighted at the December 2025 R&D Day include zanzalintinib plus XB628 in both advanced RCC and CRC.

Two Potential IND Applications in 2026. Exelixis anticipates advancing two programs into clinical development this year:

XL557 is an orally bioavailable small molecule Somatostatin Receptor 2 agonist. Somatostatin analogs are widely used in the first- and second-line NET treatment settings, but currently available therapies are administered via injection and pose associated challenges. Exelixis believes XL557 has the potential to become a best-in-class molecule that could serve NET patients across all lines of treatment as a monotherapy and potentially in combination with zanzalintinib.
XB773 is an antibody-drug conjugate (ADC) consisting of an exatecan payload conjugated to a monoclonal antibody targeting DLL3, a transmembrane protein that is expressed in neuroendocrine carcinomas such as small cell lung cancer and neuroendocrine prostate cancer. Exelixis believes XB773 could be a best-in-class molecule with better payload delivery compared to competitor ADCs and potential for improved therapeutic benefit, as well as strong combination potential that would facilitate its use in earlier lines and settings.
Corporate Updates

Stock Repurchase Program (SRP) Update. Since Exelixis’ Board of Directors authorized the first SRP in March 2023, Exelixis has repurchased a total of $2.16 billion of the company’s common stock, retiring 76.7 million shares, at an average price of $28.14 per share, as of the end of fiscal year 2025. In October 2025, Exelixis’ Board of Directors authorized the repurchase of up to an additional $750 million of the company’s common stock before December 31, 2026. Exelixis has begun executing stock repurchases under the October 2025 SRP, which is the fifth such program to be undertaken by the company since March 2023. Stock repurchases under this program may be made from time to time through a variety of methods, which may include open market purchases, in block trades, Rule 10b5-1 trading plans, accelerated share repurchase transactions, exchange transactions or any combination of such methods. The timing and amount of any stock repurchases under the SRP will be based on a variety of factors, including ongoing assessments of the capital needs of the business, alternative investment opportunities, the market price of our common stock and general market conditions. The program does not obligate Exelixis to acquire any amount of its common stock, and the SRP may be modified, suspended or discontinued at any time without prior notice.

Presentation and Webcast

Exelixis President and Chief Executive Officer Michael M. Morrissey, Ph.D., will provide a corporate overview and discuss the company’s preliminary fiscal year 2025 financial results, 2026 financial guidance and key priorities and milestones for 2026 during the company’s presentation at the J.P. Morgan 2026 Healthcare Conference beginning at 5:15 p.m. PT / 8:15 p.m. ET on Monday, January 12, 2026.

To access the webcast link, log onto www.exelixis.com and proceed to the Event Calendar page under the Investors & News heading. A replay will also be available at the same location for at least 30 days.

(Press release, Exelixis, JAN 11, 2026, View Source [SID1234661921])

On January 11, 2026 Kura Oncology, Inc. (Nasdaq: KURA), a biopharmaceutical company committed to realizing the promise of precision medicines for the treatment of cancer, reported recent accomplishments, preliminary KOMZIFTI (ziftomenib) net product revenue and outlined anticipated 2026 milestones.

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"Following the landmark FDA approval of KOMZIFTI on November 13, 2025, we are executing a robust commercial launch to drive rapid adoption and market share growth," said Troy Wilson, Ph.D., J.D., President and CEO of Kura Oncology. "With KOMZIFTI’s compelling efficacy, favorable safety profile and ease of use, we believe that we are strongly positioned for success and encouraged by the first few weeks of our commercial launch. Our comprehensive development strategy advances ziftomenib into combinations and earlier lines of therapy, including newly diagnosed patients with NPM1 mutations, KMT2A rearrangements, and FLT3 mutations, supported by our expanding pipeline programs and solid cash position. We are excited to deliver meaningful impact for patients throughout 2026 and beyond."

Preliminary Fourth Quarter Financial Highlights

$2.1 million of KOMZIFTI net product revenue in the five-week period of initial commercial availability ended December 31, 2025.
Milestone payments of $195 million under collaboration agreement with Kyowa Kirin in the fourth quarter of 2025.
Collaboration revenue (non-cash item) for the fourth quarter of 2025 estimated between $15 to $17 million.
$667.3 million in cash, cash equivalents, and short-term investments as of December 31, 2025.
Recent Program Highlights

In November 2025, KOMZIFTI was granted full approval by the U.S. Food and Drug Administration (FDA) for adult patients with relapsed or refractory (R/R) acute myeloid leukemia (AML) with a susceptible NPM1 mutation who have no satisfactory alternative treatment options. KOMZIFTI is the first and only once-daily, oral menin inhibitor approved for R/R NPM1-mutated (NPM1-m) AML, a devastating blood cancer with limited treatment options.
In November 2025, KOMZIFTI was added to the National Comprehensive Cancer Network (NCCN) Clinical Practice Guidelines in Oncology (NCCN Guidelines) as a Category 2A recommended treatment option for adults with R/R NPM1-m AML.
In December 2025, two oral presentations at the 67th Annual Meeting of the American Society of Hematology (ASH) (Free ASH Whitepaper) (ASH 2025) reported a favorable safety profile and encouraging antileukemic activity for ziftomenib in combination with venetoclax and azacitidine (ven/aza) in patients with AML harboring NPM1 mutations or KMT2A rearrangements (KMT2A-r). These data came from the ongoing Phase 1a/1b KOMET-007 trial (NCT05735184), which includes patients with newly diagnosed NPM1-m AML as well as patients with R/R NPM1-m or KMT2A-r AML.
In September 2025, the first patient was dosed in the Phase 3 KOMET-017 (NCT07007312) trial evaluating ziftomenib in combination with both intensive and non-intensive chemotherapy regimens in patients with newly diagnosed NPM1-m or KMT2A-r AML.
In October 2025, compelling preliminary data from Kura’s first- and next-generation farnesyl transferase inhibitor (FTI) programs – tipifarnib and darlifarnib – were presented at the 2025 European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) Congress.
Expected 2026 Key Milestones

