On March 17, 2026 Verastem Oncology (Nasdaq: VSTM), a biopharmaceutical company committed to advancing new medicines for patients with RAS/MAPK pathway-driven cancers, reported multiple abstracts have been accepted for presentation at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting to be held April 17-22, 2026, in San Diego, CA.

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"Preclinical data accepted for presentation at the AACR (Free AACR Whitepaper) Special Conference in Cancer Research: RAS Oncogenesis and Therapeutics and the AACR (Free AACR Whitepaper) Annual Meeting highlight our highly differentiated investigational asset VS-7375, an oral, KRAS G12D (ON/OFF) inhibitor in clinical development for pancreatic, lung, colorectal and other cancers harboring a G12D mutation, the most prevalent KRAS mutation in human cancers," said Jonathan Pachter, Ph.D., chief scientific officer at Verastem Oncology. "While most agents targeting KRAS G12D-driven cancers bind preferentially only to the "ON" (active) or "OFF" (inactive) state of KRAS, VS-7375 engages both active and inactive states with extremely high affinity and long residence time, which corresponds to superior efficacy across pre-clinical models of G12D mutated cancers."

Late-Breaking Abstracts

Late-breaking abstracts will be available on the AACR (Free AACR Whitepaper) Annual Meeting website on April 17, 2026, 12 p.m. PT.

Session: Late-Breaking Research: Experimental and Molecular Therapeutics 2
Abstract #: LB183 / 5
Title: Strong durable tumor regressions with the KRAS G12D ON/OFF inhibitor VS-7375 in combination with PRMT5 inhibition in MTAP-deleted/KRAS G12D-mutant pancreatic cancer
Date and Time: April 20, 2026, 2 p.m. – 5 p.m. PT

Session: Late-Breaking Research: Experimental and Molecular Therapeutics 2
Abstract #: LB197 / 19
Title: VS-7375, a non-covalent dual ON/OFF KRAS G12D inhibitor, displays superior activity to ON-only KRAS G12D inhibitors in preclinical models of pancreatic cancer
Date and Time: April 20, 2026, 2 p.m. – 5 p.m. PT

Regular Abstracts

The accepted abstracts are available on the AACR (Free AACR Whitepaper) Annual Meeting website: AACR (Free AACR Whitepaper) Annual Meeting 2026

Session: Novel Antitumor Agents 3
Abstract & Poster Details: Abstract/Poster #7100, Poster Section #13, Poster Board #20
Title: VS-7375: An oral, selective KRAS G12D dual ON/OFF inhibitor with potent anti-tumor activity as a single agent and in combination with other agents
Date and Time: April 22, 2026, 9 a.m. – 12 p.m. PT

In the KP4 KRAS G12D pancreatic cancer model, VS-7375 (50 mg/kg twice daily), zoldonrasib (100 mg/kg once daily) and daraxonrasib (25 mg/kg once daily), produced similar initial tumor regression through day nine. By approximately day 20, however, zoldonrasib and daraxonrasib lost anti-tumor activity with tumor outgrowth, (mean tumor volume >850 mm by day 30) whereas VS-7375 maintained sustained tumor regression (mean tumor volume ~80 mm by day 30), consistent with pharmacodynamic analyses showing durable pathway inhibition only with VS-7375. VS-7375 also showed deeper tumor regression compared to these RAS ON-only inhibitors in KRAS G12D-mutated lung and colorectal xenograft models.

Session: Therapies Targeting Metastasis
Abstract & Poster Details: Abstract/Poster #2232, Poster Section #32, Poster Board #7
Title: Investigating the combined inhibition of RAF, MEK, and FAK in melanoma molecular subtypes
Date and Time: April 20, 2026, 9 a.m. – 12 p.m. PT

In mutant BRAF-driven models, the combination of the FAK inhibitor VS-4718 and the RAF/MEK clamp avutometinib, with or without the mutant BRAF inhibitor encorafenib, significantly delayed tumor onset, induced regression of established tumors and brain metastases, and prolonged overall survival.

