On April 17, 2026 Cogent Biosciences, Inc. (Nasdaq: COGT), a biotechnology company focused on developing precision therapies for genetically defined diseases, reported that preclinical data from the Company’s KRAS and ErbB2 pipeline programs will be presented during poster sessions at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 taking place in April 17-22 in San Diego, CA.

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"As we prepare for the potential launch of bezuclastinib later this year, we are excited to share updates from two of our pipeline programs this weekend at the 2026 annual AACR (Free AACR Whitepaper) meeting," said Andrew Robbins, Cogent’s President and Chief Executive Officer. "First, we are presenting data on CGT1263, our novel pan-KRAS(ON) inhibitor, which shows best-in-class cellular potency along with evidence that its kinase selectivity advantage over multi-RAS inhibitors could drive clinical differentiation with regards to skin toxicity, a current liability of advanced clinical programs. Separately, we provide an update on CGT4255, our novel, selective ErbB2 inhibitor that was specifically designed for its best-in-class CNS penetrant properties to address a significant unmet need for HER2+ patients with brain metastases. This presentation also includes preclinical data in combination with a HER2 ADC suggesting potential synergistic activity leading to improved duration of therapy as well as re-sensitization of patients following HER2 ADC resistance. With multiple potential blockbuster programs advancing in our pipeline, we believe these new data underscore the long-term potential of Cogent Biosciences."

Poster Details

Title: Characterization of CGT1263, a KRAS (ON/OFF) inhibitor clinical candidate with selectivity for mutant KRAS over HRAS and NRAS
Session Category: Experimental and Molecular Therapeutics
Session Title: Novel Antitumor Agents 1
Session Date and Time: April 19, 2026 – 2:00 PM – 5:00 PM PT (5:00 PM – 8:00 PM ET)
Location: Poster Section 17
Poster Board Number: 13
Poster Number: 410

Mutations in KRAS are among the most prevalent mutations found in cancer, occurring most often in colorectal cancer, non-small cell lung cancer and pancreatic cancer. The preclinical poster highlights Cogent’s internally developed pan-KRAS(ON) inhibitor with >500x selectivity for KRAS over HRAS and NRAS. Plasma exposure following oral administration across species resulted in sustained pERK inhibition and robust antitumor activity. Tumor pERK inhibition was also achieved with limited skin suppression, supporting the potential of a larger therapeutic window for CGT1263 when compared to multi-RAS inhibitors currently in clinical development. This aligns with historical data implicating the RAS-MAPK-ERK pathway as essential for skin development given its role in regulation of keratinocyte proliferation, differentiation, and survival; combined suppression of multiple targets within this pathway is thought to be the driver of frequent rash observed in patients treated with multi-RAS inhibitors. Overall, these findings suggest CGT1263 could provide an advantage for patients, enabling higher dosing designed to elicit a more profound molecular response. Investigational New Drug (IND) enabling studies are ongoing with an IND submission expected later this year.

Title: Preclinical characterization of CGT4255, an EGFR sparing, pan-mutant HER2 clinical development candidate with potential best-in-class brain penetration
Session Category: Experimental and Molecular Therapeutics
Session Title: Tyrosine Kinase, Phosphatase, and Other Inhibitors
Session Date and Time: April 21, 2026 – 2:00 PM – 5:00 PM PT (5:00 PM – 8:00 PM ET)
Location: Poster Section 18
Poster Board Number: 7
Poster Number: 5869

Cogent’s EGFR-sparing, brain-penetrant ErbB2 inhibitor includes potent coverage of key mutations (YVMA, S310F, V842I, L755S) inadequately addressed by currently approved therapies. Activating mutations in the ErbB2 gene have been identified in multiple cancers and demonstrate a tumorigenic role similar to that of ErbB2 amplification. New data presented describe CGT4255’s >100-fold selectivity over EGFR while robustly engaging HER2 amplification, insertion and mutant lines in addition to reinforcing best-in-class potential CNS performance relative to other agents in development. Additional mechanistic studies presented suggest CGT4255 may have synergistic effects on efficacy and durability when combined with HER2 targeted ADCs. Preclinical evidence demonstrates that concurrent treatment of CGT4255 and T-DXd enhances receptor internalization and cancer cell apoptosis, suggesting the potential for a synergistic combination that could improve patient outcomes. The Phase 1 study of CGT4255 is ongoing.