KOMZIFTI Commercial

Accelerate U.S. uptake of KOMZIFTI in R/R NPM1-m AML.
Drive quarter-over-quarter growth in net product revenue.
Ziftomenib Development

Present updated KOMET-007 data evaluating combination with 7+3 in newly diagnosed NPM1-m or KMT2A-r AML in the first half of 2026.
Publish ven/aza combination data in R/R NPM1-m AML in the first half of 2026.
Present preliminary data from KOMET-008 cohort evaluating combination with gilteritinib in R/R NPM1-m/FLT3-m AML in the second half of 2026.
Advance enrollment of KOMET-017 Phase 3 trials for newly diagnosed AML, including combinations with intensive and non-intensive chemotherapy, in 2026.
Advance enrollment of KOMET-007 cohort evaluating combination with 7+3 and quizartinib in newly diagnosed NPM1-m/FLT3-m AML (quad) in 2026.
Expand ziftomenib to non-AML indications in 2026, including ongoing Phase 1a dose escalation trial evaluating combination with imatinib in gastrointestinal stromal tumors.
Darlifarnib Development

Initiate expansion cohorts of darlifarnib and cabozantinib in advanced renal cell carcinoma (RCC) (Phase 1b) in the first half of 2026.
Present preliminary data from darlifarnib and adagrasib in KRASG12C-mutated solid tumors (non-small cell lung cancer, colorectal cancer, pancreatic ductal adenocarcinoma) in the first half of 2026.
Present updated dose-escalation data from darlifarnib and cabozantinib in advanced RCC (Phase 1a) in the second half of 2026.
Explore opportunities to evaluate additional indications and combination agents in 2026.
Pipeline

Publish preclinical menin inhibitor data on diabetes in the second half of 2026.
Advance KO-7246, next generation menin inhibitor, in IND-enabling studies for diabetes and cardiometabolic diseases in 2026.
Advance preclinical development of a next-generation menin inhibitor development candidate for use in combination therapy for solid tumors in 2026.
2026 Financial Guidance

Kura anticipates non-cash collaboration revenue recognition of $45 million to $55 million in 2026.
$667.3 million in cash, cash equivalents and short-term investments as of December 31, 2025, together with anticipated short-term collaboration payments and product revenue, expected to support ziftomenib AML program through topline results in front-line Phase 3 trial in newly-diagnosed AML.
About KOMZIFTI (ziftomenib)
KOMZIFTI (ziftomenib) is an oral menin inhibitor approved for the treatment of adult patients with relapsed or refractory acute myeloid leukemia (AML) with a susceptible NPM1 mutation who have no satisfactory alternative treatment options.

Ziftomenib is in development for the front-line treatment of AML harboring NPM1 mutations, KMT2A translocations and FLT3 mutations, with the potential to be combined with approved therapies and benefit a broad spectrum of patients earlier in their disease course.

IMPORTANT SAFETY INFORMATION FOR KOMZIFTI FROM THE U.S. PRESCRIBING INFORMATION

Boxed WARNING: DIFFERENTIATION SYNDROME

Differentiation syndrome, which can be fatal, has occurred with KOMZIFTI. Signs and symptoms may include fever, joint pain, hypotension, hypoxia, dyspnea, rapid weight gain or peripheral edema, pleural or pericardial effusions, pulmonary infiltrates, acute kidney injury, and rashes. If differentiation syndrome is suspected, interrupt KOMZIFTI, and initiate oral or intravenous corticosteroids with hemodynamic and laboratory monitoring until symptom resolution; resume KOMZIFTI upon symptom improvement.

WARNINGS AND PRECAUTIONS

Differentiation Syndrome

KOMZIFTI can cause fatal or life-threatening differentiation syndrome (DS). DS is associated with rapid proliferation and differentiation of myeloid cells. Symptoms of DS, including those seen in patients treated with KOMZIFTI, may include fever, hypoxia, joint pain, hypotension, dyspnea, rapid weight gain or peripheral edema, pleural or pericardial effusions, acute kidney injury, and rashes.

In the clinical trial, DS occurred in 29 (26%) of 112 patients with R/R AML with an NPM1 mutation who were treated with KOMZIFTI at the recommended dosage. DS was Grade 3 in 13% and fatal in two patients. In broader evaluation of all patients with any genetic form of AML treated with KOMZIFTI monotherapy in clinical trials, DS occurred in 25% of patients. Four fatal cases of DS occurred out of 39 patients with KMT2A-rearranged AML treated with KOMZIFTI. KOMZIFTI is not approved for use in patients with KMT2A-rearranged AML.

