Foghorn Therapeutics (NASDAQ: FHTX) narrows 2025 loss and extends cash runway into 2028
Filing Impact
Filing Sentiment
Form Type
8-K
Rhea-AI Filing Summary
Foghorn Therapeutics reported 2025 results and outlined its oncology pipeline progress and financing. Collaboration revenue rose to
As of
Positive
- Strengthened balance sheet and extended runway: Cash, cash equivalents and marketable securities of
$158.9 million at December 31, 2025, plus a$50 million registered direct financing at a30% premium, support an indicated cash runway into the first half of2028 . - Improving financial profile: Collaboration revenue increased to
$30.9 million from$22.6 million , while net loss narrowed to$74.3 million from$86.6 million , reflecting higher partnered income and lower operating expenses. - Advancing and diversified pipeline: Lead SMARCA2 inhibitor FHD‑909 is in Phase 1, and selective CBP, EP300 and ARID1B degrader programs showed broad preclinical anti‑tumor activity with plans for IND‑enabling or in vivo proof‑of‑concept studies in
2026 .
Negative
- None.
Insights
Foghorn narrows losses, de-risks funding, and pushes a broad chromatin-focused pipeline toward the clinic.
Foghorn Therapeutics grew collaboration revenue to
Liquidity is a key highlight. The company ended 2025 with
On the pipeline, the Phase 1 SMARCA2 inhibitor FHD‑909 is advancing in SMARCA4‑mutant cancers under a 50/50 U.S. economics collaboration with Lilly. Preclinical selective CBP, EP300 and ARID1B degrader programs showed anti‑tumor activity and are tracking to IND‑enabling studies or in vivo proof‑of‑concept in
UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
Washington, D.C. 20549
| ________________________ | ||
FORM 8-K
| ________________________________________________________________________________________________ | ||
CURRENT REPORT
Pursuant to Section 13 or 15(d)
of the Securities Exchange Act of 1934
Date of Report (Date of earliest event reported): March 11, 2026
| ________________________________________________________________________________________________ | ||
(Exact name of registrant as specified in its charter)
| ________________________________________________________________________________________________ | ||
| (State or other jurisdiction of incorporation) | (Commission File Number) | (IRS Employer Identification No.) | ||||||||||||
| (Address of principal executive offices) | (Zip Code) | ||||||||||||||||||||||
(Registrant’s telephone number, including area code): (617 ) 586-3100
Not Applicable
(Former name or former address, if changed since last report)
| ________________________ | ||
Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:
| Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425) | |||||
| Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12) | |||||
| Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b)) | |||||
Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c)) | |||||
Securities registered pursuant to Section 12(b) of the Act:
| Title of each class | Trading Symbol(s) | Name of each exchange on which registered | ||||||||||||
Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§240.12b-2 of this chapter).
Emerging growth company ☐
If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. ☐
Item 2.02 Results of Operations and Financial Condition.
On March 11, 2026, Foghorn Therapeutics Inc. (the “Company”) issued a press release announcing certain of the Company’s financial results for the year ended December 31, 2025. A copy of the press release is furnished as Exhibit 99.1 to this Current Report on Form 8-K.
The information in this Item 2.02 (including Exhibit 99.1 attached hereto) is being furnished and shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), or otherwise subject to the liabilities of that section, nor shall it be deemed incorporated by reference into any filing by the Company under the Securities Act of 1933, as amended (the “Securities Act”), or the Exchange Act, except as expressly set forth by specific reference in such filing.
Item 7.01 Regulation FD Disclosure
The Company is furnishing as Exhibit 99.2 to this Current Report on Form 8-K a presentation, dated March 2026, which the Company intends to use in meetings with or presentations to investors. The information in this Item 7.01 (including Exhibit 99.2 attached hereto) is being furnished and shall not be deemed “filed” for purposes of Section 18 of the Exchange Act, or otherwise subject to the liabilities of that section, nor shall it be deemed incorporated by reference into any filing by the Company under the Securities Act or the Exchange Act, except as expressly set forth by specific reference in such filing.
Item 9.01 Financial Statements and Exhibits.
(d) Exhibits
| Exhibit No. | Description | ||||
99.1 | Press Release issued on March 11, 2026 | ||||
99.2 | Investor Presentation dated March 2026 | ||||
SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
FOGHORN THERAPEUTICS INC. | |||||||||||
| By: | /s/ Ryan Maynard | ||||||||||
| Ryan Maynard | |||||||||||
| Chief Financial Officer | |||||||||||
Exhibit 99.1
Foghorn Therapeutics Provides Financial Update for 2025 and 2026 Strategic Outlook
FHD-909 (LY4050784) Phase 1 dose-escalation advancing as planned, targeting SMARCA4 (BRG1)-mutant cancers with a focus on non-small cell lung cancer (NSCLC)
FHD-909 (LY4050784) Phase 1 dose-escalation advancing as planned, targeting SMARCA4 (BRG1)-mutant cancers with a focus on non-small cell lung cancer (NSCLC)
Selective CBP degrader program with potential in ER+ breast cancer tracking to IND-enabling studies in 2026
Selective EP300 degrader program tracking to IND-enabling studies in 2026 with a focus in multiple myeloma (MM) and diffuse large b-cell lymphoma (DLBCL)
Completed a $50 million registered direct financing in January 2026
Strong balance sheet with cash, cash equivalents, and marketable securities of $158.9 million as of December 31, 2025; with the addition of the January 2026 financing, the company has cash runway into the first half of 2028
WATERTOWN, Mass. -- (GLOBE NEWSWIRE) – March 11, 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, today provided a financial and corporate update in conjunction with the Company’s 10-K filing for the year ending December 31, 2025. With an initial focus in oncology, Foghorn’s Gene Traffic Control® Platform and resulting broad pipeline have the potential to transform the lives of people suffering from a wide spectrum of diseases.
“We are building meaningful momentum as we further advance our first-in-class portfolio of potential medicines targeting cancers with significant unmet needs,” said Adrian Gottschalk, President and Chief Executive Officer of Foghorn. “Our lead candidate FHD-909 continues to progress as planned through dose escalation in collaboration with Lilly. The trial is enriching for NSCLC patients with SMARCA4 mutations, where outcomes remain especially poor and deteriorate with later lines of therapy. In parallel, our wholly owned programs are moving toward the clinic. Our Selective CBP degrader program and our Selective EP300 degrader are on track for IND-enabling studies in 2026. Our recent cash infusion strengthens our balance sheet and enables us to focus on continued execution beyond our near-term milestones.”
Recent Corporate Updates
Bolstered Balance Sheet. Announced the successful closing of a $50 million registered direct financing at $6.71 (issue price), a 30% premium to the closing price on January 9, 2026. The offering also included series warrants representing 50% coverage at $13.42 per share (two times the issue price) and another 50% coverage at $20.13 per share (three times the issue price). The transaction, supported by BVF Partners, Deerfield Management, founding investor Flagship Pioneering and a leading biotech mutual fund, strengthens the Company’s balance sheet and extends the anticipated cash runway into the first half of 2028.
Strengthened Executive Leadership. In February 2026, Foghorn appointed Ryan Maynard as Chief Financial Officer. Mr. Maynard joins Foghorn with over 25 years of executive experience driving financial strategy, capital markets execution, and operational performance across public and private biopharmaceutical companies.
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.
•Phase 1 trial on track. Enrollment in the first-in-human Phase 1 multi-center trial of FHD-909 is progressing well. The trial is on track, following the dosing of the first patient in October 2024.
