On April 19, 2026 Immunocore Holdings plc (Nasdaq: IMCR) ("Immunocore" or the "Company"), a commercial-stage biotechnology company pioneering and delivering transformative immunomodulating medicines to radically improve outcomes for patients with cancer, infectious diseases and autoimmune diseases, reported that KIMMTRAK (tebentafusp-tebn) five-year overall survival (OS) was presented in an oral session at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2026 meeting.

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This is the longest, prospective Phase 3 randomized trial in patients with unresectable or metastatic uveal melanoma (mUM) – a disease with a very poor prognosis and a historical survival rate of <5% at 5 years1. KIMMTRAK doubled the likelihood of being alive at five years, with an OS for KIMMTRAK of 16% versus 8% in the control arm (hazard ratio [HR] of 0.67 [95% CI: 0.54-0.85]). These results also represent the longest follow-up reported for any T cell engager in a solid tumor.

In the trial, 378 patients were randomized to tebentafusp (252) or investigator’s choice (126; 82% pembrolizumab). The median OS was 21.6 months on KIMMTRAK, versus 16.9 months on investigator’s choice (IC). The Kaplan–Meier survival curves separated early and remained separated over time, confirming the durability of the benefit with extended follow-up.

"These important results allow us, for the first time, to speak with real confidence to patients about the possibility of long-term survival," said Professor Paul Nathan, Consultant Medical Oncologist, Mount Vernon Cancer Centre, UK. "Before tebentafusp, such conversations simply weren’t possible for metastatic uveal melanoma patients."

"These long-term overall survival results further solidify KIMMTRAK as the first-line standard of care for HLA-A*02:01 positive patients with metastatic uveal melanoma," said Mohammed Dar, Immunocore Chief Medical Officer. "The survival benefit was evident even in patients with known poor prognostic factors, including those with large tumors and extrahepatic disease."

The data confirmed that the OS benefit was primarily driven by tebentafusp rather than subsequent therapies. Among patients treated with KIMMTRAK who were alive at five years, nearly half (44%) received only KIMMTRAK, while among patients in the control arm alive at the same time point, 86% subsequently received tebentafusp.

Importantly, the OS benefit with KIMMTRAK was observed regardless of known poor prognostic factors at baseline (high tumor burden [≥10cm]; elevated lactate dehydrogenase [LDH]) or tumor location (hepatic only; hepatic and extra-hepatic). OS benefit was also observed in patients with a best response of progressive disease, including those with >20% tumor growth as best change on treatment.

More patients continued treatment beyond progression in the KIMMTRAK arm than in the control arm (57% vs 25%) – with the trial allowing this option in both arms. Patients on KIMMTRAK achieved nearly a 7-fold higher rate of tumor reduction with treatment beyond initial progression compared to IC patients (27% vs 4%). In fact, patients who continued tebentafusp treatment beyond tumor progression experienced longer post-progression survival compared to those who stopped treatment, even after accounting for variations in patient characteristics.

In tebentafusp-treated patients, longer OS was associated with undetectable ctDNA at baseline or ctDNA reductions ≥50% by week 9. Among 21 ctDNA-evaluable patients who survived ≥ 5 years, 71% had undetectable baseline ctDNA and 29% had ctDNA clearance by week 9. Deep reductions in ctDNA were seen across all RECIST categories. Early ctDNA molecular response continues to be a more sensitive marker of tebentafusp activity than radiographic measurements.

The data were presented today in an oral session during the AACR (Free AACR Whitepaper) 2026 meeting:

Title: Five-year survival with tebentafusp in previously untreated metastatic uveal melanoma in a Phase 3 trial (CT029)
Presenting author: Paul Nathan
Session: Advanced Cellular and Immune-Based Therapeutics

(Press release, Immunocore, APR 19, 2026, View Source [SID1234664542])

On April 19, 2026 Ascentage Pharma Group International (NASDAQ: AAPG; HKEX: 6855), a global, commercial stage, integrated biopharmaceutical company engaged in the discovery, development and commercialization of novel, differentiated therapies to address unmet medical needs in cancer, reported that it will present four preclinical studies in poster format at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2026 Annual Meeting, held April 17 to 22, 2026 in San Diego, CA, USA.