In the 112 patients with an NPM1 mutation, DS was observed with and without concomitant hyperleukocytosis, in as early as 3 days and up to 46 days after KOMZIFTI initiation. The median time to onset was 15 days. Two patients experienced more than one DS event. Treatment was interrupted and resumed in 15 (13%) patients, while it was permanently discontinued in 2 (2%) patients.

Prior to starting treatment with KOMZIFTI, reduce the WBC counts to less than 25 x 10⁹/L. If DS is suspected, interrupt KOMZIFTI, initiate oral or intravenous corticosteroids (e.g., dexamethasone 10 mg every 12 hours) for a minimum of 3 days with hemodynamic and laboratory monitoring. Resume treatment with KOMZIFTI at the same dose level when signs and symptoms improve and are Grade 2 or lower. Taper corticosteroids over a minimum of 3 days after adequate control or resolution of symptoms. Symptoms of DS may recur with premature discontinuation of corticosteroid treatment.

QTc Interval Prolongation

KOMZIFTI can cause QTc interval prolongation. In the clinical trial, QTc interval prolongation was reported as an adverse reaction in 12% of 112 patients treated with KOMZIFTI at the recommended dosage for R/R AML with an NPM1 mutation. QTc interval prolongation was Grade 3 in 8% of patients. The heart-rate corrected QT interval (using Fridericia’s method) (QTcF) was greater than 500 msec in 9% of patients, and the increase from baseline QTcF was greater than 60 msec in 12% of patients. KOMZIFTI dose reduction was required for 1% of patients due to QTc interval prolongation. QTc prolongation occurred in 14% of the 42 patients less than 65 years of age and in 10% of the 70 patients 65 years of age or older.

Correct electrolyte abnormalities, including hypokalemia and hypomagnesemia, prior to treatment with KOMZIFTI. Perform an ECG prior to initiation of treatment with KOMZIFTI, and do not initiate KOMZIFTI in patients with QTcF > 480 msec. Perform an ECG at least once weekly for the first four weeks on treatment, and at least monthly thereafter. Interrupt KOMZIFTI if the QTc interval is > 500 ms or the change from baseline is > 60 ms (Grade 3). In patients with congenital long QTc syndrome, congestive heart failure, electrolyte abnormalities, or those who are taking medications known to prolong the QTc interval, more frequent ECG monitoring may be necessary. Concomitant use of KOMZIFTI with drugs known to prolong the QTc interval may increase the risk of QTc interval prolongation, result in a greater increase in the QTc interval and adverse reactions associated with QTc interval prolongation, including Torsades de Pointes, other serious arrhythmias, and sudden death.

Embryo-Fetal Toxicity

Based on findings in animals and its mechanism of action, KOMZIFTI can cause embryo-fetal harm when administered to a pregnant woman. Advise pregnant women of the potential risk to the fetus. Advise females of reproductive potential to use effective contraception during treatment with KOMZIFTI and for 6 months after the last dose. Advise males with female partners of reproductive potential to use effective contraception during treatment with KOMZIFTI and for 3 months after the last dose.

ADVERSE REACTIONS

Fatal adverse reactions occurred in 4 (4%) patients who received KOMZIFTI, including 2 with differentiation syndrome, 1 with infection, and 1 with sudden death. Serious adverse reactions were reported in 79% of patients who received KOMZIFTI. Serious adverse reactions occurring in ≥ 5% of patients included infection without an identified pathogen (29%), febrile neutropenia (18%), bacterial infection (16%), differentiation syndrome (16%), and dyspnea (6%).

Dosage interruption of KOMZIFTI due to an adverse reaction occurred in 54% of patients. Adverse reactions that required dose interruption in ≥ 2% of patients included infection without an identified pathogen (15%), differentiation syndrome (13%), febrile neutropenia (5%), pyrexia (4%), electrocardiogram QT prolonged (4%), leukocytosis (4%), bacterial infection (3%), cardiac failure (2%), cholecystitis (2%), diarrhea (2%), pruritus (2%), and thrombosis (2%). Dose reduction of KOMZIFTI due to an adverse reaction occurred in 4% of patients. Permanent discontinuation of KOMZIFTI due to an adverse reaction occurred in 21% of patients. Adverse reactions that required permanent discontinuation of KOMZIFTI in ≥ 2% of patients were infection without an identified pathogen (8%), bacterial infection (4%), cardiac arrest (2%), and differentiation syndrome (2%).

Most common (≥ 20%) adverse reactions, including laboratory abnormalities, were aspartate aminotransferase increased (53%), infection without an identified pathogen (52%), potassium decreased (52%), albumin decreased (51%), alanine aminotransferase increased (50%), sodium decreased (49%), creatinine increased (45%), alkaline phosphatase increased (41%), hemorrhage (38%), diarrhea (36%), nausea (35%), fatigue (34%), edema (30%), bacterial infection (28%), musculoskeletal pain (28%), bilirubin increased (27%), potassium increased (26%), differentiation syndrome (26%), pruritus (23%), febrile neutropenia (22%), and transaminases increased (21%).

