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Monte Rosa Therapeutics Presents Preclinical Data at American Association for Cancer Research (AACR) Annual Meeting 2026 on the Potential of its Cyclin E1 (CCNE1)-directed Molecular Glue Degrader to Treat CCNE1-amplified Solid Tumors

On April 20, 2026 Monte Rosa Therapeutics, Inc. (Nasdaq: GLUE), a clinical-stage biotechnology company developing novel molecular glue degrader (MGD)-based medicines, reported the company will present preclinical data highlighting the potential of its highly selective, first-in-class cyclin E1 (CCNE1)-directed MGD, MRT-55811, to treat CCNE1-amplified solid tumors at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, being held April 17-22 in San Diego, CA.

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"CCNE1 MGDs represent a first-in-class opportunity to directly target a frequently amplified driver oncogene in several solid tumor cancer populations with high unmet medical need. In CCNE1-amplified in vivo models of ovarian, gastric, and breast cancer, MRT-55811 demonstrated compelling monotherapy anti-tumor activity," said Sharon Townson, Ph.D., Chief Scientific Officer of Monte Rosa Therapeutics. "MRT-55811 also exhibited superior selectivity when compared to clinical-stage CDK2 inhibitors, suggesting that our CCNE1-directed MGDs could avoid the dose-limiting toxicities reported for these less selective agents. We believe that our oral CCNE1 degrader has the potential to provide clinical benefit across multiple cancer types where CCNE1 is amplified. These data also reinforce the power of our QuEEN discovery engine, as cyclin E1 represents yet another previously undruggable target we’ve successfully targeted. We anticipate submitting an IND for this program later this year."

The presentation, "Selective targeting of CCNE1 using molecular glue degraders for the treatment of CCNE1 amplified cancers" (Abstract Presentation Number 6778), will be presented by Ralph Tiedt, Ph.D., Vice President, Biology, Monte Rosa Therapeutics, at the Minisymposium, "Targeted Protein Degradation and Non-canonical Oncogenic Signaling," on April 21, 2026, from 2:30 p.m. to 4:30 p.m. PT.

Summary of results:

MRT-55811 exhibited potent degradation and high selectivity for CCNE1, with no detectable degradation of closely related cyclins or cyclin-dependent kinases (CDKs), and favorable drug-like properties.
MRT-55811 induced deep cyclin E1 degradation and downstream pathway suppression, as well as co-degradation of CDK2 within the cyclin E1/CDK2 holoenzyme complex in CCNE1-amplified cell lines.
MRT-55811 demonstrated superior selectivity compared with clinical-stage CDK2 inhibitors, which exhibited significant off-target activity, as evidenced by kinome profiling and genetic modeling.
In CCNE1-amplified cancer cell lines, MRT-55811 selectively inhibited cellular proliferation, while sparing cell lines without amplification.
In vivo, MRT-55811 monotherapy resulted in tumor regression and pathway suppression in multiple CCNE1-amplified models.
MRT-55811 downmodulated retinoblastoma (RB) protein phosphorylation and E2F-driven gene expression, demonstrating on-target effects in tumors grown in vivo.

About CCNE1 MGDs
Cyclin E1 (CCNE1) is a well-recognized human oncogene and critical driver of cell cycle progression and cell proliferation and was historically considered an undruggable target. It acts as the regulatory subunit of the CCNE1-CDK2 holoenzyme, which coordinates G1-S cell cycle progression and drives cell proliferation through RB phosphorylation and repression. CCNE1 is frequently amplified or overexpressed across multiple cancer types, including ovarian, endometrial, gastric, breast, and others. Leveraging a cryptic pocket, Monte Rosa’s CCNE1-directed MGDs selectively degrade the cyclin E1/CDK2 holoenzyme complex, while sparing other proteins such as other closely related cyclins or CDKs. As a result of this exquisite selectivity, CCNE1-directed MGDs represent an opportunity to directly and selectively target a frequently amplified driver oncogene across multiple cancers.

(Press release, Monte Rosa Therapeutics, APR 20, 2026, View Source [SID1234664587])

Radiopharm Theranostics Presents Initial Findings from Phase 1 First-in-Human HEAT Clinical Trial for 177Lu-RAD202 in HER2+ Solid Tumors at American Association for Cancer Research 2026

On April 20, 2026 Radiopharm Theranostics (ASX: RAD, Nasdaq: RADX, "Radiopharm" or the "Company"), a clinical-stage biopharmaceutical company focused on developing innovative oncology radiopharmaceuticals for areas of high unmet medical need, reported that new data from the ongoing Phase 0/1 HEAT trial (NCT06824155), evaluating 177Lu-RAD202, a first-in-class HER2-targeted radiopharmaceutical therapy, will be presented as a poster at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, being held April 17–22, 2026 in San Diego, California.

