On April 22, 2026 Flatiron Health reported its presence at the ISPOR—The Professional Society for Health Economics and Outcomes Research Annual Meeting happening from May 17-20, 2026, in Philadelphia, Pennsylvania. Flatiron’s high-quality real-world data and innovative research capabilities are featured across 18+ research acceptances, including seven Flatiron authored research posters as well as a panel presentation "Beyond Black Boxes: Transparent, Validated LLM Workflows for Accelerating Global HTA Submissions and Decisions."

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Flatiron’s presence at ISPOR 2026 closely follows the publication of the Validation of Accuracy for LLM/ML-Extracted Information and Data (VALID) Framework in the Journal of Clinical Oncology Clinical Cancer Informatics.The framework represents the first and most comprehensive, peer-reviewed approach to evaluating the quality and reliability of real-world data extracted by large language models and machine learning—establishing new industry standards for data integrity in oncology research.

"The rapid advancements of large language models and AI-enabled tools have required an incredibly thoughtful approach to data validation and research methodologies," said Emily Castellanos, MD, MPH, Senior Medical Director and Head of Research Oncology at Flatiron Health. "Flatiron’s presence at ISPOR reflects our commitment to advancing the field with high-fidelity, decision-ready real world evidence, reinforcing our position as the gold standard in oncology intelligence and a trusted partner for high-stakes clinical and research decisions."

Research highlights include:

Research assessing an LLM-approach that integrates PSA and imaging data to derive real-world progression events in prostate cancer with accuracy and completeness
A study building and evaluating four different digital-twin modeling approaches to predict survival in patients with advanced non-small cell lung cancer
An application of the newly published VALID framework to assess quality of an LLM-derived prostate cancer real-world dataset
A collaborative pilot project led by Friends of Cancer Research that demonstrated success of real-world data supported external-control arms depends on the quality of data, consistent methodology, and attentive planning.
Join Flatiron Health at booth #316 Follow Flatiron Health on X and LinkedIn for more updates from #ISPORAnnual.

Speaking Sessions

Beyond Black Boxes: Transparent, Validated LLM Workflows for Accelerating Global HTA Submissions and Decisions
Moderator: Beth Devine
Speakers: Bill Malcolm, Tim Reason, Lockwood Taylor
Speaking Session Date/Time: Wednesday, May 20, 10:00–11:00 AM ET

Abstracts and Poster Presentations

Assessing quality of a LLM-derived prostate cancer (PC) real-world dataset: an application of the validation of accuracy for LLM/ML-extracted information and data (VALID) framework
Patrick J. Ward, Yunzhi Qian, Eunice A. Hankinson, Aaron Dolor, Melissa Estevez
Poster Session: Poster Session 2
Poster Code: MSR65
Poster Session Date/Time: Monday, May 18, 4:00 PM – 7:00 PM

Real-world treatment patterns and outcomes in patients with =2 lines of therapy for recurrent or progressive endometrial cancer
Rachel Bhak, Neeraj N. Iyer, Audrey Hopkins, Murat M. Ikiisik, Edward Kavalerchik, Mala Talekar, Xinye Li, Nada Boualam, Prakirthi Yerram, Fernanda Musa
Author affiliations: Genmab, Providence-Swedish Cancer Institute, Flatiron Health
Poster Session: 2
Poster Code: HSD38
Poster Session Date/Time: Monday, May 18, 4:00 PM – 7:00 PM

Impact of telemedicine encounters on survival outcomes: A time-varying cox analysis using EHR-derived data
Deepika Paratane, Blythe Adamson, Antal T. Zemplenyi
Author affiliations: University of Colorado Skaggs School of Pharmacy and Pharmaceutical Sciences, Flatiron Health
Poster Session: 3
Poster Code: HSD60
Poster Session Date/Time: Monday, May 18, 10:30 – 1:30 PM

Customization of a large language model approach to capture PSA and imaging derived real-world progression events in prostate cancer
Kelly Magee, Patrick Ward, PhD, Wanjing Chen, Eunice Hankinson, Aaron Dolor
Poster Session: Poster Session 4
Poster Code: RWD123
Poster Session Date/Time: Tuesday, May 19, 4:00 PM – 7:00 PM

Evaluating model performance for between-country survival transportability
Mohamed S. Ali, Harlan Pittell, Elsie Horne, Philani Mpofu, Qianyi Zhang, Blythe Adamson
Poster Session: Poster Session 4
Poster Code: MSR169
Poster Session Date/Time: Tuesday, May 19, 4:00 PM – 7:00 PM