•Synergistic preclinical data of FHD-909 in combination with pembrolizumab and KRAS inhibitors. Preclinical data support 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.
◦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.
•Preclinical data for the Selective CBP degrader program identified CBPd-171 as a highly potent and selective lead candidate, which is currently advancing through dose-range finding toxicology studies.
•CBPd-171 demonstrates promising efficacy in ER+ breast cancer, while showing no impact on platelet counts and sparing megakaryocytes. Additionally, it demonstrates robust anti-tumor activity in EP300-mutant solid tumors and broader CBP-dependent cancers.
•A long-acting injectable (LAI) formulation has been optimized for subcutaneous administration on a weekly or every-other-week schedule, supporting convenient and patient-friendly dosing.
•Investigational New Drug (IND)-enabling studies anticipated in 2026.
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 several hematologic malignancies, which include diffuse large b-cell lymphoma (DLBCL) and multiple myeloma (MM).
•Preclinical efficacy and safety data for selective EP300 degraders in models of hematological malignancies demonstrate broad anti-tumor activity across more than 70% of hematologic sub-lineages tested, highlighting the program’s wide therapeutic potential.
•A VHL-based selective degrader has shown impressive efficacy in MM without hematologic toxicities, including thrombocytopenia, and EP300 degraders have retained full efficacy in IMiD-resistant multiple myeloma cell lines. Together, these findings support a favorable tolerability profile and suggest broad applicability in combination regimens across hematologic cancers.
•IND-enabling studies anticipated in 2026.
Selective ARID1B degrader program. Foghorn's first-in-class 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.
•The preclinical program has made meaningful progress with the development of both VHL- and cereblon-based bifunctional degraders designed with potential for oral delivery. Both have achieved selective degradation of ARID1B, confirming effective target engagement, and have demonstrated modulation of downstream target genes consistent with ARID1B pathway disruption.
•Advancing towards in vivo proof of concept in 2026.
Chromatin Biology and Degrader Platform. Foghorn continues to advance its chromatin biology and degrader platform with investments in induced proximity, long-acting injectables, novel ligases, and oral delivery.
Full Year 2025 Financial Highlights
•Collaboration Revenues. Collaboration revenues were $30.9 million for the year ended December 31, 2025, compared to $22.6 million for the year ended December 31, 2024. The increase year-over-year was primarily driven by continued advancement of programs under the Lilly Collaboration Agreement.
•Research and Development Expenses. Research and development expenses were $85.5 million for the year ended December 31, 2025, compared to $94.5 million for the year ended December 31, 2024. This decrease was primarily due to a decrease in FHD-286 costs, decreases in personnel-related costs, early development and other research external costs and facilities and IT-related expenses, partially offset by an increase in Lilly-partnered programs.
•General and Administrative Expenses. General and administrative expenses were $27.6 million for the year ended December 31, 2025, compared to $28.4 million for the year ended December 31, 2024. This decrease was primarily due to lower facilities and IT related expenses.
•Net Loss. Net loss was $74.3 million for the year ended December 31, 2025, compared to a net loss of $86.6 million for the year ended December 31, 2024.
•Cash, Cash Equivalents and Marketable Securities. As of December 31, 2025, the Company had $158.9 million in cash, cash equivalents and marketable securities, providing cash runway into the first half of 2028.
About FHD-909
FHD-909 (LY4050784) is a potent, first-in-class, allosteric, and orally available small molecule that selectively inhibits the ATPase activity of SMARCA2 (BRM) over its closely related paralog SMARCA4
(BRG1), two proteins that are the catalytic engines across all forms of the BAF complex, one of the key regulators of the chromatin regulatory system. In preclinical studies, tumors with mutations in SMARCA4 rely on SMARCA2 for their survival. FHD-909 has shown significant anti-tumor activity across multiple SMARCA4-mutant lung tumor models.
About Foghorn Therapeutics
Foghorn® Therapeutics is discovering and developing a novel class of medicines targeting genetically determined dependencies within the chromatin regulatory system. Through its proprietary scalable Gene Traffic Control® platform, Foghorn is systematically studying, identifying, and validating potential drug targets within the chromatin regulatory system. The Company is developing multiple product candidates in oncology. Visit our website at www.foghorntx.com for more information on the Company, and follow us on X and LinkedIn.
Forward-Looking Statements
This press release contains “forward-looking statements.” Forward-looking statements include statements regarding the Company’s ongoing Phase 1 trial of FHD-909 in SMARCA4-mutated cancers, pre-clinical product candidates, expected timing of clinical data, expected cash runway, expected timing of regulatory filings, and research efforts and other statements identified by words such as “could,” “may,” “might,” “will,” “likely,” “anticipates,” “intends,” “plans,” “seeks,” “believes,” “estimates,” “expects,” “continues,” “projects” and similar references to future periods. Forward-looking statements are based on our current expectations and assumptions regarding capital market conditions, our business, the economy and other future conditions. Because forward-looking statements relate to the future, by their nature, they are subject to inherent uncertainties, risks and changes in circumstances that are difficult to predict. As a result, actual results may differ materially from those contemplated by the forward-looking statements. Important factors that could cause actual results to differ materially from those in the forward-looking statements include regional, national or global political, economic, business, competitive, market and regulatory conditions, including risks relating to our clinical trials and other factors set forth under the heading “Risk Factors” in the Company’s Annual Report on Form 10-K for the year ended December 31, 2025, as filed with the Securities and Exchange Commission. Any forward-looking statement made in this press release speaks only as of the date on which it is made.
Condensed Consolidated Balance Sheets
(In thousands)
Dec. 31, 2025 | Dec. 31, 2024 | ||||||||||
Cash, cash equivalents and marketable securities | $ | 158,894 | $ | 243,747 | |||||||
All other assets | 39,209 | 40,235 | |||||||||
Total assets | $ | 198,103 | $ | 283,982 | |||||||
Deferred revenue, total | $ | 249,154 | $ | 280,063 | |||||||
All other liabilities | 57,449 | 49,447 | |||||||||
Total liabilities | 306,603 | 329,510 | |||||||||
Total stockholders’ deficit | (108,500) | (45,528) | |||||||||
Total liabilities and stockholders’ deficit | $ | 198,103 | $ | 283,982 | |||||||
Condensed Consolidated Statements of Operations
(In thousands, except share and per share amounts)
Twelve Months Ended December 31, | |||||||||||
2025 | 2024 | ||||||||||
Collaboration revenue | $ | 30,909 | $ | 22,602 | |||||||
Operating expenses: | |||||||||||
Research and development | 85,466 | 94,528 | |||||||||
General and administrative | 27,550 | 28,359 | |||||||||
Gain on lease modification | (1,632) | — | |||||||||
Impairment of long-lived assets | 5,914 | 2,398 | |||||||||
Total operating expenses | 117,298 | 125,285 | |||||||||
Loss from operations | (86,389) | (102,683) | |||||||||
Total other income, net | 12,106 | 16,063 | |||||||||
Net loss | $ | (74,283) | $ | (86,620) | |||||||
Net loss per share attributable to common stockholders—basic and diluted | $ | (1.18) | $ | (1.58) | |||||||
Weighted average common shares outstanding—basic and diluted | 62,980,959 | 54,899,432 | |||||||||
Contact:
Karin Hellsvik, Foghorn Therapeutics Inc.