DRUG INTERACTIONS

Drug interactions may occur when KOMZIFTI is concomitantly used with:

Strong or Moderate CYP3A4 Inhibitors: Monitor patients more frequently for KOMZIFTI-associated adverse reactions.
Strong or Moderate CYP3A4 Inducers: Avoid concomitant use of KOMZIFTI.
Gastric Acid Reducing Agents: Avoid concomitant use of KOMZIFTI with proton pump inhibitors (PPIs), H2 receptor antagonists (H2RAs), or locally acting antacids. If concomitant use with H2RAs or locally acting antacids cannot be avoided, modify KOMZIFTI administration time.
Take KOMZIFTI 2 hours before or 10 hours after administration of an H2 receptor antagonist.
Take KOMZIFTI 2 hours before or 2 hours after administration of a locally acting antacid.
Drugs that Prolong the QTc Interval: Avoid concomitant use of KOMZIFTI. If concomitant use cannot be avoided, obtain ECGs when initiating, during concomitant use, and as clinically indicated. Interrupt KOMZIFTI if the QTc interval is > 500 ms or the change from baseline is > 60 ms.
USE IN SPECIFIC POPULATIONS

Pregnancy: Based on findings in animals and its mechanism of action, KOMZIFTI can cause embryo-fetal harm when administered to a pregnant woman. Advise pregnant women of the potential risk to a fetus. Verify pregnancy status in females of reproductive potential prior to starting KOMZIFTI.

Lactation: Because of the potential for adverse reactions in the breastfed child, advise women not to breastfeed during treatment with KOMZIFTI and for 2 weeks after the last dose.

Infertility: Based on findings in animals, KOMZIFTI may impair fertility in females and males of reproductive potential.

(Press release, Kura Oncology, JAN 11, 2026, View Source [SID1234661920])

On January 11, 2026 Zentalis Pharmaceuticals presented its corporate presentation.

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(Presentation, Zentalis Pharmaceuticals, JAN 11, 2026, https://www.sec.gov/Archives/edgar/data/1725160/000172516026000003/zntlcorporatepresentatio.htm [SID1234661919])

On January 10, 2026 Pfizer Inc. (NYSE: PFE) reported positive results from Cohort 3, a separate randomized cohort of the pivotal BREAKWATER trial, evaluating BRAFTOVI (encorafenib) in combination with cetuximab (marketed as ERBITUX) and FOLFIRI (fluorouracil, leucovorin, and irinotecan) in patients with previously untreated metastatic colorectal cancer (mCRC) with a BRAF V600E mutation. At the time of this analysis, the BRAFTOVI combination regimen with FOLFIRI and cetuximab demonstrated a clinically meaningful and statistically significant improvement in confirmed objective response rate (ORR) assessed by blinded independent central review (BICR) compared to patients receiving standard-of-care treatment FOLFIRI with or without bevacizumab (64.4% vs 39.2%, odds ratio =2.76, p=0.001). These data will be presented today in an oral presentation (Abstract 13) at the 2026 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Gastrointestinal (ASCO GI) Cancers Symposium and highlighted in the ASCO (Free ASCO Whitepaper) GI official press program.

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"These results represent a great advance for patients with BRAF V600E-mutant metastatic colorectal cancer. We’ve seen this approach significantly increase the response compared to FOLFIRI with or without bevacizumab, and these responses were rapid and durable," said Scott Kopetz, M.D., Ph.D., FACP, Professor and Deputy Chair of Gastrointestinal Medical Oncology at The University of Texas MD Anderson Cancer Center and co-principal investigator of the BREAKWATER trial. "The trial supports the potential for another chemotherapy backbone option that may be paired with encorafenib plus cetuximab in this patient population."

The estimated median duration of response as assessed by BICR was not estimable with BRAFTOVI plus cetuximab and FOLFIRI (95% Confidence Interval [CI]: not estimable [NE]-NE) or with FOLFIRI with or without bevacizumab (95% CI: 7.0 months-NE). Of patients on BRAFTOVI plus cetuximab and FOLFIRI, 57.4% had a response lasting 6 months or longer, compared to 34.5% with FOLFIRI with or without bevacizumab.

Overall survival (OS) data were analyzed descriptively (Hazard Ratio [HR]: 0.49, 95% CI: 0.24-1.03; median follow-up of approximately 10 months for both arms). The BREAKWATER trial is ongoing with an estimated completion in 2027.

"These data further strengthen the potential utility of BRAFOTVI for patients with BRAF V600E-mutant metastatic colorectal cancer. The significant improvement in response rates reflects the meaningful clinical benefit of this targeted combination therapy regimen for patients," said Jeff Legos, Chief Oncology Officer, Pfizer. "These results underscore the potential of BRAFTOVI as a standard of care for patients with this aggressive cancer and reflect our commitment to advancing precision medicine options that help tailor treatment based on patients’ needs."

The safety profile of BRAFTOVI in combination with cetuximab and FOLFIRI was consistent with the known safety profile of each respective agent. No new safety signals were identified. The most common side effects (≥15%) were nausea, diarrhea, vomiting, alopecia, anemia, neutrophil count decreased, decreased appetite, fatigue, neutropenia, skin hyperpigmentation, dry skin, asthenia, weight decreased, arthralgia, palmar-plantar erythrodysaesthesia syndrome, rash, white blood cell count decreased, and constipation. Among patients receiving BRAFTOVI in combination with cetuximab and FOLFIRI, 8.5% experienced an adverse reaction that resulted in permanent discontinuation of BRAFTOVI.