From real-world data (RWD) to digital twins: Building models for patient-level counterfactual prediction in oncology
Sandra Griffith, Joe Manfredonia, Marcello Ricottone, Richard Knoche, Aaron B. Cohen, Jacqueline Law, Melissa Estevez
Poster Session: Poster Session 5
Poster Code: MSR219
Poster Session Date/Time: Wednesday, May 20, 9:00 AM – 11:30 AM

External control arm feasibility across external data sources in oncology: Methodological and regulatory considerations
Bernat Navarro, Kawther Abdilleh, Amy Alabaster, Peter Ansell, Li Chen, Gregory S. Calip, Ruthanna Davi, Janet Espirito, Laura L. Fernandes, Sebastian Zavala Hoffmann, Patricia Luhn, Xinran Ma, Patricia Prince, Mark Riffon, Xiang Yin, Mark Stewart, Hillary Andrews, Jeff Allen
Author Affiliations: Friends of Cancer Research, Pancreatic Cancer Action Network, ConcertAI, AbbVie, Amgen, Medidata, Ontada, COTA Healthcare, iOMEDICO, Genentech, Flatiron Health, Aetion/Datavant, American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper)
Poster Session: Poster Session 5
Poster Code: RWD154
Poster Session Date/Time: Wednesday, May 20, 9:00 AM – 11:30 AM

(Press release, Flatiron Health, APR 22, 2026, View Source [SID1234664706])

On April 22, 2026 Vyome Holdings, Inc. ("Vyome") (Nasdaq: HIND) reported its full Phase 2 investigator initiated study results and preclinical data supporting the efficacy and safety of VT-1953 as a potential treatment for symptoms of Malignant Fungating Wounds (MFW) at the 2026 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting in San Diego, on April 21, 2026.

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MFWs are non-healing wounds that occur in ~10% of advanced cancer patients (~65K patients in the U.S. alone each year). Patients suffer symptoms such as severe ‘rotten meat’ malodor, pain, which negatively impacts quality of life. Patients feel ashamed of the malodor and socially withdraw. There are currently no FDA approved drugs to treat these symptoms of MFW.

Vyome is developing VT-1953 as a first in class treatment for symptoms of MFW. VT-1953 acts by dual mechanism of action, inhibiting DNA Gyr and modulating MD2/TLR interactions, an inflammatory signal. In the Ph2 study, advanced cancer patients with MFW who scored at a median 0.5 (corresponding to extreme malodor that is detected 6-10ft away with dressing on) at start of treatment with VT-1953 improved (P=0.0020) to a median score of 4 (mild odor detectable up close only after removing dressing) by Day 14 on a TELER scale of 0-5 scored by clinical investigator (Primary endpoint). MFW patients treated with the vehicle as a control arm showed no improvement in malodor (median score remained the same on Day 14 as Day 1; P=0.9999). VT-1953 treatment was significantly superior to the control arm (P = 0.0015).

On a secondary endpoint, where patients were asked to score the impact of malodor on their life, 70% of patients treated with VT-1953 reported an improvement to a score range of 3 to 5 by Day 14 from a baseline score of 0, as compared with 0% of patients in the vehicle-treated arm (P = 0.0256).

Patients were also asked to score the level of malodor on a 10-point visual analog scale, where 0 was no smell, while 10 was the worst smell. Treatment with VT-1953 gel treatment group improved the median score from 7.5 at the start of treatment to 2.5 by Day 14, a significant improvement (p=0.0020) from baseline. Patients treated with the vehicle reported an increase (worsening) in median malodor score from 6.0 at baseline to 7.0 by Day 14 (p=0.0625). Patients treated with VT-1953 also reported a clinically significant 2-point improvement in lesion pain by Day 14 (p= 0.0020) as scored using a 10-point VAS scale, while patients treated with vehicle reported no improvement from baseline score. Treatment did not change exudate levels. There were no treatment-associated adverse effects reported.

"These compelling Phase 2 results, where treatment with VT-1953 resulted in clinically meaningful improvements in malodor and pain symptoms associated with MFW and quality of life of patients, provide a strong rationale to advance VT-1953 into registrational studies. To be able to be close to loved ones rather than socially withdraw due to the shame of malodor can be meaningful to a cancer patient," said Dr. Shiladitya Sengupta, co-founder of Vyome and associate professor of medicine at Harvard Medical School.