AACR Special Conference in Cancer Research: RAS Oncogenesis and Therapeutics

At the AACR (Free AACR Whitepaper) Special Conference in Cancer Research: RAS Oncogenesis and Therapeutics held March 5-8, 2026, Dr. Jonathan Pachter, delivered a plenary oral presentation titled, "Anti-tumor efficacy of the selective oral KRAS G12D dual ON/OFF inhibitor VS-7375 as a single agent and in combination with targeted agents." This presentation can be found on the Company’s website on the Resources page.

About VS-7375, an Oral KRAS G12D (ON/OFF) Inhibitor

VS-7375 is a potential best-in-class, potent, and selective oral KRAS G12D dual ON/OFF inhibitor. VS-7375 is the lead program from the Verastem Oncology discovery and development collaboration with GenFleet Therapeutics. Verastem initiated VS-7375-101, an international Phase 1/2 clinical trial, in June of 2025 in the U.S., that is evaluating the safety and efficacy of VS-7375 in patients with advanced KRAS G12D mutant solid tumors. In July 2025, U.S. Food and Drug Administration (FDA) granted Fast Track Designation (FTD) to VS-7375 for the first-line treatment of patients with KRAS G12D-mutated locally advanced or metastatic adenocarcinoma of the pancreas (PDAC) and for the treatment of patients with KRAS G12D-mutated locally advanced or metastatic PDAC who have received at least one prior line of standard systemic therapy.

About the GenFleet Therapeutics Collaboration

The collaboration with GenFleet Therapeutics aims to advance three oncology discovery programs related to RAS/MAPK pathway-driven cancers. The collaboration provides Verastem with an exclusive option to obtain a license for each of the three compounds in the collaboration after the successful completion of pre-determined milestones in a Phase 1 trial. Verastem selected VS-7375 (also known as GFH375), an oral KRAS G12D (ON/OFF) inhibitor, as its lead program in December 2023 and the license for VS-7375 that was exercised in January 2025 is the first one from this collaboration. The licenses would give Verastem development and commercialization rights outside the GenFleet markets of mainland China, Hong Kong, Macau, and Taiwan.

(Press release, Verastem, MAR 17, 2026, View Source [SID1234663631])

On March 17, 2026 SingleCell Biotechnology, a biotechnology company developing technologies to measure tumor cell behavior at single-cell resolution, reported that data from its platform will be presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, to be held in San Diego, April 17-21, 2026.

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Relapse remains one of the most persistent challenges in oncology. While many therapies successfully reduce tumor size, a subset of tumor cells can survive treatment and later regenerate disease. These cells often exhibit behaviors, such as slow proliferation, migration or transient dormancy, that are difficult to detect using traditional preclinical models, where measurements are typically averaged across large populations of rapidly dividing tumor cells. As a result, promising drug candidates may advance through development without being evaluated against the cell populations most responsible for treatment resistance and recurrence.

SingleCell Biotechnology is developing a high-throughput single-cell phenotyping platform designed to measure tumor cell growth, migration and quiescent states at scale. The platform enables large-scale measurement of clonal tumor cell proliferation while preserving the diversity of cellular behaviors within tumors. By combining functional phenotyping with molecular analysis, the approach aims to provide deeper insight into tumor heterogeneity and support more informed decision-making in oncology drug discovery.

Presentation Details:

Poster Title: An Integrated High-throughput Assay for Proliferative Phenotypic and Omics
Presenter: Shiska Raut, Machine Learning Engineer
Location: Poster Section 51
Poster Board Number: 9
Session Date/Time: Sunday, April 19, 2026, 2:00 PM – 5:00 PM

(Press release, Single Cell Technology, MAR 17, 2026, View Source [SID1234663647])

On March 17, 2026 Perspective Therapeutics, Inc. ("Perspective" or the "Company") (NYSE AMERICAN: CATX), a radiopharmaceutical development company pioneering advanced treatments for cancers throughout the body, reported that updated data on the Company’s [212Pb]VMT-α-NET program have been accepted as a poster presentation at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 taking place from April 17 to 22, 2026 in San Diego, CA as detailed below. AACR (Free AACR Whitepaper) has announced that it will release further details for clinical trial abstracts for the conference on April 17, 2026.