BRAFTOVI in combination with cetuximab and FOLFIRI is an investigational regimen and is not currently approved for use. BRAFTOVI in combination with cetuximab and mFOLFOX6 received accelerated approval by the U.S. Food and Drug Administration (FDA) in December 2024 for patients with BRAF V600E -mutant mCRC based on a clinically meaningful and statistically significant improvement in confirmed ORR in treatment-naïve patients, one of the study’s primary endpoints. Continued approval for this indication is contingent upon verification of clinical benefit.

Pfizer is continuing its commitment to help non-scientists understand the latest findings with the development of abstract plain language summaries (APLS) for company-sponsored research being presented, which are written in non-technical language. Those interested in learning more can visit www.Pfizer.com/apls to access the summaries.

About BREAKWATER
BREAKWATER is a Phase 3, randomized, active-controlled, open-label, multicenter trial of BRAFTOVI with cetuximab, alone or in combination with chemotherapy (mFOLFOX6 or FOLFIRI) in participants with previously untreated BRAF V600E-mutant mCRC. Patients were randomized to receive BRAFTOVI 300 mg orally once daily in combination with cetuximab (discontinued after randomization of 158 patients), BRAFTOVI 300 mg orally once daily in combination with cetuximab and mFOLFOX6 (n=236) or mFOLFOX6, FOLFOXIRI, or CAPOX, with or without bevacizumab (control arm) (n=243). The dual primary endpoints for these study groups are ORR and PFS as assessed by BICR. OS is a key secondary endpoint. In Cohort 3, patients were randomized to receive BRAFTOVI 300 mg orally once daily in combination with cetuximab and FOLFIRI (n=73) or FOLFIRI, with or without bevacizumab (control-arm) (n=74). The primary endpoint of Cohort 3 is ORR as assessed by BICR. PFS is a key secondary endpoint; OS is a secondary endpoint.

About Colorectal Cancer (CRC)
CRC is the third most common type of cancer in the world, with approximately 1.8 million new diagnoses in 2022.1 It is the second leading cause of cancer-related deaths.2 Overall, the lifetime risk of developing CRC is about 1 in 24 for men and 1 in 26 for women.2 In the U.S. alone, an estimated 154,270 people will be diagnosed with cancer of the colon or rectum in 2025, and approximately 53,000 are estimated to die from the disease each year.3 For 20% of those diagnosed with CRC, the disease has metastasized, or spread, making it harder to treat, and up to 50% of patients with localized disease eventually develop metastases.4

BRAF mutations are estimated to occur in 8-12% of people with mCRC and are associated with a poor prognosis for these patients.5 The BRAF V600E mutation is the most common BRAF mutation and the risk of mortality in CRC patients with the BRAF V600E mutation is more than double that of patients with no known mutation present.5-7 Despite the high unmet need in BRAF V600E-mutant mCRC, prior to December 20, 2024, there were no approved biomarker-driven therapies specifically indicated for people with previously untreated BRAF V600E-mutant mCRC.8,9

About BRAFTOVI (encorafenib)
BRAFTOVI is an oral small molecule kinase inhibitor that targets BRAF V600E. Inappropriate activation of proteins in the MAPK signaling pathway (RAS-RAF-MEK-ERK) has been shown to occur in certain cancers, including CRC.

Pfizer has exclusive rights to BRAFTOVI in the U.S., Canada, Latin America, Middle East, and Africa. Ono Pharmaceutical Co., Ltd. has exclusive rights to commercialize the product in Japan and South Korea, Medison has exclusive rights to commercialize the product in Israel and Pierre Fabre Laboratories has exclusive rights to commercialize the product in all other countries, including Europe and Asia (excluding Japan and South Korea).

INDICATION AND USAGE
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 an FDA-approved test. This indication is approved under accelerated approval based on response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial(s).

BRAFTOVI is also indicated, in combination with cetuximab, for the treatment of adult patients with mCRC with a BRAF V600E mutation, as detected by an FDA-approved test, after prior therapy.

Limitations of Use: BRAFTOVI is not indicated for treatment of patients with wild-type BRAF CRC.

IMPORTANT SAFETY INFORMATION

Refer to the prescribing information for cetuximab and individual product components of mFOLFOX6 for recommended dosing and additional safety information.

WARNINGS AND PRECAUTIONS

New Primary Malignancies: New primary malignancies, cutaneous and non-cutaneous, can occur. In BEACON CRC (previously treated BRAF V600E mutation-positive mCRC), cutaneous squamous cell carcinoma (cuSCC), including keratoacanthoma (KA), occurred in 1.4% of patients with CRC, and a new primary melanoma occurred in 1.4% of patients who received BRAFTOVI in combination with cetuximab. In BREAKWATER (previously untreated BRAF V600E mutation-positive mCRC) skin papilloma was reported in 2.6%, basal cell carcinoma in 1.3%, squamous cell carcinoma of skin in 0.9%, keratoacanthoma in 0.4% and malignant melanoma in situ in 0.4% of patients who received BRAFTOVI in combination with cetuximab and mFOLFOX6. Perform dermatologic evaluations prior to initiating treatment, every 2 months during treatment, and for up to 6 months following discontinuation of treatment. Manage suspicious skin lesions with excision and dermatopathologic evaluation. Dose modification is not recommended for new primary cutaneous malignancies. Based on its mechanism of action, BRAFTOVI may promote malignancies associated with activation of RAS through mutation or other mechanisms. Monitor patients receiving BRAFTOVI for signs and symptoms of non-cutaneous malignancies. Discontinue BRAFTOVI for RAS mutation-positive non-cutaneous malignancies. Monitor patients for new malignancies prior to initiation of treatment, while on treatment, and after discontinuation of treatment.