"We are delighted with the Phase 2 data," said Venkat Nelabhotla, CEO of Vyome. "The highly statistically significant results, far exceeding the standard threshold of P<0.05, offer us a high degree of confidence as we design the registrational studies. It also means we need fewer patients to power the study. VT-1953 can be a transformative treatment for patients with MFW, who currently have no FDA-approved choices. Recent independent third-party analysis estimates the total addressable U.S. MFW market to be approximately USD 2.2 billion. We are pleased to have presented this data at the prestigious AACR (Free AACR Whitepaper) conference."

(Press release, Vyome Therapeutics, APR 22, 2026, View Source [SID1234664705])

On April 22, 2026 A2 Biotherapeutics, Inc. (A2 Bio), a clinical-stage immunotherapy company developing first-in-class logic-gated therapies for solid tumors, reported the acceptance of three abstracts for presentation during the 2026 Annual Meeting of the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) taking place May 29 – June 2, 2026, in Chicago.

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A2 Bio will present two posters from the ongoing phase 1/2 EVEREST-2 study: The first provides the safety and efficacy of A2B694, a logic-gated mesothelin (MSLN)-targeted Tmod chimeric antigen receptor T-cell (CAR T) therapy. The second is a trials-in-progress poster about A2B543, which uses the same logic-gated construct as A2B694 but also includes a membrane-tethered IL-12 booster. A third poster describes modules based on IL-12 and other molecules that boost potency and preserve selectivity of Tmod-based precision cell therapies. Titles of accepted abstracts are available online on the ASCO (Free ASCO Whitepaper) website.

Poster Presentation Details

Abstract Title

Presenting Author

Abstract Number

Poster Board Number

Poster Presentation Date/Time

Poster Session

Initial safety and efficacy of A2B694, a logic-gated mesothelin (MSLN)-targeted Tmod chimeric antigen receptor T-cell (CAR T) therapy in patients with advanced solid tumors with HLA-A*02 loss of heterozygosity (LOH)

Julian R. Molina, M.D., Ph.D.

Mayo Clinic

Rochester, Minn.

8579

369

Sunday, May 31, 2026

9:00 AM-12:00 PM CDT

Lung Cancer—Non-Small Cell Metastatic

A logic-gated chimeric antigen receptor T-cell (CAR T) therapy with an armored, membrane-tethered IL-12 booster in patients with advanced solid tumors with HLA-A*02 loss of heterozygosity (LOH): EVEREST-2, a Phase 1/2 study

Salman R. Punekar, M.D.

NYU Langone Health

New York

TPS2673

459a

Saturday, May 30, 2026

1:30 PM-4:30 PM CDT

Developmental Therapeutics— Immunotherapy

Influence of onboard, tethered IL-12 on potency of the Tmod NOT gate and selectivity

Jushen Liang

A2 Biotherapeutics,

Agoura Hills, Calif.

2562

352

Saturday, May 30, 2026

1:30 PM-4:30 PM CDT

Developmental Therapeutics— Immunotherapy

About EVEREST-2

The EVEREST-2 master protocol (NCT06051695) is a seamless Phase 1/2 study evaluating the safety and efficacy of A2B694 (Arm 1) and A2B543 (Arm 2), autologous logic-gated investigational cell therapies developed from the A2 Bio proprietary Tmod platform. The Tmod platform provides selective killing of tumor cells and protection of normal cells via a dual-receptor design consisting of an activator that targets tumor cells and a blocker that protects normal cells. A2B694 consists of an activator that targets MSLN and a blocker that targets HLA-A*02. HLA-A*02 is lost in tumor cells and present in normal cells in the eligible patient population. A2B543 contains the same Tmod construct as A2B694 with an added mem-IL-12 booster. The EVEREST-2 study is recruiting patients with colorectal cancer, pancreatic cancer, non-small cell lung cancer, ovarian cancer, mesothelioma, and other solid tumors that express MSLN and have lost HLA-A*02 expression.

About the Tmod Platform

Invented at A2 Bio, the Tmod platform is a precision-targeting cellular system, designed with logic-gate technology to enable immune cells to unequivocally differentiate tumors from normal tissues. The system consists of activator and blocker receptors. The activator recognizes antigens on tumor cells and triggers their destruction, while the blocker recognizes antigens on normal cells and protects them. This novel blocker technology enables precise, personalized, and effective T-cell targeting specifically against tumors.