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These posters feature three of the Company’s drug candidates, Olverembatinib (HQP1351), a novel BCR-ABL inhibitor; APG-2449, a FAK/ALK/ROS1 triple tyrosine kinase inhibitor; and APG-5918, a PRC2/EED inhibitor.

Yifan Zhai, M.D., Ph.D., Chief Medical Officer of Ascentage Pharma, said, "These preclinical findings reflect our continued commitment to advancing innovative therapies across multiple cancer types. The four studies demonstrate the breadth and versatility of our pipeline, exploring the therapeutic potential of our key assets in combination with other approved treatment options in both hematologic malignancies and solid tumors.

Notably, the research examines Olverembatinib’s potential beyond its approved use in China for chronic myeloid leukemia (CML), exploring new applications in areas such as endometrial carcinoma and mantle cell lymphoma, including combination approaches with BTK inhibitors. In addition, our evaluation of APG-2449 in BRAF-mutant tumors, and APG-5918 in small-cell lung cancer, underscores our strategic focus on addressing resistance mechanisms and exploring combination strategies.

These preclinical investigations are designed to inform our clinical development strategies and complement our ongoing global registrational trials as we bring new treatment options to patients with significant unmet medical needs."

Detailed data presented at AACR (Free AACR Whitepaper) 2026 Annual Meeting are summarized below:

(Abstract #4583)

Multitarget kinase inhibitor Olverembatinib (HQP1351) is efficacious and synergizes with chemotherapy in preclinical models of endometrial carcinoma (EC)

Background:

EC is the most common gynecologic malignancy in developed countries, with an incidence that is steadily increasing globally. Patients with advanced-stage, high-risk non-endometrioid EC subtypes or recurrent disease have a poor prognosis and limited treatment options.
Olverembatinib is a tyrosine kinase inhibitor approved by the National Medical Products Administration (NMPA) of China for the treatment of patients with CML. It targets multiple kinases, including VEGFR1–3, FGFR1–4, Src family kinases, RAF, KIT, RET, and PDGFR.
Drug sensitivity screening of 883 human cancer cell lines using the PRISM (Profiling Relative Inhibition Simultaneously in Mixtures) platform showed that EC is one of the tumor types most sensitive to Olverembatinib. This study further explored the antitumor effects of Olverembatinib alone or in combination with standard-of-care chemotherapy in preclinical EC models.

Summary:

In a broad range of preclinical in vitro and in vivo EC models, Olverembatinib was efficacious and synergized with chemotherapy agents to promote antitumor effects.
Mechanistically, Olverembatinib combined with chemotherapy suppressed FGFR2, PI3K/AKT, and MEK/ERK signaling pathways, induced DNA damage, and resulted in enhanced cell apoptosis.
These findings support future clinical evaluation of Olverembatinib and its combination with other approved treatment options in EC.

(Abstract #5875)

Multikinase inhibitor Olverembatinib (HQP1351) is efficacious and synergizes with BTK inhibitor acalabrutinib in mantle cell lymphoma (MCL) preclinical models

Background:

MCL is a rare, aggressive type of non-Hodgkin lymphoma. Although BTK inhibitors have transformed MCL treatment, response to monotherapy is limited, and efforts are underway to develop combination therapies.
Olverembatinib, an investigational multikinase inhibitor (approved in China for CML), inhibits Src-family kinases (e.g., Lyn, Fyn, YES1) and BTK, which are essential for B-cell receptor (BCR) signaling and B-cell proliferation, differentiation, and activation.
Hypothesizing that dual inhibition of Lyn and BTK pathways could enhance antitumor effects, this study evaluated Olverembatinib in combination with acalabrutinib in preclinical MCL models and explored potential mechanisms of action.

Summary:

Olverembatinib potently inhibited MCL cell proliferation both in vitro and in vivo and showed synergistic effects when combined with acalabrutinib. The combination significantly promoted apoptosis and induced G0/G1 cell cycle arrest.
Mechanistically, Olverembatinib inhibited phosphorylation of Lyn and its downstream BTK, while the combination further downregulated NF-kB activity.
These data provide a scientific rationale for further clinical evaluation of this novel combination therapy in patients with MCL.