khellsvik@foghorntx.com
khellsvik@foghorntx.com
Unique biology Precision therapeutics Broad impact NASDAQ LISTED FHTX March 2026 Exhibit 99.2
| Forward Looking Statements 2 This presentation contains forward-looking statements that are based on management's beliefs and assumptions and on information currently available to management. All statements other than statements of historical facts contained in this presentation are forward- looking statements. In some cases, you can identify forward-looking statements by terms such as “could,” “may,” “might,” “will,” “likely,” “anticipates,” “intends,” “plans,” “seeks,” “believes,” “estimates,” “expects,” “continues,” “projects” or the negative of these terms or other similar expressions, although not all forward-looking statements contain these words. Forward-looking statements include, but are not limited to, statements concerning: the potential outcomes from our collaboration agreement with Lilly; the initiation, timing, progress and results of our research and development programs and pre-clinical studies and clinical trials, including with respect to our Phase 1 dose escalation trial of FHD-909 with Lilly; our ability to advance product candidates that we may develop and to successfully complete preclinical and clinical studies; our ability to leverage our initial programs to develop additional product candidates using our Gene Traffic Control Platform®; the impact of exogeneous factors, including macroeconomic and geopolitical circumstances, on our and our collaborators’ business operations, including our research and development programs and pre-clinical studies; developments related to our competitors and our industry; our ability to expand the target populations of our programs and the availability of patients for clinical testing; our ability to obtain regulatory approval for FHD-909 and any future product candidates from the FDA and other regulatory authorities; our ability to identify and enter into future license agreements and collaborations; our ability to continue to rely on our CDMOs and CROs for our manufacturing and research needs; regulatory developments in the United States and foreign countries; our ability to attract and retain key scientific and management personnel; the scope of protection we are able to establish, maintain and enforce for intellectual property rights covering FHD-909, our future products and our Gene Traffic Control Platform; and our use of proceeds from capital-raising transactions, estimates of our expenses, capital requirements, and needs for additional financing. You should, therefore, not rely on these forward-looking statements as representing our views as of any date subsequent to the date of this presentation. Additional important factors to be considered in connection with forward-looking statements are described in the Company's filings with the Securities and Exchange Commission, including withing the section entitled "Risk Factors" in the Company's Annual Report on Form 10-K for the fiscal year ended December 31, 2025. Any forward-looking statements represent the Company’s views only as of the date of this presentation and should not be relied upon as representing its views as of any subsequent date. The Company explicitly disclaims any obligation to update any forward-looking statements. The Company’s business is subject to substantial risks and uncertainties.
| Foghorn is a Leader in Chromatin Biology, Successfully Drugging Challenging Targets 3 Targeting chromatin regulation Implicated in up to 50% of all tumors Multi-billion $ Opportunities Unlocking selectivity of previously undruggable targets First-and-Best-in-Class Approaches Innovating selective protein degradation with capabilities in induced proximity Selective Target Engagement Leveraging a proven drug development platform with expansive potential Strategic Partnership: Multiple Programs
| Chromatin Regulatory System Orchestrates Gene Expression: Multiple Opportunities for Targets and Therapeutics 4 Chromatin – compacted form of DNA inside the nucleus of the cell Chromatin Remodeling Complexes – specialized multiprotein machines that allow access to DNA Targets: SMARCA2, ARID1B Transcription Factors – proteins that help turn specific genes "on" or "off" by working in concert with the chromatin remodeling complex to bind to DNA Targets: Multiple TFs Other Chromatin Binding Proteins involved in gene expression / function Targets: CBP, EP300 Chromatin Regulatory System genes are implicated across a wide range of cancers Leveraging synthetic lethality and lineage dependencies
| Foghorn’s Platform Has Delivered Precision First-in-Class Therapeutics, and is Poised to Unlock New Biology 5 1. Chromatin Biology 2. Chemistry, Biochemistry & Formulations 3. Degraders / Selective Targeting Deep mechanistic understanding of chromatin regulatory system Expertise in rules of degrader optimization Track record with previously undruggable targets Expansion into New TAs & Induced Proximity Track record of delivering precision therapeutics
| Foghorn: Precision Therapies with Potential for Multi-Billion Dollar Opportunities Across Oncology 6 Modality Program and Partner Phase 1 Enzyme Inhibitors Protein Degraders FHD-909* (Selective SMARCA2) 3 Discovery Programs Undisclosed Partnered** Undisclosed Disease SMARCA4-mutant cancers (e.g., NSCLC) Selective SMARCA2 SMARCA4-mutant cancers (e.g., NSCLC) Selective ARID1B ARID1A-mutant cancers (e.g., endometrial, gastric, bladder, NSCLC) Selective CBP ER+ Breast and EP300-mutant cancers (e.g., endometrial, cervical, ovarian, bladder) Selective EP300 MM and DLBCL and other heme cancers Undisclosed Undisclosed Pre-Clinical Anticipated MilestonesDiscovery *LY4050784, 50/50 U.S. economic split, ex-U.S. royalties. **Pending Lilly decision to proceed, 50/50 U.S. economic split, ex-U.S. royalties. SMARCA2 = BRM DLBCL: Diffuse Large B-Cell Lymphoma; ER+: Estrogen Receptor-positive; MM: Multiple Myeloma; NSCLC: Non-Small Cell Lung Cancer Ph 1 Monotherapy Data; Confidential Transition to Lilly; Confidential IND-enabling Studies; 2026 Transition to Lilly; Confidential IND-enabling Studies; 2026 In vivo PoC; 2026
| FHD-909 is Being Developed in Collaboration with Lilly; Landmark Agreement Signed in December 2021 Significant Upfront and Economics Strong Momentum and Shared Vision Ongoing Discovery Programs • $300 million cash • $80 million in Foghorn common stock at a price of $20 per share • 50/50 U.S. economic split on SMARCA2- target and another undisclosed program • Tiered ex-U.S. royalties ranging from low double-digit into 20s • Lilly is a leading oncology company with a track record of innovation and execution • Lilly selected FHD-909 for development and initiated the first clinical trial in 2024 • Thorough evaluation of FHD-909 in models of SMARCA2-dependent tumors • Three additional programs as part of collaboration (undisclosed) • Potential to earn royalties and up to $1.3 billion in potential milestones across these three programs 7
| Developing First-in-Class Precision Medicines Targeting Major Unmet Needs in Cancer 8 Large Market Potential Chromatin biology is implicated in up to 50% of tumors, potentially impacting ~2.5 million patients Foghorn’s current pipeline potentially addresses more than 500,000 of these patients Broad pipeline across a range of targets and small molecule modalities Major Strategic Collaboration Strategic collaboration with Lilly; $380 million upfront; 50/50 U.S. economic split on two lead programs Well- Funded $158.9 million in cash and equivalents (as of 12/31/2025) $50 million gross proceeds from January 2026 financing Cash runway into H1 2028 Shares outstanding: approximately 70.6M* Value Drivers Selective SMARCA2 Inhibitor, FHD-909, partnered with Lilly, in Phase 1 trial Advancement of preclinical assets (Selective SMARCA2, CBP, EP300, ARID1B degraders) towards INDs Protein degrader platform with expansion into induced proximity Leader in Unique Area of Cancer Biology Foghorn is a leader in targeting chromatin biology, which has the potential to address underlying dependencies of many genetically defined cancers Platform with initial focus in oncology, therapeutic area expansion potential *Includes pre-funded warrants as of 02/28/2026.