"These first-in-human results represent an important early milestone for our HER2-targeted radiopharmaceutical program," said Dr. Dimitris Voliotis, Chief Medical Officer of Radiopharm Theranostics. "In a heavily pre-treated patient population with significant unmet need, 177Lu-RAD202 demonstrated encouraging tumor uptake and a favorable safety profile at the lowest dose level. Importantly, the observed dosimetry supports continued dose escalation, which was recently approved by the Data Safety and Monitoring Committee (DSMC) to advance to the third cohort at 130 mCi dosing. We look forward to further evaluating the therapeutic potential of this novel approach and expect to see signs of antitumor activity at higher, more therapeutic dose levels."

The AACR (Free AACR Whitepaper) poster highlights first-in-human safety, biodistribution, dosimetry and tumor uptake clinical findings from the initial lowest dose cohort of three patients with advanced HER2-positive breast and urothelial cancers who had received multiple prior metastatic therapies and were dosed at 30 mCi.

Key Findings from the AACR (Free AACR Whitepaper) Abstract and Poster

Meaningful tumor uptake of 177Lu-RAD202 was observed at the initial and lowest dose level of 30 mCi, particularly in breast cancer lesions
177Lu-RAD202 was generally well tolerated in the first three treated patients, with predominantly Grade 1–2 treatment-emergent adverse events
No dose-limiting toxicities or treatment discontinuations due to adverse events were observed
Organ-level absorbed radiation doses were within expected and clinically acceptable ranges, supporting continued dose escalation
Poster Presentation Details

Title: A First-in-Class HER2-Targeted Radiopharmaceutical Therapy: Initial Findings from the Phase 0/1 HEAT Trial of 177Lu-RAD202 in HER2+ Advanced Solid Tumors
Abstract Number: CT046
Presenter: Dimitris Voliotis, M.D., Chief Medical Officer of Radiopharm Theranostics
Session: Poster Session
Dates: April 20, 2026 at 9:00 AM PT
The complete poster can be found on the Company’s website here.

On April 8, 2026, Radiopharm Theranostics announced the positive recommendation from the Data Safety and Monitoring Committee (DSMC) to advance 177Lu-RAD202 to the third cohort at a dose level of 130mCi in the Phase 1 ‘HEAT’ clinical trial in patients with HER2-positive advanced solid tumors1. The DSMC is a multidisciplinary committee that conducts detailed reviews of study data, discusses potential safety events and provides recommendations regarding trial continuation.

About the HEAT Trial

177Lu-RAD202 is a Lutetium-177–labeled single-domain antibody (sdAb) designed to target HER2-expressing tumors. The sdAb format enables deep tumor penetration and rapid systemic clearance, while the beta-emitting isotope 177Lu delivers cytotoxic radiation with potential bystander effects independent of HER2 receptor density.

The HEAT trial (HER2-Antibody Therapy with Lutetium-177; (NCT06824155) is a first-in-human, open-label, multicenter integrated Phase 0/1 study evaluating 177Lu-RAD202 in patients with HER2-positive locally-advanced or metastatic solid tumors.

Phase 0 evaluates biodistribution, pharmacokinetics, and radiation dosimetry using an imaging dose
Phase 1 consists of multiple-dose escalation to assess safety, tolerability, tumor targeting, and to determine the recommended Phase 2 dose
About RAD202:

RAD202 is a proprietary single-domain monoclonal antibody (sdAb) that targets the Human Epidermal Growth Factor Receptor 2 (HER2)-positive expression in advanced solid tumors. HER2 is overexpressed in breast cancer and several other solid tumors and represents a validated target in oncology. In a previous diagnostic study of ten HER2-positive breast cancer patients, RAD202 demonstrated clinical proof-of-concept and had positive safety and biodistribution.