(Abstract #1858)

FAK inhibition by APG-2449 enhances the antitumor activity of MAPK pathway blockade in BRAF V600E-mutant tumor models

Background:

BRAF mutations occur in approximately 4% to 8% of all cancers, most frequently in colorectal cancer (CRC), melanoma, and non-small-cell lung cancer. The V600E mutation is the most common and functionally activating form, leading to constitutive activation of the mitogen activated protein kinase (MAPK) signaling cascade.
Combined BRAF and MAPK kinase (MEK) inhibition has shown substantial clinical benefit in BRAF V600Emutant melanoma and CRC. However, resistance frequently develops through feedback reactivation of extracellular signal-regulated kinase (ERK) or compensatory activation of the phosphoinositide-3 kinase (PI3K)-AKT signaling pathway.
Recent evidence indicates that focal adhesion kinase (FAK) signaling is also adaptively reactivated upon MAPK inhibition, contributing to therapeutic resistance.
This study evaluated the effects of APG-2449, a potent and selective multi-kinase inhibitor that also targets FAK, on the antitumor activities of the BRAF inhibitor dabrafenib and the MEK inhibitor trametinib in BRAF V600E-mutant CRC and melanoma preclinical models.

Summary:

The results showed selective sensitivity of BRAF V600E-mutant cancer cell lines to APG-2449.
APG-2449 suppresses compensatory signaling activation induced by MAPK pathway blockade and synergistically enhances the antitumor activity of dabrafenib + trametinib in preclinical models.
These results warrant clinical development of APG-2449 for patients with melanoma or CRC harboring the BRAF V600E mutation.

(Abstract #4500)

Embryonic ectoderm development (EED) inhibitor APG-5918 synergizes with topoisomerase I inhibitors in preclinical small-cell lung cancer (SCLC) models through epigenetic priming of chemosensitivity

Background:

Although SCLC initially responds to platinum-based chemotherapy, it rapidly develops resistance, resulting in a poor prognosis.
PRC2-mediated epigenetic silencing represses Schlafen 11 (SLFN11), a biomarker of sensitivity to DNA-damaging therapies, thereby contributing to treatment resistance.
EZH2, the catalytic subunit of PRC2, promotes chemoresistance in part through SLFN11 repression. EED, another core PRC2 component, stabilizes the complex and maintains its methyltransferase activity, making it an attractive therapeutic target in SCLC.
Topoisomerase I inhibitors, such as topotecan and irinotecan, are used in relapsed SCLC; however, their efficacy is limited when SLFN11 is epigenetically suppressed.
APG-5918 is a selective and investigational EED inhibitor that disrupts PRC2 function. This study evaluated the antitumor activity of APG-5918 in combination with topoisomerase I inhibitors in preclinical SCLC models.

Summary:

In preclinical SCLC models, combination treatment with APG-5918 and topoisomerase I inhibitors synergistically inhibited cell proliferation and induced apoptosis.
In vivo, APG-5918 combined with irinotecan demonstrated synergistic antitumor activity in the NCI-H446 SCLC cell-derived xenograft (CDX) model without significant body-weight loss, indicating favorable tolerability.
Mechanistically, APG-5918 reduced the repressive histone mark H3K27me3, indicating on-target inhibition of PRC2 activity. Consistent with this effect, APG-5918 treatment increased SLFN11 and p21 expression. Notably, treatment with topotecan or SN-38 increased H3K27me3 levels, whereas APG-5918 reduced this effect. Combination treatment further decreased expression of PRC2 core components, suppressed cell-cycle progression, and enhanced DNA damage and apoptotic signaling, supporting a synergistic proapoptotic effect.
The findings support clinical investigation of APG-5918 in combination with DNA-damaging agents as a promising therapeutic strategy for SCLC.

(Press release, Ascentage Pharma, APR 19, 2026, View Source [SID1234664528])

On April 19, 2026 Immunocore Holdings plc (Nasdaq: IMCR) ("Immunocore" or the "Company"), a commercial-stage biotechnology company pioneering and delivering transformative immunomodulating medicines to radically improve outcomes for patients with cancer, infectious diseases and autoimmune diseases, reported that KIMMTRAK (tebentafusp-tebn) five-year overall survival (OS) was presented in an oral session at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2026 meeting.