Tumor Promotion in BRAF Wild-Type Tumors: In vitro experiments have demonstrated paradoxical activation of MAP-kinase signaling and increased cell proliferation in BRAF wild-type cells exposed to BRAF inhibitors. Confirm evidence of BRAF V600E or V600K mutation using an FDA-approved test prior to initiating BRAFTOVI.

Cardiomyopathy: Cardiomyopathy manifesting as left ventricular dysfunction associated with symptomatic or asymptomatic decreases in ejection fraction, has been reported in patients. Assess left ventricular ejection fraction (LVEF) by echocardiogram or multi-gated acquisition (MUGA) scan prior to initiating treatment, 1 month after initiating treatment, and then every 2 to 3 months during treatment. Safety has not been established in patients with a baseline ejection fraction that is either below 50% or below the institutional lower limit of normal (LLN). Patients with cardiovascular risk factors should be monitored closely. Withhold, reduce dose, or permanently discontinue based on severity of adverse reaction.

Hepatotoxicity: Hepatotoxicity can occur. In BREAKWATER (previously untreated BRAF V600E mutation-positive mCRC), the incidence of Grade 3 or 4 increases in liver function laboratory tests in patients receiving BRAFTOVI in combination with cetuximab and mFOLFOX6 was 2.2% for alkaline phosphatase, 1.3% for ALT, and 0.9% for AST. Monitor liver laboratory tests before initiation of BRAFTOVI, monthly during treatment, and as clinically indicated. Withhold, reduce dose, or permanently discontinue based on severity of adverse reaction.

Hemorrhage: In BEACON CRC (previously treated BRAF V600E mutation-positive mCRC), hemorrhage occurred in 19% of patients receiving BRAFTOVI in combination with cetuximab; Grade 3 or higher hemorrhage occurred in 1.9% of patients, including fatal gastrointestinal hemorrhage in 0.5% of patients. The most frequent hemorrhagic events were epistaxis (6.9%), hematochezia (2.3%), and rectal hemorrhage (2.3%). In BREAKWATER (previously untreated BRAF V600E mutation-positive mCRC), hemorrhage occurred in 30% of patients receiving BRAFTOVI in combination with cetuximab and mFOLFOX6; Grade 3 or 4 hemorrhage occurred in 3% of patients. Withhold, reduce dose, or permanently discontinue based on severity of adverse reaction.

Uveitis: Uveitis, including iritis and iridocyclitis, has been reported in patients treated with BRAFTOVI. Assess for visual symptoms at each visit. Perform an ophthalmological evaluation at regular intervals and for new or worsening visual disturbances, and to follow new or persistent ophthalmologic findings. Withhold, reduce dose, or permanently discontinue based on severity of adverse reaction.

QT Prolongation: BRAFTOVI is associated with dose-dependent QTc interval prolongation in some patients. In BREAKWATER (previously untreated BRAF V600E mutation-positive mCRC), an increase of QTcF >500 ms was measured in 3.6% (8/222) of patients receiving BRAFTOVI in combination with cetuximab and mFOLFOX6. Monitor patients who already have or who are at significant risk of developing QTc prolongation, including patients with known long QT syndromes, clinically significant bradyarrhythmias, severe or uncontrolled heart failure and those taking other medicinal products associated with QT prolongation. Correct hypokalemia and hypomagnesemia prior to and during BRAFTOVI administration. Withhold, reduce dose, or permanently discontinue for QTc >500 ms.

Embryo-Fetal Toxicity: BRAFTOVI can cause fetal harm when administered to pregnant women. BRAFTOVI can render hormonal contraceptives ineffective. Advise females of reproductive potential to use effective nonhormonal contraception during treatment with BRAFTOVI and for 2 weeks after the final dose.

Risks Associated with Combination Treatment: BRAFTOVI is indicated for use as part of a regimen in combination with cetuximab, or in combination with cetuximab and mFOLFOX6. Refer to the prescribing information for cetuximab and individual product components of mFOLFOX6 for additional risk information.

Lactation: Advise women not to breastfeed during treatment with BRAFTOVI and for 2 weeks after the final dose.

Infertility: Advise males of reproductive potential that BRAFTOVI may impair fertility.

ADVERSE REACTIONS

BREAKWATER Trial (previously untreated BRAF V600E mutation-positive mCRC)

Serious adverse reactions occurred in 38% of patients who received BRAFTOVI in combination with cetuximab and mFOLFOX6. Serious adverse reactions in >3% of patients included intestinal obstruction (3.5%) and pyrexia (3.5%).
Fatal gastrointestinal perforation occurred in 0.9% of patients who received BRAFTOVI in combination with cetuximab and mFOLFOX6.
Most common adverse reactions(≥25%, all grades) in the BRAFTOVI with cetuximab and mFOLFOX6 arm compared to the control arm (mFOLFOX6 ± bevacizumab or FOLFOXIRI ± bevacizumab or CAPOX ± bevacizumab) were peripheral neuropathy (62% vs 53%), nausea (51% vs 48%), fatigue (49% vs 38%), rash (31% vs 4%), diarrhea (34% vs 47%), decreased appetite (33% vs 25%), vomiting (33% vs 21%), hemorrhage (30% vs 18%), abdominal pain (26% vs 27%), and pyrexia (26% vs 14%).
Most common laboratory abnormalities(≥10%, grade 3 or 4) in the BRAFTOVI with cetuximab and mFOLFOX6 arm compared to the control arm (mFOLFOX6 ± bevacizumab or FOLFOXIRI ± bevacizumab or CAPOX ± bevacizumab) were: increased lipase (51% vs 25%), decreased neutrophil count (36% vs 34%), decreased hemoglobin (13% vs 5%), decreased white blood cell count (12% vs 7%), and increased glucose (11% vs 2%).
BEACON CRC Trial (previously treated BRAF V600E mutation-positive mCRC)

