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 [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])

On April 19, 2026 Synthetic Design Lab, a next-generation antibody-drug conjugate (ADC) and protein engineering company, reported preclinical data in an oral presentation at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 demonstrating that its proprietary SYNTHBODY therapeutic platform delivers log-order improvements in internalization, potency, and efficacy compared to current ADCs. The presentation marks the company’s first public disclosure of platform and lead candidate data and introduces a new paradigm for ADC and biologic therapy design.

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Where today’s antibody-drug conjugates are limited by single- or bi-specific protein targeting, a SYNTHBODY therapeutic employs engineered design principles to achieve, in a combinatorial fashion, a multi-protein binding architecture and geometry that adjusts its binding and payload delivery to different cancer cell conformations and presentations. Unlike past approved protein therapeutics, which passively bind to a target and either inhibit or activate it, SYNTHBODY functions like a molecular processor, using built-in logic gates to adjust its behavior based on what it encounters in the body.

"The modern approach in drug development is the right drug for the right patient. Smart drugs capable of adjusting their own behavior may eventually upend that model entirely, because you may not need to match drug to patient when the drug itself can adapt," said Daniel S. Chen, M.D., Ph.D., founder and CEO of Synthetic Design Lab. "That type of inherent advanced drug intelligence has never existed in an approved medicine. Today’s data are the first demonstration that it is possible."

That intelligence addresses one of the field’s most stubborn limitations: limited targets that are expressed specifically at high levels on cancer cells. ADCs such as trastuzumab deruxtecan (ENHERTU) have demonstrated that when therapeutic payloads are delivered to high expressing targets with precision and efficacy, metastatic HER2+ breast cancer can be treated with complete responses exceeding 20% and durability of response greater than 30 months. But HER2 is an outlier: its high specific expression levels on tumor cells are rarely replicated by other targets, leaving most cancers beyond the reach of current ADC approaches. SYNTHBODY was engineered to solve this problem by creating synthetic targeting equivalents, coordinating multiple lower-expression targets and higher-expression non-specific targets across a much wider range of tumors.

Data Highlights

Synthetic Design Lab presented data on a multiple myeloma-targeting SYNTHBODY that incorporates affinity- and geometry-tuned binders for BCMA, GPRC5D, and CD38 – three antigens that individually fall short of HER2-like expression and specificity. When combined in a properly designed SYNTHBODY architecture, it creates a synthetic high-expression high-specificity target through multi-layered logic-gating.

In head-to-head studies, the presented SYNTHBODY demonstrated more than 30x greater internalization versus the BCMA-targeting IgG antibody belantamab, and when bioconjugated to MMAF, achieved more than 80x greater potency versus belantamab mafodotin in human myeloma cells. The molecule retained its activity in cell lines with both high and low expression of each of its three targets and evaded clinically relevant concentrations of soluble BCMA, a known resistance mechanism that limits belantamab efficacy. The SYNTHBODY platform also demonstrated tunable IgG-like pharmacokinetics in vivo. In mouse tumor models, the molecule achieved ≥10x increased potency compared to an IgG-based comparator.

Similar early results were observed in a Non-Hodgkin’s Lymphoma (NHL)-targeting SYNTHBODY construct, and a high-throughput SYNTHBODY ENGINE approach is being used to rapidly generate and optimize multiple solid tumor SYNTHBODY ADCs, supporting the platform’s broad applicability across cancer types.

The SYNTHBODY architecture introduces something with no precedent in protein-based medicine: advanced logic-gated drug behavior. The constructs behave like molecular transistors, with "AND-BETTER" logic-gated control, layered with "AND" safety gates and "MULTIPLIER" functions that produce synergistic activity absent from conventional antibody ADCs. Optimized SYNTHBODY constructs also demonstrate strong manufacturability in CHO cells, favorable developability, and tunable IgG-like pharmacokinetics in vivo.

"Our platform is a fundamentally different way of thinking about how to target a cancer cell," said Ramesh Baliga, Ph.D., Chief Scientific Officer and co-founder of Synthetic Design Lab. "By controlling the geometry and biophysics of the targeting architecture itself, we can generate capabilities and emergent properties that simply aren’t possible with conventional IgG-based formats."