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Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

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This is the longest, prospective Phase 3 randomized trial in patients with unresectable or metastatic uveal melanoma (mUM) – a disease with a very poor prognosis and a historical survival rate of <5% at 5 years1. KIMMTRAK doubled the likelihood of being alive at five years, with an OS for KIMMTRAK of 16% versus 8% in the control arm (hazard ratio [HR] of 0.67 [95% CI: 0.54-0.85]). These results also represent the longest follow-up reported for any T cell engager in a solid tumor.

In the trial, 378 patients were randomized to tebentafusp (252) or investigator’s choice (126; 82% pembrolizumab). The median OS was 21.6 months on KIMMTRAK, versus 16.9 months on investigator’s choice (IC). The Kaplan–Meier survival curves separated early and remained separated over time, confirming the durability of the benefit with extended follow-up.

"These important results allow us, for the first time, to speak with real confidence to patients about the possibility of long-term survival," said Professor Paul Nathan, Consultant Medical Oncologist, Mount Vernon Cancer Centre, UK. "Before tebentafusp, such conversations simply weren’t possible for metastatic uveal melanoma patients."

"These long-term overall survival results further solidify KIMMTRAK as the first-line standard of care for HLA-A*02:01 positive patients with metastatic uveal melanoma," said Mohammed Dar, Immunocore Chief Medical Officer. "The survival benefit was evident even in patients with known poor prognostic factors, including those with large tumors and extrahepatic disease."

The data confirmed that the OS benefit was primarily driven by tebentafusp rather than subsequent therapies. Among patients treated with KIMMTRAK who were alive at five years, nearly half (44%) received only KIMMTRAK, while among patients in the control arm alive at the same time point, 86% subsequently received tebentafusp.

Importantly, the OS benefit with KIMMTRAK was observed regardless of known poor prognostic factors at baseline (high tumor burden [≥10cm]; elevated lactate dehydrogenase [LDH]) or tumor location (hepatic only; hepatic and extra-hepatic). OS benefit was also observed in patients with a best response of progressive disease, including those with >20% tumor growth as best change on treatment.

More patients continued treatment beyond progression in the KIMMTRAK arm than in the control arm (57% vs 25%) – with the trial allowing this option in both arms. Patients on KIMMTRAK achieved nearly a 7-fold higher rate of tumor reduction with treatment beyond initial progression compared to IC patients (27% vs 4%). In fact, patients who continued tebentafusp treatment beyond tumor progression experienced longer post-progression survival compared to those who stopped treatment, even after accounting for variations in patient characteristics.

In tebentafusp-treated patients, longer OS was associated with undetectable ctDNA at baseline or ctDNA reductions ≥50% by week 9. Among 21 ctDNA-evaluable patients who survived ≥ 5 years, 71% had undetectable baseline ctDNA and 29% had ctDNA clearance by week 9. Deep reductions in ctDNA were seen across all RECIST categories. Early ctDNA molecular response continues to be a more sensitive marker of tebentafusp activity than radiographic measurements.

The data were presented today in an oral session during the AACR (Free AACR Whitepaper) 2026 meeting:

Title: Five-year survival with tebentafusp in previously untreated metastatic uveal melanoma in a Phase 3 trial (CT029)
Presenting author: Paul Nathan
Session: Advanced Cellular and Immune-Based Therapeutics

(Press release, Immunocore, APR 19, 2026, View Source [SID1234664527])

On April 19, 2026 Researchers from Inocras, a bioinformatics-led company harnessing the power of whole-genome data and proprietary analytics to advance precision health, and the Broad Institute of MIT and Harvard reported new insights from a collaborative initiative to analyze large-scale whole genome data during the AACR (Free AACR Whitepaper) Annual Meeting 2026 in San Diego. The collaboration delivers one of the largest cancer whole-genome analyses from over 8,000 cancer whole-genomes, generated by the NCI’s The Cancer Genome Atlas (TCGA), across more than 30 cancer types.