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Presenter Abstract Title Presentation Details
Thorvardur Halfdanarson, Mayo Clinic Comprehensive Cancer Center [212Pb]VMT-a-NET in advanced SSTR2+ neuroendocrine tumors: safety and preliminary efficacy results from dose-finding cohorts 1, 2 and 3 Abstract Number: CT088
Session Type: Poster presentation
Session Title: Phase I Clinical Trials in Progress
Session Date: April 20, 2026
Session Time: 9:00 am – 12:00 pm
About [212Pb]VMT-α-NET
Perspective designed [212Pb]VMT-α-NET to target and deliver 212Pb to tumor sites expressing somatostatin receptor type 2 (SSTR2). The Company is conducting a multi-center, open-label, dose-escalation, dose-expansion study (clinicaltrials.gov identifier NCT05636618) of [212Pb]VMT-α-NET in patients with unresectable or metastatic SSTR2-positive neuroendocrine tumors who have not received prior radiopharmaceutical therapies (RPT).

Interim analysis with a data cut-off date of December 10, 2025 was previously reported at the 2026 ASCO (Free ASCO Whitepaper) Gastrointestinal Cancers Symposium (ASCO-GI) in January 2026, including efficacy data on half of the patients in Cohort 2 and both patients in Cohort 1. Initial efficacy data for the remaining patients in Cohort 2 and eight patients in Cohort 3 are pending, and submissions for presentations at additional medical conferences during 2026 are planned.

Highlights from the previously presented ASCO (Free ASCO Whitepaper)-GI analysis included the following:

Safety findings based on 56 patients who received at least one treatment:

The 56 patients in this safety analysis comprised 2 patients in Cohort 1 (2.5 mCi), 46 patients in Cohort 2 (5.0 mCi), and 8 patients in Cohort 3 (6.0 mCi).
There were no reports of dose limiting toxicities (DLTs), treatment-related discontinuations, serious renal complications, dysphagia, or clinically significant treatment-related myelosuppression.
Grade 3 or higher treatment-emergent adverse events were reported in 21 patients (37.5%). One of these patients, who was enrolled in Cohort 3, experienced a transient Grade 4 event (lymphocyte count decrease). This event was transient and resolved without medical intervention. The patient continues to receive [212Pb]VMT-α-NET treatment. There were no Grade 5 events.
Serious adverse events were reported in 5 patients, with none deemed related to the study medication.
Anti-tumor activity based on both patients in Cohort 1 and 23 (half) of the patients enrolled in Cohort 2:

Updated efficacy analysis in the same 25 patients from ESMO (Free ESMO Whitepaper) Congress 2025 (ESMO 2025) in October 2025 was presented with an additional ~13 weeks of follow-up since the previous presentation at ESMO (Free ESMO Whitepaper) 2025.
19 of the 25 patients (76%) were without progression and remained alive, including both patients in Cohort 1.
Nine (39%) patients in Cohort 2 were observed to have response according to investigator-assessed RECIST v1.1. Eight (35%) of those responses were confirmed and previously reported at ESMO (Free ESMO Whitepaper) 2025. One additional patient experienced an initial response in their most recent tumor assessment after the prior update at ESMO (Free ESMO Whitepaper) 2025. As the patient remains on study, the patient is expected to receive a subsequent tumor assessment.
Seven patients were observed to have deepening of best response, including one patient with stable disease.

(Press release, Perspective Therapeutics, MAR 17, 2026, View Source [SID1234663663])

On March 17, 2026 CoRegen, Inc., a biopharmaceutical company pursuing novel treatments for patients impacted by some of the most aggressive forms of cancer, reported the publication of research conducted at the Baylor College of Medicine describing how the disruption of steroid receptor coactivator 3 (SRC-3) expression in regulatory T cells (Treg cells) can reprogram the tumor immune microenvironment and enable the immune system to eliminate multiple solid tumors. The article, titled, "Steroid receptor coactivator 3-deficient regulatory T cells eradicate multiple solid tumors in syngeneic mouse models," was published in the open access, peer-reviewed journal, OncoImmunology. One of the lead researchers, Sang Jun Han, PhD, Director of Lab Research, CoRegen, describes how selectively eliminating SRC-3 in Treg cells reprograms their function, shifting them from immunosuppressive regulators to promoters of anti-tumor immunity without inducing immune-related toxicities, a finding demonstrated across multiple preclinical tumor models including breast cancer, glioblastoma, melanoma, and lung cancer.