For more information about A2 Bio clinical studies and how to enroll, visit www.a2bioclinicaltrials.com.

(Press release, A2 Biotherapeutics, APR 22, 2026, View Source [SID1234664704])

On April 22, 2026 Fulgent Genetics, Inc. (NASDAQ: FLGT) ("Fulgent" or the "Company"), a technology-based company with a well-established laboratory services business and a therapeutic development business, reported that its abstract was selected to be presented within the Head and Neck Cancer Track of the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) rapid oral abstract session on June 1, 2026, from 4:30pm to 6:00pm (CDT) in hall D1 of McCormick Place, Chicago.

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The abstract is entitled "FID-007 in combination with cetuximab in recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC)", clinical trial identifier, NCT06332092. This is a Phase 2 study designed to evaluate the efficacy of different dosing regimens as well as to characterize the pharmacokinetics (PK) and safety and tolerability of FID-007 in combination with cetuximab in patients with disease progression after treatment with PD-L1-based immune checkpoint inhibitor.

Ming Hsieh, Chairman of the Board of Directors and Chief Executive Officer, said, "We are honored to be selected by ASCO (Free ASCO Whitepaper) to present our findings on the interim data of our Phase 2 results for FID-007. We are encouraged by the clinical progress achieved so far and believe in the potential of FID-007 for the treatment of (R/M) HNSCC patients, currently having very few effective treatment options."

Details of the presentation are as follows:

Abstract Title: FID-007 in combination with cetuximab in recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC).

Session: Head and Neck Cancer Track Rapid Oral Abstract Session from 4:30pm to 6pm (CDT) within hall D1 of McCormick Place, Chicago.

Presenter: Guilherme Rabinowits, MD, senior member of the Head and Neck-Endocrine Oncology Department at Moffitt Cancer Center.

Authors: Guilherme Rabinowits, Christine H. Chung, Aditya Shreenivas, Eric S. Nadler, Donald A. Richards, Nabil F. Saba, Ray Yin, Jorge J. Nieva, Jacob S. Thomas.

Presentation Date and Time: Monday, June 1, 2026, from 4:30pm to 6:00pm.

Presentation Type: Rapid Oral Abstract Session within the Head and Neck Cancer Track Session.

Abstract #6020.

The abstract will be available on the ASCO (Free ASCO Whitepaper) website on May 21, 2026, at 5:00pm EST. The full presentation will be available on Fulgent’s investor relations website at the start of the session.

(Press release, Fulgent Genetics, APR 22, 2026, View Source [SID1234664703])

On April 22, 2026 Abbisko Therapeutics (HKEX: 02256) reported that the company presented six latest preclinical and translational research findings in poster sessions at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, held from April 17 to 22, 2026, in San Diego, USA.

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The presentations span multiple key innovation areas, including the pan-KRAS inhibitor ABSK211, the 4th generation EGFR inhibitor ABK-EGFR-1, the CDK4 selective inhibitor ABK-CDK4, the MTA-cooperative PRMT5 inhibitor ABSK131, as well as a ctDNA-based study investigating resistance mechanisms to the FGFR2/3 inhibitor ABSK061.

pan-KRAS Inhibitor ABSK211

ABSK211 is a potent, highly selective, and orally bioavailable small-molecule pan-KRAS inhibitor developed by Abbisko Therapeutics. It demonstrates broad inhibitory activity against multiple KRAS mutations, addressing significant unmet medical needs in KRAS-driven cancers. At AACR (Free AACR Whitepaper) 2026, Abbisko presented preclinical data for both monotherapy and combination strategies of ABSK211.

Monotherapy: Broad and Potent Inhibition Across KRAS Mutations

KRAS mutations are highly prevalent across multiple cancers, including pancreatic (~90%), colorectal (~35%), and lung cancer (~25%). While several pan-KRAS inhibitors have entered clinical development, there remains a critical need for enhanced potency.