Posters will be available on the ‘Posters and Publications’ page of Cogent’s website.

(Press release, Cogent Biosciences, APR 17, 2026, View Source [SID1234664468])

On April 17, 2026 Asgard Therapeutics, a privately held biotech company pioneering in vivo direct cell reprogramming for cancer immunotherapy, reported that it will be presenting a poster on its lead asset AT-108 at the AACR (Free AACR Whitepaper) Annual Meeting, held in San Diego, California, US, from 17-22 April 2026.

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AT-108 is a transformative gene therapy utilizing Asgard’s in vivo cell reprogramming technology to directly reprogram tumor cells into dendritic cells. This approach forces these tumor cells to present their tumor antigens, ultimately leading to a personalized anti-tumor immune response. Asgard is progressing its first-in-class therapy toward clinical development, with a focus on solid tumors, and is advancing IND-enabling studies and CMC development.

The poster presentation, titled ‘Preclinical efficacy and biomarker characterization of AT-108, a first-in-class in situ tumor-to-dendritic cell reprogramming agent’, will detail preclinical data demonstrating that AT-108 induces systemic, dose-dependent efficacy with broad tumor activity. Key biomarker parameters were highlighted to be explored in future clinical development.

Details of the poster presentation are as follow:

Poster title: Preclinical efficacy and biomarker characterization of AT-108, a first-in-class in situ tumor-to-dendritic cell reprogramming agent

Presenter: Fabio Rosa, Asgard Therapeutics

Authors: Fritiof Åkerström1, Xavier Catena1, Marta Santiago2, Ana Perego1, Ruixian Liu1, Arun Sundaramurthy1, Lihan Xie1, Emilie Renaud1, Andreea-Medeea Matei1, Xiaoli Huang1, Emma Leire1, Ozcan Met2, Inge-Marie Svane2, Shane Olwill1, Cristiana Pires1, Filipe Pereira3, Fabio Rosa1

Poster session: Session LBPO.ET04 – Late-Breaking Research: Experimental and Molecular Therapeutics 4

Session date and time: 22 April, 2026, 9:00 AM – 12:00 PM PDT

Location: Section 53

Poster number: LB455 / 2

1Asgard Therapeutics AB, Lund, Sweden,2National Center of Cancer Immune Therapy (CCIT-DK), Department of Oncology, Copenhagen University Hospital, Copenhagen, Denmark,3Molecular Medicine and Gene Therapy, Lund Stem Cell Centre, Lund University, Lund, Sweden

The abstract is available to view via the AACR (Free AACR Whitepaper) online planner.

(Press release, Asgard Therapeutics, APR 17, 2026, View Source [SID1234664467])

On April 17, 2026 Adagene Inc. ("Adagene") (Nasdaq: ADAG), a company transforming the discovery and development of novel antibody-based therapies, reported new data from two ongoing Phase 1b/2 studies of muzastotug in triple combination regimens at the American Association of Cancer Research (AACR) (Free AACR Whitepaper) annual meeting 2026, held April 17-22 in San Diego. Results support muzastotug’s mechanistic advantages over traditional anti-CTLA-4 therapies, and its continued development as a potential backbone therapy in combination regimens for difficult-to-treat cancers. FDA has previously designated muzastotug in combination with Merck’s (known as MSD outside of the United States and Canada) anti-PD-1 therapy, KEYTRUDA (pembrolizumab), as a Fast Track product for adult patients with microsatellite stable metastatic colorectal cancer (MSS mCRC) without current or active liver metastases.

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"At AACR (Free AACR Whitepaper), Adagene shared new data from two triplet regimens supporting muzastotug’s potential as a combination backbone for multiple tumor types, said Peter Luo, Ph.D., CEO and President of R&D at Adagene. In HCC, adding muzastotug to the atezolizumab plus bevacizumab combo resulted in higher efficacy, with a safety profile consistent with historical studies of the doublet alone. In MSS CRC, adding muzastotug to pembrolizumab plus fruquintinib showed dose-dependent response rates, with no DLTs or Grade 4 or 5 treatment related adverse events. As muzastotug continues to generate more data in additional settings, we are increasingly convinced that its intentionally designed wider therapeutic index has potential to improve the efficacy of current immunotherapies without worsening the toxicity for patients with difficult to treat solid tumors."