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The full paper can be accessed here.

SRC-3 co-regulates cell behavior that controls immune response. When knocked out, the expression of several genes involved in Treg signaling is altered, ultimately enhancing the immune system’s ability to combat cancer without causing pathological autoimmune reactions. This unique mechanism of action allows immune effector cells to recognize, attack, and kill cancer by allowing CD8+, CD4+ and NK tumor-killing effector cells to infiltrate into tumors. The SRC-3 engineered Treg cells block pathogenic tumor-protective transcriptional programs in the Treg cell, thereby altering the tumor microenvironment in a way that supports tumor destruction by the patient’s own immune system.

"We are delighted to have these findings that support our SRC-3 technology published in such a well-respected journal," said Suneet Varma, Chairman of the Board, CoRegen. "This research highlights a powerful new way to harness the immune system against cancer by reprogramming Treg cells so that tumors cannot evade immune attack. If these findings translate to patients, engineering SRC-3 disrupted Treg cells could represent a watershed moment for therapies capable of eradicating multiple, difficult-to-treat cancers while avoiding many of the immune-related side effects seen with current immunotherapies."

David Lonard, Ph.D., Chief Scientific Officer of CoRegen and Professor of Molecular & Cell Biology at the Baylor College of Medicine, added, "This publication provides important proof-of-concept data showing that selectively targeting SRC-3 in Treg cells can reprogram the tumor microenvironment to drive potent anti-tumor activity. The eradication and durable immune protection observed across multiple solid tumor models strongly support the translational potential of CoRegen’s lead program."

CoRegen remains on track to submit an investigational new drug application (IND) for its lead candidate in Spring 2026 and initiate a Phase 1 clinical trial thereafter.

(Press release, CoRegen, MAR 17, 2026, View Source [SID1234663680])

On March 17, 2026 Immuneering Corporation (Nasdaq: IMRX), a late-stage clinical oncology company focused on keeping cancer patients alive and helping them thrive, reported it will present a poster on one of the three key mechanisms by which atebimetinib aims to improve overall survival: shrinking tumors durably. The poster will be presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting taking place April 17-22, 2026 in San Diego, CA.

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Inhibitors of RAS, RAF, or MEK often provide only temporary benefit due to resistance, as tumors acquire new mutations or mechanisms of escape within the MAPK pathway. Atebimetinib, a novel Deep Cyclic Inhibitor of MEK, is engineered to mitigate the selective pressure that typically drives these resistance mechanisms, with the goal of more durable anti-tumor activity. Immuneering will present an analysis of circulating tumor DNA (ctDNA) from ≥64 patients with RAS-mutant solid tumors treated with atebimetinib, showing that acquired MAPK pathway alterations are rarely seen in patients treated with atebimetinib. These findings suggest that Deep Cyclic Inhibitors have the potential to overcome the limitations of conventional MAPK inhibition and provide a more sustained clinical benefit for patients.

Poster Presentation Details:
Title: Atebimetinib’s Deep Cyclic Inhibition of MEK Constrains MAPK-Axis Adaptive and Acquired Alterations in Patients with RAS-Mutant Tumors
Session Category: Experimental and Molecular Therapeutics
Session Title: Targeting Drug Resistance 2: RAS Signaling
Poster Number: 1873
Poster Board Number: 6
Session Date: April 20, 2026
Session Time: 9:00 AM – 12:00 PM ET
Location: Poster Section 19

The abstract will be available on the AACR (Free AACR Whitepaper) website. Following presentation, the poster will be available on the publications section of Immuneering’s website at View Source

(Press release, Immuneering, MAR 17, 2026, View Source [SID1234663615])