In preclinical studies, ABSK211 demonstrated:

Robust in vitro activity: ABSK211 significantly reduced cell viability across multiple KRAS alterations (including G12, G13, Q61, and WT amplification) at sub-nanomolar to nanomolar concentrations. Meanwhile ABSK211 displayed marginal inhibition in KRAS wild-type cell line with normal copy.
Strong in vivo efficacy: Oral administration induced deep tumor regression in multiple KRAS G12V xenograft models, with robust target engagement.
Broad mutation coverage: Consistent and significant antitumor activity was observed in models harboring KRAS G12D/C/S and G13D mutations.
These findings support the clinical advancement of ABSK211, which is currently undergoing IND-enabling studies.

Poster Information

Title: Preclinical characterization of ABSK211: A highly potent, orally bioavailable and selective pan-KRAS inhibitor with broad and robust activity in KRAS-driven tumors
Time: April 22, 2026, 9:00 AM – 12:00 PM (PT)
Location: Poster Section 13, Board #10
Abstract #: 7090
Combination Therapy: Multi-Mechanistic Synergy Enhances Antitumor Activity

Combination therapy is widely considered a key strategy to improve treatment outcomes in KRAS-mutant cancers. ABSK211 demonstrated synergistic antitumor activity with multiple therapeutic agents:

In vitro synergy: Significant anti-proliferative synergy with PRMT5 inhibitors across KRAS mutations; strong synergy observed with EGFR monoclonal antibodies and chemotherapy in KRAS G12D/G12V models.
Enhanced in vivo efficacy: Combination regimens with PRMT5 inhibitors, cetuximab, immunotherapies, and chemotherapy showed superior tumor growth inhibition and improved durability compared to monotherapy.
These results demonstrate that ABSK211 can significantly enhance antitumor efficacy through multi-mechanistic synergy, supporting its further development in combination strategies.

Poster Information

Title: ABSK211, a highly potent and orally available pan-KRAS inhibitor, demonstrates robust antitumor efficacy in combination with multiple agents
Time: April 22, 2026, 9:00 AM – 12:00 PM (PT)
Location: Poster Section 13, Board #3
Abstract #: 7083
4th Generation EGFR Inhibitor ABK-EGFR-1

ABK-EGFR-1 is a novel 4th generation EGFR inhibitor developed by Abbisko Therapeutics, specifically designed to target the EGFR C797S resistance mutation. It combines high selectivity with central nervous system (CNS) penetration to address key clinical challenges following resistance to 3rd generation EGFR TKIs.

Targeting C797S-Mediated Resistance

The EGFR C797S mutation is a clinically validated mechanism of resistance to third-generation EGFR TKIs, with an estimated 51,000–146,000 cases annually worldwide. Currently, no approved therapies specifically target this mutation, representing a significant unmet clinical need. Preclinical studies showed that ABK-EGFR-1:

Exhibits high selectivity over wild-type EGFR and other kinases.
Demonstrates significant in vivo antitumor activity in multiple EGFR C797S-driven xenograft models, effectively inhibiting tumor growth.
Possesses excellent blood-brain barrier penetration and favorable drug-like properties.
These findings support further development of ABK-EGFR-1 as a next-generation targeted therapy for EGFR-resistant cancers, particularly for patients with brain metastases.

Poster Information

Title: Discovery and characterization of ABK-EGFR-1, a 4th generation EGFR C797S Inhibitor with excellent selectivity and brain penetration
Time: April 21, 2026, 2:00 PM – 5:00 PM (PT)
Location: Poster Section 53, Board #7
Abstract #: LB350
CDK4 Selective Inhibitor ABK-CDK4

ABK-CDK4 is a highly selective, brain-penetrant small-molecule CDK4 inhibitor developed by Abbisko Therapeutics. It is designed to selectively target CDK4, reduce CDK6-related toxicity, and expand treatment potential for patients with brain metastases.

Differentiation Through Selectivity and CNS Penetration

1st generation CDK4/6 inhibitors (e.g., palbociclib, ribociclib, and abemaciclib) have demonstrated clinical benefit in breast cancer, but CDK6 inhibition is associated with dose-limiting hematologic toxicities. In addition, 20–40% of breast cancer patients develop brain metastases, while current therapies have limited CNS exposure.

Preclinical studies showed that ABK-CDK4:

High selectivity: Over 50-fold selectivity for CDK4 versus CDK6, potentially reducing CDK6-related toxicity.
CNS penetration: Favorable CNS exposure (Kpuu > 0.5) and drug-like properties.
Antitumor activity: Effective inhibition of Rb phosphorylation and tumor growth in HR+/HER2− breast cancer models
These results suggest that ABK-CDK4 may overcome key limitations of current CDK4/6 inhibitors and provide a differentiated therapeutic option.