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For two decades, cancer genomic data has underpinned many of the most important discoveries in cancer genomics. However, most studies have relied primarily on whole-exome sequencing (WES), which covers only ~1–2% of the genome, leaving the majority of the genome unexplored. The Inocras-Broad collaboration analyzes whole-genome sequences (WGS) released by TCGA, delivering an unprecedented, well-curated genomic dataset that can serve as an ideal training set for building artificial intelligence (AI) models to usher in a new era of whole-genome AI-driven precision oncology.

Cancer WGS analysis and dataset comparison

TCGA WGS data was analyzed in parallel with two variant calling pipelines from Broad and Inocras; the December 1, 2025 analysis freeze marks a joint commitment to ensure variant call quality, integrity, and reproducibility. All the data were consolidated into a single frozen dataset to enable a consistent analysis across both groups and robust benchmarking of computational and AI methods.

"With this analysis initiative, we are collectively setting a new standard for cancer genomics," said the principal investigators (PIs) of the Inocras-Broad collaboration: Drs. Gad Getz, PhD, a professor of pathology at Harvard Medical School, Director of Bioinformatics at the Krantz Family Center for Cancer Research and Dept. of Pathology at Massachusetts General Hospital and Core Institute Member at Broad Institute of MIT and Harvard; Esther Rheinbay, PhD, Assistant Professor of Medicine at Harvard Medical School and Massachusetts General Hospital Cancer Center and Associate Member at the Broad Institute of MIT and Harvard; and Young Seok Ju, MD, PhD, co-founder of Incoras and Associate professor at the Korea Advanced Institute of Science and Technology. "Whole-exome data has already transformed our understanding of cancer based on a narrow slice of the genome. Now, with harmonized full whole-genome insights, researchers can explore the complete landscape of cancer to identify noncoding driver mutations, genome ploidy assessment, structural variants (SVs) across intergenic and intronic regions, and mutational signatures, among other new insights to further advance translational cancer research."

Key insights from the Inocras-Broad collaboration

Leveraging high-depth, PCR-free WGS, the new analysis of the somatic mutation landscape in 31 cancer types improved the discovery of new driver events by incorporating the analysis of non-coding regions, genome-wide copy number alterations, and genomic rearrangements.

Some of the insights include: Across all tumors, (i) more than 250 million variants were identified with >1 million somatic SVs, as well as (ii) new coding and non-coding candidate driver mutations, (iii) new genomic signatures of chromosomal instability, (iv) new promoter/enhancer somatic copy number alterations, (v) new patterns of alterations in the previously understudied X and Y chromosomes, and (vi) new candidate SV drivers; moreover, the data show (vii) pathogenic and likely pathogenic germline variants in established cancer predisposition genes affecting about 10% of all cases.

Strong foundation for future cancer research and cancer intelligence

Through the initiative, the PIs have together built a robust foundation to analyze cancer whole genomes at industry-scale. "The Inocras-Broad collaboration reflects our belief that the most impactful discoveries emerge from open, rigorous, and deeply collaborative science," said Jehee Suh, CEO of Inocras. "Through this partnership, we are not just generating findings—we are building the foundation of a scalable, whole-genome–driven ecosystem for cancer research and clinical translation. I believe this foundation will accelerate discovery, enable clinical adoption, and advance the next generation of cancer intelligence."

The PIs from Inocras and the Broad Institute will jointly present data highlights and discuss future initiatives during the Exhibitor Spotlight session "TCGA and Beyond: Whole-Genome Data Powering the Next Era of Cancer Intelligence" on Monday, April 20th.

(Press release, Broad Institute of Harvard and MIT, APR 19, 2026, View Source [SID1234664526])

On April 19, 2026 EpiBiologics, a leader in tissue-selective extracellular protein degradation, reported that the first patient has been dosed with EPI-326 in its global Phase 1 clinical study. EPI-326 is the company’s tissue-selective bispecific antibody that degrades all oncogenic mutant and wild type forms of EGFR for EGFR-driven cancers. The first-in-human study is evaluating EPI-326 in patients with advanced non-small cell lung cancer (NSCLC) and head and neck squamous cell carcinoma (HNSCC) with the potential to expand into colorectal cancer (CRC).