Final copies of the two posters from AACR (Free AACR Whitepaper) can be found on the Pipeline Publications section of the company’s website.

AACR Poster Presentations

Abstract CT054

The MORPHEUS-Liver study (NCT04524871) is a Phase 1b/2 open-label randomized umbrella study designed to evaluate immunotherapy-based combinations as first line therapy in patients with locally advanced or metastatic hepatocellular carcinoma (HCC). As of July 11, 2025, six patients had been randomized to the triple combination of muzastotug (6 mg/kg Q6W), atezolizumab and bevacizumab and 40 patients had received atezolizumab and bevacizumab in the active control arm. Interim results from patients in the muzastotug arm (18.8 months median duration of follow-up) demonstrated a 66.7% overall response rate (ORR; 4/6) using HCC-specified modified RECIST v1.1 criteria1. ORR was 50.0% (3/6) using RECIST v1.1 criteria. The median progression free survival (mPFS) was 8.2 months (same for both RECIST criteria) and the median overall survival (mOS) was not yet reached at the data cut but was greater than 22 months.

These results compared favorably to the 40 patients in the active control arm (17.2 months median duration of follow-up) that demonstrated an ORR of 32.5% (13/40) using HCC-specified modified RECIST v1.1 criteria, mPFS of 5.5 months, and mOS of 17.5 months. Using RECIST v1.1 criteria, the ORR was 17.5% (7/40) and the mPFS was 4.3 months. The mOS in the doublet control arm was largely overlapping with that reported in the IMbrave150 Phase 3 study2,3 (19.2 months), which served as the basis for approval of atezolizumab (Tecentriq) for HCC in 20204.

The triplet regimen of muzastotug, atezolizumab and bevacizumab was well-tolerated with safety data comparable to the doublet active control arm of atezolizumab and bevacizumab. Grade 3 or greater TRAEs were 50% (3/6) in the muzastotug arm and 45% (18/40) in the active control arm, which supports the potential for continuous dosing with muzastotug. Muzastotug was safely administered continuously at 6 mg/kg Q6W in a triplet setting, which is twice the dose of ipilimumab in the currently approved HCC doublet regimen, (capped at 3 mg/kg Q3W for only 4 cycles)5. In addition, encouraging durability was observed with responses maintained beyond 84 weeks in some patients. Ongoing muzastotug plus atezolizumab treatment after bevacizumab discontinuation suggests potential flexibility to modify individual agents during safety-related interruptions while preserving durable clinical benefit.

Abstract CT083

A Phase 1b/2 single arm study (NCT05405595) is evaluating the triple combination of muzastotug, pembrolizumab and fruquintinib in patients with advanced and metastatic microsatellite stable (MSS) colorectal cancer (CRC). As of February 21, 2026, nine patients have been treated with the triple combination — four (4) patients at a dose of 10 mg/kg every 6 weeks (Q6W) of muzastotug and five (5) patients at a dose of 15 mg/kg Q6W of muzastotug. All patients were without liver metastases (NLM). Interim results demonstrated a 25% ORR (1/4) among patients in the 10 mg/kg arm (6.7 months median follow-up), and a 40% ORR (2/5) among patients in the 15 mg/kg arm (5.9 months median follow-up).

The triplet regimen was well-tolerated with no new safety signals relative to known CTLA-4, PD-1, and fruquintinib monotherapy and combination safety data. There were no dose-limiting toxicities, 25 – 60% Grade 3 TRAEs, and no Grade 4 or Grade 5 TRAEs. Given that fruquintinib is known to be active in MSS CRC patients with liver metastases, the triple combination may have therapeutic benefit beyond the NLM population being evaluated in this study.

(Press release, Adagene, APR 17, 2026, View Source [SID1234664466])

On April 17, 2026 Abbott (NYSE: ABT) reported it will present new data at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 demonstrating continued advancements in its multi-biomarker, multi-cancer early detection (MCED) program supporting the commercially available Cancerguard test. Additionally, the AACR (Free AACR Whitepaper) Cancer Prevention Research Award for Outstanding Journal Article will recognize a publication on MCED multiyear outcomes from the DETECT-A study.

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Multi-biomarker approach enables broader and earlier cancer detection
New data demonstrate how combining methylation (M) and protein (P) biomarkers improves cancer detection across stages, with each biomarker contributing independently to overall performance. Cancerguard is currently the only commercially available MCED test designed with a multi-biomarker class approach, combining methylation and protein signals to improve detection.