Poster Information

Title: Discovery of ABK-CDK4, a selective and brain-penetrant CDK4 inhibitor
Time: April 20, 2026, 9:00 AM – 12:00 PM (PT)
Location: Poster Section 20, Board #13
Abstract #: 1905
MTA-cooperative PRMT5 inhibitor ABSK131

ABSK131 is a potent and selective small-molecule MTA-cooperative PRMT5 inhibitor developed by Abbisko Therapeutics, targeting MTAP-deleted tumors, and is currently in clinical development.

Broad Synergy Across Multiple Therapeutic Modalities

MTAP homozygous deletion occurs in approximately 10–15% of solid tumors and frequently co-exists with oncogenic drivers such as KRAS and EGFR. In addition, MTAP abnormities are associated with poor prognosis following standard-of-care therapies across multiple cancer types. Therefore, there remains a significant unmet need for novel and effective combination therapies centered on MTA-cooperative PRMT5 inhibitor for MTAP-deleted tumors, with the potential to enable precision patient stratification and deliver synergistic therapeutic benefits.

Preclinical studies demonstrated that ABSK131 exhibits strong synergistic activity with multiple therapies:

KRAS inhibitors: Enhanced tumor growth inhibition in KRAS-mutant, MTAP-deleted models when combined with AMG 510 or ABSK141.
EGFR inhibitors: Improved anti-proliferative and in vivo antitumor activity in EGFR-mutant, MTAP-deleted NSCLC models when combined with osimertinib.
MAT2A inhibitors: Consistent synergistic effects across multiple tumor models when combined with IDE397.
Chemotherapy: Synergistic activity observed both in vitro and in vivo when combined with carboplatin in NSCLC models.
These findings support ABSK131 as a potential backbone therapy for combination strategies in MTAP-deleted tumors.

Poster Information

Title: Synergistic antitumor activity of the MTA-cooperative PRMT5 inhibitor ABSK131 in combination with multiple therapeutic agents in diverse cancer models
Time: April 21, 2026, 9:00 AM – 12:00 PM (PT)
Location: Poster Section 14, Board #23
Abstract #: 4504
FGFR2/3 Inhibitor ABSK061

ABSK061 is a highly potent and selective small-molecule FGFR2/3 inhibitor developed by Abbisko Therapeutics. It has demonstrated encouraging efficacy and safety in Phase I studies and is currently being evaluated in a Phase II trial for gastric cancer.

ctDNA Analysis Reveals Resistance Mechanisms

Acquired resistance remains a major challenge limiting the long-term benefit of targeted therapies. Using ctDNA-based next-generation sequencing (NGS), Abbisko conducted longitudinal genomic analyses comparing baseline and progression samples to elucidate resistance mechanisms to ABSK061:

On-target resistance: Polyclonal acquired FGFR2 mutations in the FGFR2 kinase domain were commonly observed in gastric cancer and cholangiocarcinoma.

Off-target resistance: FGFR2-Atered NSCLC was prone to develop acquired alterations in genes involved in RTK/RAS pathways.

These findings provide important molecular insights into resistance mechanisms and inform the design of future combination and sequential treatment strategies.

Poster Information

Title: Circulating tumor DNA (ctDNA)-based profiling of acquired resistance to the fibroblast growth factor receptor (FGFR)2/3 inhibitor lavengratinib(ABSK061) in patient(pt)s with advanced solid tumors
Time: April 21, 2026, 9:00 AM – 12:00 PM (PT)
Location: Poster Section 45, Board #14
Abstract #: 5319

At AACR (Free AACR Whitepaper) 2026, Abbisko Therapeutics showcased the latest preclinical and translational research advances across multiple pipeline programs, demonstrating its strong capabilities in drug discovery and development. As these programs continue to advance into clinical stages, the company is further strengthening its globally competitive R&D platform.

Looking ahead, Abbisko Therapeutics will continue to focus on addressing unmet medical needs and accelerating the translation of innovative discoveries into clinical applications, with the goal of delivering more first-in-class and best-in-class therapies to patients worldwide.

(Press release, Abbisko Therapeutics, APR 22, 2026, View Source;abbisko-therapeutics-showcases-six-research-advances-highlighting-pan-kras-4th-generation-egfr-and-synthetic-lethality-approaches-302751184.html [SID1234664702])