Selective SMARCA2 Program For SMARCA4-mutant Cancers • FHD-909 (LY4050784) – Selective SMARCA2 Inhibitor 9
| SMARCA2: Clinical-stage FHD-909 Selective SMARCA2 Inhibitor and Preclinical Selective SMARCA2 Degrader 10 Selective SMARCA2 Inhibitor FHD-909* Selective SMARCA2 Degrader Biology Exploit the synthetic lethal relationship between SMARCA2 and mutated SMARCA4 Status Phase 1 monotherapy dose escalation trial ongoing Advancing through late preclinical development Opportunity SMARCA4-mutated cancer including ~10% of NSCLC and up to 5% of all solid tumors Lilly Partnership 50/50 global R&D cost share | 50/50 U.S. economics | tiered ex-U.S. royalties starting in the low double-digit range and escalating into the twenties *LY4050784
| Selective SMARCA2 Inhibition: Promising Strategy to Exploit Synthetic Lethal Relationship Between SMARCA2 and Mutant SMARCA4 11 No SMARCA4 Mutations SMARCA4 Mutation SMARCA4 Mutation and SMARCA2i Cell Survival Cell Death Healthy Cells Cancer Cells SMARCA4 SMARCA2 BAF Complex BAF Complex Mutant SMARCA4 BAF Complex SMARCA2i Precision medicine targeting synthetic lethal relationships is a proven clinical approach now used in multiple cancers (e.g., PARP inhibitors) SMARCA4 SMARCA2
| SMARCA4 is Mutated in Up to 10% of NSCLC; Up to 5% of Solid Tumors 12 SMARCA4 mutated across a broad range of tumors Accounts for ~5% of solid tumors AACR GENIE via cBioPortal
| FHD-909: Overall Goal is to Become a First-Line Treatment for SMARCA4- mutated NSCLC 13 1st Line NSCLC Pembrolizumab-based regimens Other immune checkpoint inhibitor-based regimens Chemotherapy-based regimens 2nd Line NSCLC Chemotherapy-based regimens Ramucirumab (anti-VEGF) + chemotherapy Checkpoint inhibitor monotherapy 3rd Line NSCLC Chemotherapy-based regimens Other targeted agents + chemotherapy Relevant treatment regimens in each line of therapy for metastatic NSCLC* Agents evaluated preclinically in combination with FHD-909 KRAS inhibitors Targeted agents Note: *Generalized across squamous and non-squamous metastatic NSCLC without driver mutation Source: CancerMPact 2024 US NSCLC TA report
| 14 Significant Unmet Medical Need in NSCLC Metastatic Setting for SMARCA4 Patients ~15 months ~8 months 1L (SMARCA4 WT) 1L (SMARCA4 Mut) 39.1% 21.9% 2.7 months Response Rate (%) PFS (months) OS (months) Significant Unmet Need Frontline NSCLC Metastatic – PD1 + Chemo1 Source: 1. Alessi, J Thorac Oncol, 2023 2. Rittmeyer, Lancet, 2017; Fehrenbacher, J Thorac Oncol, 2018; Mazieres, J Thorac Oncol, 2021 Herbst, Lancet, 2016; Herbst, Abs OA03.07 3. S1800A – Lung-MAP Sub-study – ASCO 2022; Garon, Lancet, 2014 • Poor response to 1L chemo-immunotherapy for patients with SMARCA4 mutations1 • 2L outcomes with docetaxel are poor for all patients (ORR 10-20% depending on agent/s2,3; PFS ~5-months) • SMARCA4-mutated patients are expected to fare even worse in the 2L setting • 3L+ setting – experience suggests less than 10% ORR and 1 to 2 months PFS Significant Unmet Need in SMARCA4-mutated NSCLC 8.1 t 6.1 months 15.0 t s
| NSCLC patients with SMARCA4 mutations: ─ Poor prognosis ─ Shorter overall survival ─ Less responsive to immune checkpoint inhibitors ─ Clinically definable, high unmet need population SMARCA4 Mutated in Up to 10% of NSCLC Tumors, Minimal Overlap w/ Other Mutations2 Overall Survival for SMARCA4 wt vs SMARCA4 mut1; Frontline Metastatic NSCLC w/ Chemoimmunotherapy SMARCA4 Mutations are Consequential – in NSCLC, Patients with Mutated SMARCA4 Have Significantly Worse Clinical Outcomes 15 SMARCA4 10% KRAS 29% EGFR 26% ALK 7% RET 4% MET 7% Source: 1. Alessi et al DOI: 10.1016/j.jtho.2023.01.091; 2. TCGA via cBioPortal O ve ra ll Su rv iv al (% ) Months Supporting references: • Gandhi, et al, 2025; DOI: 10.1016/j.jtho.2025.01.016 • Alessi, et al, 2023; DOI: 10.1016/j.jtho.2023.01.091 • Negrao, et al, 2023; DOI: 10.1158/2159-8290.Cd-22-1420 • Liu, et al, 2021; DOI: 10.1002/1878-0261.12831 • Fernando, et al, 2020; DOI: 10.1038/s41467-020-19402-8 • Schoenfeld, et al, 2020DOI: 10.1158/1078-0432.ccr-20-1825
| When SMARCA4 and KRAS Mutations Co-Occur, Patients Have Even Worse Outcomes to Standard of Care Treatment In response to PD(L)-1 therapy, patients with co-occurring SMARCA4 and KRAS mutations have a shorter ORR, PFS, and OS than patients with only KRASmut 16 Overall Response Rate (ORR) Source: Alessi et al DOI: 10.1016/j.jtho.2021.03.024 Progression-Free Survival (PFS) Overall Survival (OS) Median PFS, months (95% CI) Median OS, months (95% CI) KRAS mut + SMARCA4 wt (n:159): 15.1 (11.2–20.1) KRAS mut + SMARCA4 mut (n:17): 3.0 (1.0–9.3) HR = 0.25 [95% CI: 0.14–0.42] P < 0.001 HR = 0.29 [95% CI: 0.17–0.50] P < 0.001 0.0% (0/17) KRAS mut + SMARCA4 wt (n:159): 4.1 (2.8–6.0) KRAS mut + SMARCA4 mut (n:17): 1.4 (0.9–2.0) P = 0.03 22.0% (35/159)
| A First-in-Human Phase 1 Trial of FHD-909 in Advanced Solid Tumor Patients with SMARCA4 Mutations Phase 1a Dose Escalation Advanced solid tumors with any SMARCA4 alteration (mTPI-2 method with backfillinga) Dose Level 1 Dose Level 2 Dose Level 3 Dose Level n Phase 1b Dose Expansionb Presence of a Known or Likely Loss of Function of SMARCA4 Part A: 2L + NSCLCc (Optional Randomized Dose Optimization) Part B: Other Solid Tumors Cohort A1 Cohort A2 (optional) Cohort A3 (optional) R an d om iz ed Cohort B1 • FHD-909 is administered orally BID, in 28-day cycles • Phase 1b may begin prior to completion of backfill in Phase 1a • In Phase 1b, no prior SMARCA2 (BRM) inhibitors/degraders are allowed Note: aEach dose level will enroll 3-6 DLT-evaluable patients; select dose levels may backfill up to 20 patients; N~80; b Phase 1b may open prior to completion of backfill; N~80; c prior platinum doublet, immunotherapy, and antibody-drug conjugate therapy allowed; sponsor may initiate a randomized dose optimization cohort within Phase 1b across 2 or more dose levels 17