Most common adverse reactions(≥25%, all grades) in the BRAFTOVI with cetuximab arm compared to irinotecan with cetuximab or FOLFIRI with cetuximab (control) were: fatigue (51% vs 50%), nausea (34% vs 41%), diarrhea (33% vs 48%), dermatitis acneiform (32% vs 43%), abdominal pain (30% vs 32%), decreased appetite (27% vs 27%), arthralgia (27% vs 3%), and rash (26% vs 26%).
Other clinically important adverse reactions occurring in <10% of patients who received BRAFTOVI in combination with cetuximab was pancreatitis.
Most common laboratory abnormalities (all grades) (≥20%) in the BRAFTOVI with cetuximab arm compared to irinotecan with cetuximab or FOLFIRI with cetuximab (control) were: anemia (34% vs 48%) and lymphopenia (24% vs 35%).
DRUG INTERACTIONS

Strong or moderate CYP3A4 inhibitors: Avoid coadministration of BRAFTOVI with strong or moderate CYP3A4 inhibitors, including grapefruit juice. If coadministration is unavoidable, reduce the BRAFTOVI dose.

Strong CYP3A4 inducers: Avoid coadministration of BRAFTOVI with strong CYP3A4 inducers.

Sensitive CYP3A4 substrates: Avoid the coadministration of BRAFTOVI with CYP3A4 substrates (including hormonal contraceptives) for which a decrease in plasma concentration may lead to reduced efficacy of the substrate. If the coadministration cannot be avoided, see the CYP3A4 substrate product labeling for recommendations.

Dose reductions of drugs that are substrates of OATP1B1, OATP1B3, or BCRP may be required when used concomitantly with BRAFTOVI.

Avoid coadministration of BRAFTOVI with drugs known to prolong QT/QTc interval.

(Press release, Pfizer, JAN 10, 2026, View Source [SID1234661926])

On January 9, 2026 Foghorn Therapeutics Inc. (Nasdaq: FHTX), a clinical-stage biotechnology company pioneering a new class of medicines that treat serious diseases by correcting abnormal gene expression, reported its strategic objectives for 2026.

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"We are pleased to have raised $50 million in an equity financing, priced at a 30% premium to the closing stock price on January 9, 2026. As part of the financing, we issued premium-priced warrants with an exercise price of 2 and 3 times the issue price. This equity raise represents an important vote of confidence from key biotech investors in our vision and execution," said Adrian Gottschalk, President and Chief Executive Officer of Foghorn. "We continue to execute across our first-in-class pipeline focused on developing new treatment options for cancers with significant unmet need. For FHD-909, our partnered program with Lilly, the Phase 1 dose-escalation trial is on track. The trial is enrolling patients with SMARCA4-mutated cancers, particularly those with NSCLC where prognosis is poor and worsens with each additional line of therapy. We are also making strong progress across our degrader portfolio as we advance our Selective CBP degrader, with promise in ER+ breast cancer, and our Selective EP300 degrader, with potential in hematologic malignancies, toward anticipated Investigational New Drug (INDs) filings. With unique programs across our partnered and proprietary pipeline, we look forward to providing updates during the coming year."

*
Unaudited and estimated.

Corporate Update

Strengthens Balance Sheet with Equity Financing to Advance Pipeline. On January 9, 2026, Foghorn entered into agreements with BVF Partners, Deerfield Management, founding investor Flagship Pioneering and a leading biotech mutual fund for the purchase and sale of 2,030,314 shares of its common stock at a purchase price of $6.71 per share and in lieu of common stock to certain investors, pre-funded warrants to purchase up to an aggregate of 5,421,250 shares of its common stock at a price of $6.7099 per pre-funded warrant, which represents the per share offering price for the common stock less the $0.0001 per share exercise price for each such pre-funded warrant as well as warrants to purchase up to 3,725,782 shares of common stock at an exercise price of $13.42 per share and up to 3,725,782 shares of common stock at an exercise price of $20.13 per share. The purchase price of the shares of common stock to be sold in the offering represents a premium of 30% to the last reported sale price of our common stock on the Nasdaq Global Market on January 9, 2026. (The offering is expected to close on or about January 13, 2026, subject to satisfaction of customary closing conditions). All of the shares of common stock in the offering are to be sold by Foghorn.

Program Overview and Upcoming Milestones

FHD-909 (LY4050784). FHD-909 is a first-in-class oral SMARCA2 selective inhibitor that has demonstrated in preclinical studies to have high selectivity over its closely related paralog SMARCA4, two proteins that are the catalytic engines across all forms of the BAF complex. Selectively blocking SMARCA2 activity is a promising synthetic lethal strategy intended to induce tumor death while sparing healthy cells. SMARCA4 is mutated in up to 10% of NSCLC alone and implicated in a significant number of solid tumors. Across lines of therapy, significant unmet needs remain for patients with SMARCA4 (BRG1)-mutant cancers with both poor response rates and short progression-free survival.