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"Patients face persistent challenges with current EGFR-targeted therapies, including resistance and poor tolerability," said Eric Humke, M.D., Ph.D., Chief Medical Officer of EpiBiologics. "EPI-326 was designed to address those limitations through a mutation-agnostic, tissue-selective approach to localize EGFR degradation to tumors while sparing healthy tissue. We believe EPI-326 can drive strong durable efficacy as a monotherapy and in combinations, and ultimately enable treatment in earlier settings."

The Phase 1 study (NCT07462377) is designed to evaluate the safety, tolerability, pharmacokinetics and preliminary anti-tumor activity of EPI-326 as a monotherapy in patients with advanced NSCLC and HNSCC. The study is currently enrolling patients at sites in the U.S. and is planned to initiate sites in the Asia-Pacific region, including South Korea.

AACR Highlights

New data presented today at the AACR (Free AACR Whitepaper) New Drugs on the Horizon session highlight EPI-326’s activity across multiple tumor models, potential in combination settings, and encouraging tolerability profile:

Broad anti-tumor activity: EPI-326 showed robust preclinical in vivo efficacy in both classical and drug-resistant (C797S) EGFR-mutant NSCLC models, as well as in wildtype HNSCC and CRC tumor models. In an EGFR-mutant NSCLC preclinical model, EPI-326 monotherapy drove a high complete response rate and demonstrated stronger activity than EGFR inhibitors.
Combination potential: Preclinical studies combining EPI-326 with frontline standard-of-care therapies, including tyrosine kinase inhibitors (TKIs) and KRAS inhibitors for NSCLC and CRC cancers respectively, led to deeper and more durable anti-tumor responses.
Favorable tolerability profile: EPI-326 was well tolerated in multidose non-human primate toxicology studies to a maximal feasible dose of 204 mg/kg, with no evidence of stereotypical EGFR-related toxicities. This safety window supports the company’s monotherapy strategy and provides a strong basis for evaluating EPI-326 in combination with standard-of-care therapies.
"What stands out in these data is the combination of robust anti-tumor activity with an excellent tolerability profile," said Shyra Gardai, Ph.D., Chief Scientific Officer of EpiBiologics. "This is the central promise of tissue-selective degradation. We are now pursuing similar therapeutic approaches across multiple targets in oncology and immunology."

Additional AACR (Free AACR Whitepaper) presentations highlight EpiBiologics’ pipeline progress. New data from the company’s cMET degrader-ADC support advancement of this dual mechanism EpiTAC, which combines targeted degradation with a cytotoxic payload and may safely address high unmet needs, including tumors with low cMET expression. Together with new data from the company’s cKIT program, these presentations underscore the potential to generate tissue-selective EpiTACs against receptor tyrosine kinases implicated across multiple tumor types.

"Advancing EPI-326 into the clinic, alongside key data presented at AACR (Free AACR Whitepaper), gives us an early view into the broader opportunity for EpiTACs," said Ann Lee-Karlon, Ph.D., Chief Executive Officer of EpiBiologics. "This milestone builds on the momentum of our recent Series B financing, and we are delighted to welcome Roche Venture Fund as a new investor in our syndicate. Our goal is to build highly differentiated bispecific antibodies to selectively degrade membrane and soluble targets for oncology and immunology where new approaches are needed the most."

Details of the poster presentations are as follows:

Title: "Dual modality of EpiTAC bispecific degrader ADCs combines c-MET degradation with cytotoxic payload delivery to overcome limitations of current c-MET-targeted therapies"
Date & Time: Mon., April 20th, 9 a.m.-12 p.m. PT
Presenters: Lisa Marshall, Kenneth Ng, Shruti Yadav

Title: "Discovery of mutation-independent cKit degrading bispecific antibodies that suppress tumor growth in preclinical models of GIST"
Date & Time: Tues., April 21st, 9 a.m.-12 p.m. PT
Presenters: Ken Flanagan, Kenneth Ng, Shruti Yadav

About EPI-326
EPI-326 is a tissue-selective bispecific antibody that degrades all oncogenic forms of EGFR, is mutation-agnostic, and overcomes limitations of existing EGFR therapies by localizing degradation to the tumor while sparing normal healthy tissue. It is currently being evaluated in a global Phase 1 clinical trial (NCT07462377) in patients with NSCLC and HNSCC with the potential to expand to CRC.

(Press release, EpiBiologics, APR 19, 2026, View Source [SID1234664525])