Degrader Programs • Selective CBP Degrader • Selective EP300 Degrader • Selective ARID1B Degrader 18
| Developing a Portfolio of Novel and Selective Degraders 19 Selective ARID1B Degrader Selective CBP Degrader • Mutated in up to 5% of all solid tumors • First to demonstrate robust and selective degradation of the protein • Developing VHL and cereblon degraders, potential for oral delivery • Program advancing towards in vivo proof-of-concept in 2026 • EP300-mutant and CBP- dependent Cancers • Anti-tumor activity demonstrated including promising potential in ER+ breast cancer • Long-Acting Injectable (LAI) formulation • No significant preclinical heme toxicity • IND-enabling studies in 2026 • CBP-mutant and EP300- dependent Cancers • Potential across range of heme malignancies, including MM and DLBCL • Highly selective and potent • No significant preclinical heme toxicity • IND-enabling studies in 2026 Selective EP300 Degrader
| CBP and EP300 Proteins – A Decades-long Challenge in Selectivity 20 CBP and EP300 Biology • CBP and EP300 are highly homologous, paralog histone acetyltransferases regulating enhancer-mediated transcription and protein stability • Dysregulation of CBP and EP300 has been implicated in multiple cancers • Dual targeting has revealed tolerability and safety issues Foghorn’s Solution... Highly Selective Degradation • Achieved selective targeting which results in improved tolerability and efficacy • Advancing two separate programs with defined dependencies and patient populations CoA TF TF TF RNA Polymerase Ac Ac CoA Ac Ac Ac CBP/ EP300 MYC Cell growth Cell survival Ac EP300 Degrader Approach Focus on EP300 Lineage- dependent Cancers CBP Degrader Approach Focus on EP300-mutant Cancers via Synthetic Lethality
Selective CBP Degrader, FHT-171 For EP300-mutant and CBP-dependent Cancers 21
| Summary: Selective CBP Degrader for CBP-dependent & EP300-mutant Cancers 22 • CREB binding protein (CBP) • Targeted protein degrader Gynecological cancers1 Other cancers2 Bladder cancer ER+ Breast cancer Target / Approach • Preclinical • IND-enabling studies in 2026 Stage / Next Milestone • Highly selective and potent • Increased tolerability relative to non- selective compounds • Long-acting formulation • Compelling combination potential Asset Description Initial Opportunity (U.S.) Incidence* EP300 mut. Frequency EP300 mut. Incidence 105K 8% 8.4K 84K 10% 8.4K 349K 6% 21K 210K NA NA *Per year incidence in the U.S.. Source: Clarivate DRG Mature Markets Data; 1Endometrial, Cervical, and Ovarian Cancers; 2Gastric, CRC, NSCLC **CBP-dependent cancers do not exploit synthetic lethal relationships in paralogs EP300 mut. Cancers CBP-dependent Cancers** Incidence* Key Differentiation
| In Breast Cancer, FHT-171 Disrupts Estrogen Receptor (ER) Signaling and Inhibits Tumor Cell Growth Robust & Potent CBP Degradation …Resulting in Cancer Cell Growth Inhibition 23 0. 00 01 0. 00 1 0. 01 0. 1 1 10 10 0 10 00 10 00 0 10 00 00 10 00 00 0 % d e te c te d C B P p ro te in CBP degradation in MCF7 cells(24h) …Leads to Reduced Expression of ER and its Target Genes MCF7 colony formation assay (14d) 33311137 12.34.11.370.46 0.150.050.017 1000 0 FHT-171 [nM] 1nM FHT-171 treated MCF7 (7d)
| FHT-171 Demonstrates Anti-tumor Efficacy as a Monotherapy in Standard-of-care Resistant ER+ Breast Cancer Models ER+ Metastatic Breast Cancer CDX (ST941C; ESR1m) ER+ Metastatic Breast Cancer PDX (ST4887B, ESR1 wt) ER+ Metastatic Breast Cancer PDX (ST4680D, ESR1m) 24 T u m o r V o lu m e (m m 3 ) + /- S E M *Data were generated as part of a Mouse Clinical Trial executed by Xenostart. PDX models are from patients who have progressed from endocrine and CDK4/6 inhibitor therapies. 0 20 40 0 200 400 600 800 1000 Days on treatment Untreated control FHT-171, 10mg/kg QD, s.c. 0 5 10 15 0 250 500 750 1000 Days on treatment T u m o r V o lu m e ( m m 3 ) + /- S E M Untreated control FHT-171, 10mg/kg QD, s.c.
| FHT-171 Shows No Impact on Platelet Counts and Spared Megakaryocytes • C B P Platelet Counts Post Two Weeks of Dosing (In Vivo – Control Mice) Human Megakaryocyte Cell Viability Assay (In Vitro**) *CCS1477 (Inobrodib) inhibition study used 3 weeks of dosing Platelet counts are unaffected by selective CBP degrader in in vivo models **Human megakaryocytes derived from primary human hematopoietic stem cells 25 PLT (x109cells/L) 0 500 1,000 1,500 2,000 2,500 Study Day 14 P la te le ts (X 1 0 3 c e ll s /u L ) Vehicle FHT-171, 10mg/kg, SC, QD Dual BD inhibitor, (GNE-781), 30mg/kg, PO, BID FHT-171 Dual CBP/EP300 Bromodomain Inhibitors Vehicle Dual BD inhibitor (CCS1477, Inobrodib), 20mg/kg, PO, QD GNE-781 Inobrodib *
| FHT-171: Potent and Selective CBP Degrader • C B P Global Proteomics Confirms that FHT-171 is Selective 26 FHT-171 Rapidly and Potently Degrades CBP, but not its Paralog EP300 Dmax: 97% Max Rate: 3.2 hr-1 DC50: 30pM Dmax: 5% Max Rate: N/A 100nM CBPd-171/DMSO 3hr Log2FC FHT-171 CBP Kinetics FHT-171 EP300 Kinetics