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Phase 1 trial on track. Enrollment in the first-in-human Phase 1 multi-center trial of FHD-909 is progressing well. The trial in patients with NSCLC as the primary target population is on track, following the dosing of the first patient in October 2024.

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Synergistic preclinical data of FHD-909 in combination with pembrolizumab and KRAS inhibitors. Preclinical data supports enhanced anti-tumor activity of FHD-909 in combination with standard-of-care (SoC) chemotherapies, anti-PD-1 pembrolizumab and several novel KRAS inhibitors in NSCLC animal models.

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Pending successful Phase 1 dose escalation results, Foghorn and Lilly anticipate evaluating FHD-909 in combination studies in the front-line setting of NSCLC.

Ongoing strategic collaboration with Lilly. Foghorn is collaborating with Lilly to develop novel oncology medicines, including a 50/50 U.S. co-development and co-commercialization agreement for its selective SMARCA2 oncology program that includes both a selective inhibitor and a selective degrader, as well as an additional undisclosed oncology target. The collaboration also includes three discovery programs from Foghorn’s proprietary Gene Traffic Control platform.

Selective CBP degrader program. Foghorn’s Selective CBP degrader selectively targets CBP, an acetyltransferase closely related to EP300. CBP lineage dependencies are established in several cancers, including breast cancer and there is also a synthetic relationship in EP300-mutated cancers, which include endometrial, cervical, ovarian, bladder, and colorectal cancer. Attempts to selectively drug CBP have been challenging due to the high level of similarity between the two proteins, while dual inhibition of CBP/EP300 has been associated with dose-limiting toxicities.

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CBP degrader program – IND-ready anticipated in 2026. In October 2025, preclinical data for Selective CBP degraders CBP-dependent cancers and ER+ breast cancer was presented during a Foghorn virtual investor event, which included:

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Highly potent and selective lead candidate CBPd-171 in ongoing dose range finding toxicology studies

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Anti-tumor activity in EP300 mutant solid tumors and in CBP-dependent cancers, including promising potential in ER+ breast cancer

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No impact on platelet counts and spared megakaryocytes with CBPd-171

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Long Acting Injectable (LAI) formulation optimized for subcutaneous injection weekly or every other week for convenient administration

Selective EP300 degrader program. Foghorn is developing a Selective EP300 degrader for the treatment of hematological malignancies and prostate cancer. Attempts to selectively drug EP300 have been challenging due to the high level of similarity between EP300 and CBP, while dual inhibition of CBP/EP300 has been associated with dose limiting toxicities. EP300 lineage dependencies are established in diffuse large b-cell lymphoma (DLBCL) and multiple myeloma (MM).

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EP300 degrader program – IND-enabling studies expected in 2026, with a focus in MM and DLBCL. In October 2025, efficacy and safety data of Selective EP300 degraders in preclinical models of hematological malignancies was presented during a Foghorn virtual investor event which included:

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Broad anti-tumor activity in over 70% of all heme sub-lineages tested

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VHL-based selective degrader shows impressive efficacy in MM without hematological toxicities including thrombocytopenia

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EP300 degraders show full efficacy in IMiD-resistant MM cell lines

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Tolerability profile with widespread potential for combinations

Selective ARID1B degrader program. Foghorn’s Selective ARID1B degrader selectively targets and degrades ARID1B in ARID1A-mutated cancers. ARID1A is the most mutated subunit in the BAF complex and amongst the most mutated proteins in cancer. These mutations lead to a dependency on ARID1B in several types of cancer, including endometrial, gastric, gastroesophageal junction, bladder and NSCLC. Attempts to selectively drug ARID1B have been challenging because of the high degree of similarity between ARID1A and ARID1B and the fact that ARID1B has no enzymatic activity to target. ARID1B is a major synthetic lethal target implicated in up to 5% of all solid tumors.

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First-in-class Selective ARID1B degrader program advancing towards in vivo proof of concept in 2026. In October 2025, progress for the Selective ARID1B degrader was presented during a Foghorn virtual investor event which included:

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Developed VHL and cereblon based bifunctional degraders with potential for oral delivery

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Selective degradation of ARID1B achieved

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Modulation of downstream target genes following ARID1B degradation

Strong Balance Sheet and Cash Runway.

As of January 13, 2026, the Company expects to have approximately $208.9 million (unaudited) in cash, cash equivalents, and marketable securities, inclusive of proceeds from the recent equity financing, allowing for continued investment in the pipeline and extending cash into the first half of 2028.

The securities described under Corporate Update are being offered by Foghorn pursuant to a shelf registration statement on Form S-3 declared effective by the Securities and Exchange Commission ("SEC") on January 31, 2025. This press release does not constitute an offer to sell or a solicitation of an offer to buy the securities in this offering, nor shall there be any sale of these securities in any state or other jurisdiction in which such offer, solicitation, or sale would be unlawful prior to the registration or qualification under the securities laws of any such state or other jurisdiction. A prospectus supplement and accompanying prospectus relating to the offering will be filed with the SEC and will be available on the SEC’s website at www.sec.gov.

(Press release, Foghorn Therapeutics, JAN 9, 2026, View Source [SID1234661950])