In a prospectively collected case-control study, nearly half of positive cancer signals were driven by methylation alone (47.1%), with additional detection from protein-only (7.4%) and combined biomarker signals (45.5%), supporting broader detection across cancer types and stages.1 In early-stage disease, many cancer signals were detected by a single biomarker class, demonstrating how each contributes uniquely to overall detection. Notably, none of the 2.6% false-positive results were positive for both biomarkers.1

"We designed Cancerguard as the first-of-its-kind multi-biomarker test because no one signal tells the whole story," said Tom Beer, M.D., chief medical officer, multi-cancer early detection, Abbott’s cancer diagnostics business. "By combining biomarkers, we can detect cancer earlier, when it matters most."

AACR recognizes impactful MCED research with journal award
The AACR (Free AACR Whitepaper) Cancer Prevention Research Award for Outstanding Journal Article will be presented to the authors of a 2024 Cancer Prevention Research publication reporting multi-year outcomes from the DETECT-A study, the first large prospective interventional trial of a blood-based MCED test. The study identified nine cancer types, including several without routine screening, and showed that, after a median follow-up of approximately four years, all patients treated for stage I or II cancers remained alive and cancer-free.2,3

The award recognizes the significance of these multi-year outcomes data in advancing evidence for the clinical impact of MCED, an area where long-term outcomes data have historically been limited.

"Long-term follow-up provides critical insight into how multi-cancer early detection can shape the future of cancer screening," said Beer. "With nearly 70 percent of cancers occurring in types without recommended screening, these findings highlight the potential for MCED to increase early detection and improve outcomes."4

About the DETECT-A study
The DETECT-A (Detecting cancers Early Through Elective mutation-based blood Collection and Testing) study was the first-ever large, prospective, interventional study to use a blood test to detect multiple types of cancer in a real-world setting. The DETECT-A study enrolled more than 10,000 women with no history of cancer to determine if a blood test in combination with standard-of-care screenings could detect cancers before signs and symptoms appeared. The CancerSEEK test, the MCED test studied in DETECT-A, was the forerunner to the Cancerguard test.

About the Cancerguard test
Cancerguard is a laboratory-developed test (LDT) designed to detect multiple cancers, including the most aggressive cancers, in early stages from a simple blood draw. It integrates two classes of biomarkers to enable broader detection and follows a streamlined, imaging-based diagnostic pathway to help reduce unnecessary follow-up procedures. Developed with high specificity to minimize false positives, the test helps detect a wide range of cancers, including those that lack guideline-recommended screening options.5 The Cancerguard test has not been cleared or approved by the U.S. Food and Drug Administration or any other regulatory authority. To learn more, visit cancerguard.com.

(Press release, Abbott, APR 17, 2026, View Source [SID1234664465])

On April 16, 2026, Rigel Pharmaceuticals, Inc. ("Rigel") reported to have received written notice from Eli Lilly and Company ("Lilly") of Lilly’s election to terminate that certain License and Collaboration Agreement, dated February 18, 2021 (the "Agreement"), between Rigel and Lilly.

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Pursuant to the terms of the Agreement, Lilly has elected to terminate the Agreement in its entirety. The termination will become effective June 15, 2026.

The Agreement granted Lilly an exclusive worldwide license to develop and commercialize ocadusertib (previously R552), an investigational, potent and selective receptor interacting serine/threonine protein kinase 1 ("RIPK1") inhibitor, for the treatment of non-central nervous system ("non-CNS") diseases, and additional RIPK1 inhibitors for the treatment of central nervous system ("CNS") diseases. The Agreement also provided for collaboration between the parties on development activities, as well as potential milestone payments and royalties to Rigel.

Following the effective date of termination, the Agreement will terminate in accordance with its terms, including the cessation of Lilly’s rights to the licensed compounds, subject to any applicable transition provisions. Rigel expects to regain full rights to the licensed compounds and related programs upon termination.

Rigel is currently evaluating the impact of the termination. Following termination of the Agreement, including the prior termination of the CNS disease program under the Agreement, effective in November 2025, the Company does not expect to receive future milestones or royalties under the Agreement.

(Filing, Rigel, APR 16, 2026, View Source [SID1234664622])