| Selective CBP Degradation Results in Significant Anti-Tumor Activity in EP300-mutant Solid Tumor Models EP300mut Bladder Cancer CDX (639V) EP300mut Gastric Cancer CDX (AGS) EP300mut Gastric Cancer PDX (ST020326) T u m o r V o lu m e (m m ³ + S E M ) B o d y W ei g h t C h an g e (% ) 20 30 40 50 60 0 500 1,000 1,500 Vehicle FHT-CBPd-59, 10mg/kg (QD) FHT-CBPd-59, 3mg/kg (QD) FHT-CBPd-59, 1mg/kg (QD) FHT-CBPd-59, 0.3mg/kg (QD) FHT-CBPd-59, 0.1mg/kg (QD) T u m o r V o lu m e ( m m 3 ± S E M ) B o d y w e ig h t c h a n g e ( % ) Fold Selectivity >20x >10000x EP300 0.15 uM 30uM CBP 0.005 uM 0.0024uM Degrader Selectivity FHT-CBPd-59 DC50 @24h FHT-CBPd-41 DC50 @24h 27
| Long-Acting Injectable Formulation of CBPd-171 Enables Weekly Sub-cutaneous (SC) Delivery 28 Tumor Growth Inhibition Observed in EP300mut (AGS) Gastric Model (Daily Injections and SC weekly LAI Injection) • Weekly LAI injection of CBDd-171 results in efficacy comparable to daily SC injections in AGS (gastric) model • We observe robust, dose- dependent CBP degradation across tumor models in PK/PD studies • LAI characterization in additional pharmacology studies planned to refine human dose predictionsT u m o r V o lu m e (m m ³ + S E M )
| 29 Development Vision: CBP Degrader has the Potential to be an Attractive Combination Partner in ER+ Breast Cancer and Beyond Phase 1b Dose Expansion / Combination ER+ BC patients who failed at least 2L in advanced / metastatic setting In parallel, explore combos Dose Level 1 Dose Level 2 Dose Level 3 Dose Level n Expansion cohorts based on Ph1a Advance selected combinations into registrational studies Expanding to earlier lines of therapy Additional combinations to enable future label expansion Endocrine Therapy: Fulvestrant Elacestrant Tamoxifen CDK4/6: Abemaciclib Palbociclib Ribociclib CBPd Phase 1a Dose Escalation Registration
Selective EP300 Degrader For CBP-mutant and EP300-dependent Cancers 30
| Summary: Selective EP300 Degrader for CBP-mutant & EP300-dependent Cancers 31 • E1A binding protein p300 (EP300) • Targeted protein degrader MM AML + MDS DLBCL Target / Approach • Preclinical • IND-enabling studies in 2026 Stage / Next Milestone • Deeper efficacy response vs non- selective molecules • Improved tolerability profile vs non- selective molecules • Patient selection biomarker for DLBCL Asset Description Initial Opportunity (U.S.) Incidence* 31K 32K 38K *Per year incidence in the U.S. Source: Clarivate DRG Mature Markets Data EP300-dependent Hematological Malignancies Key Differentiation • Broad range of heme malignancies focused on MM and DLBCL • AR+ prostate • Bladder, melanoma, others Indications
| EP300 Degradation Shows Anti-Proliferative Activity in Broad Range of Hematological Malignancies 32MM: Multiple Myeloma; DLBCL: Diffuse Large B-Cell Lymphoma; AML: Acute Myeloid Leukemia; BL: Burkitt’s Lymphoma; PTCL: Peripheral T-cell Lymphomas; T-ALL: T-cell Acute Lymphoblastic Leukemia; B-ALL: B-cell Acute Lymphoblastic Leukemia; CML: Chronic Myeloid Leukemia; HL: Hodgkin Lymphoma; MCL: Mantle Cell Lymphoma, FL: Follicular Lymphoma Anti-Tumor Activity Across Full Range of Heme Sub-Lineages (~ 70% of All Tested Cell Lines are Sensitive)
| Multiple Myeloma (MM1S) CDX DLBCL (KARPAS422) CDX AR+ Prostate (VCaP) CDX EP300 Degradation Results in Significant Tumor Growth Inhibition in MM, DLBCL and Prostate Models 33 B o d y W ei g h t C h an g e ( % ) 5 10 15 20 25 30 35 40 45 0 500 1,000 1,500 2,000 Vehicle FHT-EP300d - 32, SC, 50mg/kg (BID) Days After Tumor Inoculation FHT-EP300d - 32, SC, 20mg/kg (BID) FHT-EP300d - 32, SC, 10mg/kg (BID) B o d y W e ig h t C h an g e ( % ) 10 15 20 25 30 0 500 1,000 1,500 2,000 2,500 3,000 Days After Tumor Inoculation Vehicle FHT-EP300d - 53, SC, 30mg/kg (QD) FHT-EP300d - 53, SC, 10mg/kg (QD) CCS1477 (Inobrodib), PO, 20mg/kg (QD) Fold Selectivity >1000x EP300 0.7 nM CBP >1 uM Degrader Selectivity FHT-EP300d-53 DC50 @24h Fold Selectivity >40x EP300 23 nM CBP >1 uM Degrader Selectivity FHT-EP300d-32 DC50 @24h
| Selective EP300 Degradation Results in Significant Responses In Vivo, and Spares Platelets 34 • The max efficacious dose for inobrodib results in stasis with daily dosing. However, inobrodib use in the clinic is limited by thrombocytopenia, which requires dosing holidays • Selective EP300 degraders can achieve deeper responses at tolerated doses with no thrombocytopenia MM1S – A Multiple Myeloma Study Platelet Count
| Selective EP300 Degrader Spares Platelets, Red Blood Cells and Neutrophils No Change in Platelets, Red Blood Cells or Neutrophils Following 14 Days of Daily Dosing in Immunocompetent Mice 35 WBC: White Blood Cells; RBC: Red Blood Cells; PLT: Platelets; Neut: Neutrophils W BC (x 10 9 ce lls /L ) RBC (x 10 6 ce lls /μ L) PLT (x 10 9 ce lls /L ) Neu t ( x1 0 9 ce lls /L )
| VHL-based Selective EP300 Degrader Maintains Activity in IMiD Resistant Cell Lines 36 Resistant MM1S cell lines were developed through 5–6 months of in vitro exposure to gradually increasing concentrations of lenalidomide, pomalidomide, iberdomide, or mezigdomide dEP300-9 dEP300-9 pomalidomide lenalidomide mezigdomide iberdomide
| 20 25 30 35 40 0 100 200 300 400 1000 2000 3000 4000 Days After Tumor Inoculation Vehicle FHT-EP300d-007, 30mpk, BID, s.c. CCS1477 (Inobrodib), 10mpk, BID (4d on / 3d off), p.o CCS1477 (Inobrodib), 20mpk, QD, p.o. Pomalidomide, 10mpk, QD, p.o. Selective EP300 Degrader Shows Superior Efficacy Compared to Pomalidomide and Inobrodib in an IMiD Resistant Multiple Myeloma Model Pomalidomide-Resistant Multiple Myeloma CDX (MM1S-PomR) Treated with EP300d-007 37 • Selective EP300 degrader achieves deeper responses (regressions) in a Pomalidomide-resistant Multiple Myeloma model • Selective EP300 degrader with improved therapeutic window enables sustained target coverage and improved efficacy .