(Press release, Synthetic Design Lab, APR 19, 2026, View Source [SID1234664524])

On April 19, 2026 Whitehawk Therapeutics, Inc. (Nasdaq: WHWK), a clinical-stage oncology therapeutics company applying advanced technologies to established tumor biology to efficiently deliver improved antibody drug conjugate (ADC) cancer treatments, reported the presentation of new preclinical data across its ADC portfolio at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17-22, 2026, in San Diego, CA.

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"Across our three ADC programs, we have a consistent preclinical profile characterized by potent tumor regressions, high plasma stability and favorable tolerability in non‑human primates, coupled with low systemic levels of free payload," said David Dornan, PhD, Chief Scientific Officer of Whitehawk Therapeutics. "These data support the potential for our next‑generation bioconjugation and proprietary Carbon Bridge Cysteine Re-pairing linker-payload to deliver a differentiated, potentially best-in-class therapeutic index among TOP1i-based ADCs, which is fundamental to realizing the promise of ADCs for patients."

Overview of Preclinical Presentations

"Preclinical assessment of HWK-007, a next-generation, PTK7-targeting ADC with novel bioconjugation and linker-payload technology" (Poster #4439)

HWK-007 targets PTK7, the third most highly expressed tumor marker among clinically validated and emerging ADC targets, present in ~70% of tumors. HWK‑007 is being evaluated in an ongoing Phase 1 clinical trial in patients with non-squamous, EGFR wild-type non-small cell lung cancer; platinum-resistant ovarian cancer; and endometrial cancer (NCT07444814). Key preclinical findings include:

High‑affinity binding and efficient internalization across a range of PTK7 expression levels
Demonstrates potent binding, internalization and tumor cell-killing in a range of solid cancer cell lines
Exhibits bystander activity and produces tumor regressions at doses as low as 1 mg/kg in small cell lung cancer and ovarian cancer models
Demonstrates favorable pharmacokinetics and is well tolerated in non‑human primates with an HNSTD of 60 mg/kg (the maximal dose tested)
Demonstrates high stability with free payload of 0.0067% AUC detected in circulation
"Preclinical assessment of HWK-016, a next-generation, MUC16-targeting ADC with novel bioconjugation and linker-payload technology" (Minisymposium Oral Presentation #1324)

HWK‑016 targets the non‑shed extracellular domain of MUC16 to avoid binding to circulating CA125 and associated antigen sink effects observed with earlier MUC16‑directed ADCs. HWK‑016 is being evaluated in an ongoing Phase 1 clinical trial in patients with advanced ovarian and endometrial cancers (NCT07470853). Key preclinical findings include:

Selectively binds membrane‑bound MUC16 to ensure delivery to the tumor instead of circulating CA125
Demonstrates potent binding, internalization and tumor cell-killing, and is minimally impacted by exogenous CA125
Exhibits bystander activity, and produces tumor regressions at doses as low as 1 mg/kg in ovarian cancer xenograft models that shed high levels of CA125
Demonstrates favorable pharmacokinetics and is well tolerated in non‑human primates with an HNSTD of 60 mg/kg (the maximal dose tested)
Demonstrates high stability with free payload of <0.01% AUC detected in circulation
"Preclinical assessment of HWK-206, a next-generation, biparatopic, SEZ6-targeting ADC with novel bioconjugation and linker-payload technology" (Poster #4440)

HWK‑206 targets SEZ6 with a biparatopic antibody designed to enhance binding, receptor clustering and internalization. Whitehawk plans to submit an Investigational New Drug (IND) application for HWK‑206 in mid-2026 and initiate a Phase 1 clinical trial in Q3 2026. Key preclinical findings include:

Increased binding and internalization compared with a parental monoclonal antibody alone, and compared with clinical-stage ADC, ABBV-706
Greater inhibition of cell viability compared with ABBV-706 in cell lines with varying SEZ6 expression
Produces tumor regressions at doses as low as 2 mg/kg in small cell lung cancer models
Demonstrates favorable pharmacokinetics and is well tolerated in non‑human primates with an HNSTD of 60 mg/kg (the maximal dose tested)
Demonstrates high stability with free payload of 0.01% AUC detected in circulation
More information can be found on the AACR (Free AACR Whitepaper) 2026 meeting website. The posters and presentation will be accessible on the Presentations page of the Investors & News section of the Company’s website at www.whitehawktx.com following presentation at the meeting.

(Press release, Whitehawk Therapeutics, APR 19, 2026, View Source [SID1234664523])