| EP300d-007: Potent and Selective EP300 Degrader EP300d-007 Rapidly and Potently Degrades EP300, but Not its Paralog CBP Global Proteomics Confirms that EP300d-007 is Selective 38 Dmax: 97% Max Rate: 2.2 hr-1 DC50: 3 nM 333nM EP300d-007/DMSO 6hr Log2FC Dmax: 15% Max Rate: N/A
| 39 Development Vision: EP300 in Hematological Malignancies e patients with r/r hematological malignancies Dose Level 1 Dose Level 2 Dose Level 3 Dose Level n Register in specific hematological malignancies single agent or as part of combination regimen AML/MDS T-Cell Malignancies Expand into earlier lines of therapy MM DLBCL EP300 Explore combinations with SoC Phase 1a Dose Escalation Dose Expansion/ Explore Combinations Registration
Selective ARID1B Degrader For ARID1A-mutant Cancers 40
| ARID1B is a Major Synthetic Lethal Target with Potential in Up To 5% of All Solid Tumors 41 • ARID1B • Targeted protein degrader Endometrial cancers Gastric cancers Bladder cancer Non-small cell lung cancer • Preclinical • In vivo proof-of-concept in 2026 • Multiple ARID1B binders with nM affinity and selectivity • Selective ARID1B degradation Asset Description Initial Opportunity (U.S.) Incidence* ARID1A mut. Frequency ARID1A mut. Incidence 66K 38% 25K 37K 20% 7K 84K 24% 20K 195K 7% 14K *Per year incidence in the U.S.. Source: Clarivate DRG Mature Markets Data. Target / Approach Stage / Next Milestone Key Differentiation
| ARID1B: Drugging A Previously Undruggable Target • Large and highly unstructured protein ~ 240 kDa • No known enzymatic function • Member of large, multi-subunit complex • High sequence homology (~60%) to ARID1A 42 ARID1A/B BAF Nucleosome PDB ID: 6LTJ • Discover binders to ARID1B • Use binders to develop bifunctional degraders Drug Targeting Considerations Approach
| Maximum Optionality Achieved Through Progression of Both Cereblon and VHL-based Degraders in Parallel 43 C E R E B L O N V H L
| Selective ARID1B Degrader Demonstrates Robust Degradation Across Multiple Cell Lines 44 IMMUNOBLOT HiBiT – ENDPOINT HCT116 (Colorectal)HT-1376 (Bladder) HiBiT – KINETICS HCT116 (Colorectal) 24 hours 24 hours R e la ti v e L u m in es c e n c e U n it s (% C o n tr o l)
| Selective ARID1B Degradation Demonstrated by Global Proteomics 45
| 0.0 0.2 0.4 0.6 0.8 1.0 1 2 3 4 5 6 Selective ARID1B Degradation has Demonstrated Effects on Downstream Target Genes – Progressing Towards In Vivo Proof-of-concept 46 3 Day ARID1B shRNA Treatment ARID1B Degrader Treatment y = 0.6782x + 0.2591 R² = 0.7754 0.00 0.20 0.40 0.60 0.80 1.00 1.20 0.0 0.5 1.0 ARID1B expression y = -2.6042x + 3.1832 R² = 0.8159 0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 0.0 0.5 1.0 ARID1B expression ARID1B Gene Expression ARID1B Expression ARID1B ExpressionRange of Dox Treatment R e la ti v e E x p re s si o n R e la ti v e E x p re s si o n R e la ti v e E x p re s si o n Down Gene A Expression Up Gene B Expression 24h Treatment 48h Treatment Down Gene A Expression Up Gene B Expression Putative target genes identified from literature and confirmed via internal shRNA efforts
| Developing First-in-Class Precision Medicines Targeting Major Unmet Needs in Cancer 47 Large Market Potential Chromatin biology is implicated in up to 50% of tumors, potentially impacting ~2.5 million patients Foghorn’s current pipeline potentially addresses more than 500,000 of these patients Broad pipeline across a range of targets and small molecule modalities Major Strategic Collaboration Strategic collaboration with Lilly; $380 million upfront; 50/50 U.S. economic split on two lead programs Well- Funded $158.9 million in cash and equivalents (as of 12/31/2025) $50 million gross proceeds from January 2026 financing Cash runway into H1 2028 Shares outstanding: approximately 70.6M* Value Drivers Selective SMARCA2 Inhibitor, FHD-909, partnered with Lilly, in Phase 1 trial Advancement of preclinical assets (Selective SMARCA2, CBP, EP300, ARID1B degraders) towards INDs Protein degrader platform with expansion into induced proximity Leader in Unique Area of Cancer Biology Foghorn is a leader in targeting chromatin biology, which has the potential to address underlying dependencies of many genetically defined cancers Platform with initial focus in oncology, therapeutic area expansion potential *Includes pre-funded warrants as of 02/28/2026.
Unique biology Precision therapeutics Broad impact 48 March 2026
Appendix 49
SMARCA2 Program 50
| FHD-909 Monotherapy Demonstrated Regression In Vivo in NCI-H2126 SMARCA4-mutant NSCLC Model at Tolerated Doses 51 NCI-H2126 Reduction in Tumor Volume NCI-H2126 Body Weight Genetic Background: SMARCA4 W764R, TP53 E62*, STK11-/-, CDKN2A-/-, KEAP1 R272C Note: All doses were well tolerated. Dosing holidays were applied at the high dose, as appropriate. T u m o r v o lu m e (m m 3 ) Tu m o r V o lu m e (m m 3 )
| FHD-909 Monotherapy Demonstrated Strong In Vivo Activity Across SMARCA4-mutant NSCLC Models at Tolerated Doses 52 0 7 14 21 28 100 200 300 400 500 Days of Dosing (Dose Start Day1) Vehicle Control FHD-909, 20mg/kg, BID, PO FHD-909, 40mg/kg, BID, PO FHD-909, 60mg/kg, BID, PO A549 Model RERF-LC-AI Model NCI-H1793 Model Genetic Background: SMARCA4, Q729fs / H736Y, KRAS G12S, STK11-/-, CDKN2A-/-, KEAP1 G333C Genetic Background: SMARCA4 mut p.E1496*, TP53 p.Q104*, NF1 p.E1699* Genetic Background: SMARCA4, E514*, TP53 R209* R273H, ARID1A C884* Note: All doses were well tolerated. Dosing holidays were applied to the 60 mg/kg dose groups, as appropriate.
| FHD-909 in Combination with Standard Therapies Demonstrates Significant Activity in the A549 (SMARCA4-mutant, KRAS G12S) Xenograft NSCLC Model 53 0 7 14 21 28 200 400 600 800 1000 1200 Days of Dosing (Dose Start Day 1) T u m o r vo lu m e (m m 3 ) * * * * ** ## Note: *p≤0.05 for pairwise comparisons for combination group vs vehicle and single agent groups and all treatment groups vs vehicle control, # additive by Bliss Independence analysis. Dosing holidays were applied to the 60mg/kg FHD-909 dose groups as appropriate. FHD-909 + cisplatin + pemetrexed A549 (SMARCA4mt, KRAS G12S) In vivo, combining FHD-909 with cisplatin and pemetrexed increased antitumor effect, resulting in tumor regression Additivity and synergy were also observed in vitro when FHD-909 was combined with cisplatin or pemetrexed
| FHD-909 in Combination with Standard Therapies Demonstrates Significant Activity in the RERF-LC-AI (SMARCA4-mutant) Xenograft NSCLC Model 54 0 7 14 21 28 200 400 600 800 1000 1200 1400 Days of Dosing (Dose Start Day 1) T u m o r V o lu m e (m m 3 ) * * * * **# # Note: *p≤0.05 for pairwise comparisons for combination group vs vehicle and single agent groups and all treatment groups vs vehicle control, # additive by Bliss Independence analysis. In vivo, combining FHD-909 with cisplatin and paclitaxel increased antitumor effect, resulting in tumor regression Additivity and synergy were also observed in vitro when FHD-909 was combined with cisplatin or paclitaxel FHD-909 + cisplatin + paclitaxel RERF-LC-AI (SMARCA4mt)
| Synergistic Activity Observed for FHD-909 in Combination with KRAS Inhibitors In Vitro 55 In h ib it io n ( % ) In h ib it io n ( % ) FHD-909 + olomorasib (KRAS G12C inhibitor) FHD-909 + pan-KRAS inhibitor In h ib it io n ( % ) In h ib it io n ( % ) 1 10 100 1000 10000 -20 0 20 40 60 80 100 120 FHD-909 concentration (nM) DMSO 7 14 28 56 113 225 450 900 [LY4066434](nM) In h ib it io n ( % ) NCI-H2030, Lung, NSCLC SMARCA4-/- KRAS(G12C) PATU-8988T, Pancreas, PDAC SMARCA4 - / fusion, KRAS(G12D)* SNU-407, Colon, CRC SMARCA4 P109fs194, R466C, Y507H, M1109V, KRAS(G12D) A549, Lung, NSCLC SMARCA4 Q729fs/H736Y, KRAS(G12S) PATU-8988T, Pancreas, PDAC SMARCA4 - / fusion, KRAS(G12V) Note: FHD-909 is reported in unbound concentrations in the assays; *CRISPR KI, fs frameshift FHD-909 + LY3962673 (KRAS G12D inhibitor) FHD-909 + LY4066434 (pan-KRAS inhibitor) FHD-909 + LY3962673 (KRAS G12D inhibitor) FHD-909 + LY4066434 (pan-KRAS inhibitor) NCI-H2030, Lung, NSCLC SMARCA4-/- KRAS(G12C)
| Combination of FHD-909 with KRAS Inhibitors Demonstrates Synergistic Activity in SMARCA4, KRAS Co-mutated Human NSCLC Xenograft Models In Vivo FHD-909 + olomorasib (KRAS G12C inh) NCI-H2030 (SMARCA4mt, KRAS G12C) 56 0 7 14 21 28 0 500 1000 1500 2000 2500 3000 Days of Dosing (Dose Start Day1) T u m o r V o lu m e (m m 3 ) ## synergistic (p<0.05) * * * ## Combination of FHD-909 with olomorasib demonstrated synergistic antitumor activity and sustained tumor regression in vivo Note: Olomorasib – LY3537982; * p≤0.05 for pairwise comparisons for combination group vs vehicle and single agent groups and all treatment groups vs vehicle control, ## synergistic by Bliss Independence analysis.
| Combination of FHD-909 with KRAS Inhibitors Demonstrates Synergistic Activity in SMARCA4, KRAS Co-mutated Human NSCLC Xenograft Models In Vivo FHD-909 + pan-KRAS inh A549 (SMARCA4mt, KRAS G12S) 57 Combination of FHD-909 with pan-KRAS inhibitor resulted in synergistic antitumor activity and sustained tumor regression in vivo Note: pan-KRAS inhibitor - LY4066434; * p≤0.05 for pairwise comparisons for combination group vs vehicle and single agent groups and all treatment groups vs vehicle control, ## synergistic by Bliss Independence analysis.
| FHD-909 in Combination with Pembrolizumab Shows Significantly Enhanced Anti-Tumor Activity in A549 CD34+ HSC Humanized Xenograft NSCLC Model 58 FHD-909 sensitized the tumor cells to pembrolizumab treatment resulting in enhanced combination activity Pembrolizumab alone had no effect on tumor growth compared to vehicle control Note: HSC, hematopoietic stem cells; * p≤0.05 for pairwise comparisons for combination group vs vehicle and single agents; # additive, ## synergistic by Bliss Independence analysis. FHD-909 (20 mg/kg) + pembrolizumab A549 (SMARCA4mt, KRAS G12S) FHD-909 (40 mg/kg) + pembrolizumab A549 (SMARCA4mt, KRAS G12S)
| Selective SMARCA2 Degrader Achieved Complete SMARCA2 Degradation and Cell Growth Inhibition In Vitro 59 Degraders Caused Time- and Dose-dependent SMARCA2 Degradation Antiproliferative Effects in A549-mutant NSCLC Model A549 Ten-Day Proliferation AssaySMARCA2 / SMARCA4 HIBIT Data SMARCA2 SMARCA4 % D eg ra d a ti o n Concentration (uM) 0 25 50 75 100 1E-3 0.01 0.1 1 10 Note: Data as of Q4 2021.
Protein Degradation Importance of Rate Analysis FHD-609 is a Selective, Potent, Protein Degrader of the BRD9 component of the BAF complex 60
| Degradation Rates and Their Relationship to Dmax 61 • Slower rates lead to partial degradation, faster rates to complete loss • Rate is an indicator of degrader efficiency. If rate is slow, the process is inefficient and reflective of a degrader which does not have a high turnover rate of target Native Deg Rate Ta rg e t L ev e l Time Dmax10 Dmax25 Dmax50 Dmax80 Dmax95 Experimental Rate vs. Dmax Experimental Kinetic Profile Theoretical Kinetic Profile F ra ct io na l L os s
| Degradation Rate Dictates Dmax – Program Independent 62 Foghorn CBP ProgramFoghorn BRD9 Program Foghorn EP300 Program Large scale experimental kinetic analysis for a program reveals the relationship between rate and Dmax
| Prelude VHL and CRBN Compounds Have Incomplete Dmax and also Have a Hook Effect 63 • Prelude’s SMARCA2 (VHL) degrader was faster and achieved improved Dmax across concentrations as compared to SMARCA2 (CRBN) • The SMARCA2 (CRBN) degrader is considerably slower and therefore even at high concentration will be incomplete • Both degraders show a bifunctional hook effect which slows rate and impedes Dmax at high concentrations Prelude SMARCA2 (CRBN) DegraderPrelude SMARCA2 (VHL) Degrader F ra c ti o n a l L u m in e s c e n c e (R L U ) Concentration F ra ct io n a l L u m in es ce n ce (R L U ) Concentration Hook Effect Hook Effect Rate max (ƛ) hr-1: 0.4Rate max (ƛ) hr-1: 1.5 F ra ct io na l L os s F ra ct io na l L os s
| Foghorn Analysis and Dmax Results Match Published Prelude Data 64 Prelude Published Data Prelude PRT3789 (VHL) 1 Prelude PRT7732 (CRBN) 2 % P ro te in Prelude (CRBN) Degrader Prelude (VHL) Degrader Foghorn Replicated Data from Prelude Patents 1. AACR-NCI-EORTC 2023 Poster B113 – Ito et al. 2. AACR 2024 Poster 4503 -Shvartsbart et al. % D eg ra d at io n % D e g ra d a ti o n
FAQ
How did Foghorn Therapeutics (FHTX) perform financially in 2025?
Foghorn reported 2025 collaboration revenue of $30.9 million, up from $22.6 million in 2024. Research and development expenses fell to $85.5 million and general and administrative costs to $27.6 million, resulting in a narrower net loss of $74.3 million versus $86.6 million a year earlier.
What is Foghorn Therapeutics’ cash position and runway after the January 2026 financing?
As of December 31, 2025, Foghorn held $158.9 million in cash, cash equivalents and marketable securities. A $50 million registered direct financing completed in January 2026 leads the company to state it has cash runway into the first half of 2028, supporting its development plans.
What were the key terms of Foghorn Therapeutics’ January 2026 financing?
Foghorn closed a $50 million registered direct financing at an issue price of $6.71 per share, a 30% premium to the January 9, 2026 close. The deal included series warrants: 50% coverage exercisable at $13.42 per share and another 50% at $20.13 per share.
What is the status of Foghorn’s lead program FHD-909 with Lilly?
FHD‑909, a selective SMARCA2 inhibitor, is in a first‑in‑human Phase 1 dose‑escalation trial for SMARCA4‑mutant cancers, including non‑small cell lung cancer. Foghorn and Lilly share 50/50 U.S. co‑development and co‑commercialization economics on this SMARCA2 program under their collaboration agreement.
Which new degrader programs is Foghorn Therapeutics advancing toward the clinic?
Foghorn highlighted selective CBP, EP300 and ARID1B degrader programs. The CBP degrader FHT‑171 and selective EP300 degraders showed promising preclinical efficacy and tolerability, with IND‑enabling studies anticipated in 2026. The ARID1B degrader program is progressing toward in vivo proof‑of‑concept in 2026.
How did Foghorn’s operating expenses change year over year in 2025?
In 2025, research and development expenses decreased to $85.5 million from $94.5 million, largely from lower FHD‑286 and other costs. General and administrative expenses declined slightly to $27.6 million from $28.4 million, contributing to an improved overall loss from operations.
What strategic collaboration economics does Foghorn have with Lilly?
Foghorn’s collaboration with Lilly includes $300 million in cash and $80 million in Foghorn stock upfront, a 50/50 U.S. economic split on the SMARCA2 program and another undisclosed target, plus tiered ex‑U.S. royalties ranging from low double‑digit percentages into the twenties.
Filing Exhibits & Attachments
5 documents
Foghorn Therapeutics Inc.
NASDAQ:FHTX
FHTX Rankings
FHTX Latest News
FHTX Latest SEC Filings
Mar 11, 2026
[10-K] Foghorn Therapeutics Inc. Files Annual Report