(Press release, Radiopharm Theranostics, APR 20, 2026, View Source [SID1234664586])

BriaCell Presents Positive Phase 3 Quality of Life and Phase 2 Biomarker Data at the 2026 AACR Meeting

On April 20, 2026 BriaCell Therapeutics Corp. (Nasdaq: BCTX, BCTXL) (TSX: BCT) ("BriaCell" or the "Company"), a clinical-stage biotechnology company developing novel immunotherapies to transform cancer care, reported that it is presenting positive data in three clinical posters at the 2026 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, taking place April 17–22 at the San Diego Convention Center in San Diego, California. The presentations will include one poster featuring data from BriaCell’s ongoing pivotal Phase 3 study of Bria-IMT plus an immune checkpoint inhibitor (ClinicalTrials.gov identifier: NCT06072612), and two posters highlighting further analyses of Phase 2 data. Abstracts will be published in the online Proceedings of the AACR (Free AACR Whitepaper).

"Standards of care in cancer are evolving rapidly as innovative immunotherapy approaches emerge with potentially better safety profiles than chemotherapy. Clinical data, including BriaCell’s, highlight that maintaining quality of life is an important treatment goal alongside efficacy and safety," stated lead author, Saranya Chumsri, MD, Principal Investigator of BriaCell Phase 3 study of Bria-IMT+CPI, and Professor of Oncology, Mayo Clinic.

"At BriaCell, we are focused on bringing novel therapeutics to cancer patients with unmet medical needs with the ultimate goal of improving patients’ lives," noted William V. Williams, MD, BriaCell’s President & CEO. "Our new quality of life data from the Phase 3 Bria-IMT + CPI study in patients with metastatic breast cancer who failed prior therapies show very positive trends, bringing us one step closer to transforming care for these patients."

Session Title: Phase II and Phase III Clinical Trials
Session: 4/20/2026 2:00-5:00 PM PST
Location: Poster Section 52
Poster Board Number: 1
Poster Number: CT137
Title: QOL Outcomes in Bria-ABC Late-Stage Metastatic Phase 3 Trial
Summary: Heavily pretreated metastatic breast cancer patients in the pivotal Phase 3 study of Bria-IMT plus an immune check point inhibitor maintained overall health status and key functional measures with a favorable safety profile. These findings are encouraging because they suggest meaningful preservation of quality of life for late-stage metastatic breast cancer patients with limited treatment options.

QOL largely preserved in a heavily pretreated population with prior antibody-drug conjugate (ADC), check point inhibitor (CPI), and cyclin-dependent kinase 4/6 (CDK4/6) inhibitor exposure
European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire-Core 30 Survey showed:
1) Global health status stable through early and mid-treatment
2) Emotional and cognitive functioning maintained; symptom burden stable
Safety profile and time-to-deterioration analyses support durable tolerability in a late-line setting
BriaCell clinical data supports feasibility of decentralized treatment approaches, including potential home self-administration strategies
Session Category: Clinical Research
Session: 4/19/2026 2:00-5:00 PM PST
Location: Poster Section 42
Poster Board Number: 5
Poster Number: 1065
Title: Mitosis in Circulating Tumor Cells Correlates with Highly Aggressive Disease in Metastatic Breast Cancer

Summary: Circulating tumor cells (CTCs) are a well-established non-invasive blood-based biomarker that can help stratify prognosis in patients with metastatic breast cancer (MBC), particularly in aggressive disease subtypes. Early pilot studies had identified a distinct subset of CTCs undergoing mitosis (dividing cells), whose presence appeared to correlate with worse survival outcomes. However, their prognostic significance and potential interaction with different treatment regimens have not been clinically evaluated. In this multi-institutional prospective study, patients with mitotic CTCs were found to have poorer outcomes than those with non-mitotic CTCs or no CTCs, but appeared to have overall survival benefit when treated with targeted therapy. Overall, these findings support mitotic CTCs as a novel potential prognostic biomarker in metastatic breast cancer.

Session Category: Clinical Research
Session Title: Biomarkers Predictive of Therapeutic Benefit 1
Session: 4/19/2026 2:00-5:00 PM PST
Location: Poster Section 40
Poster Board Number: 19
Poster Number: 1025
Title: Monitoring PD-L1 in tumor macrophage fusion cells in blood identifies high PD-L1 checkpoint inhibitor responses in metastatic breast cancer

Summary: Tissue biopsy PD-L1 combined positive score (CPS≥10) has been identified as a positive prognostic marker in metastatic breast cancer. However, a significant percentage of MBC patients with CPS <10 seem to benefit from immune check point inhibitor (ICI) therapy. Circulating tumor-macrophage fusion cells (TMFCs) express PD-L1 and changes in TMFC PD-L1 expression during ICI treatment may explain this outcome. This Phase 2 prospective study found no correlation between tumor PD-L1 CPS and clinical response while demonstrating that patients with PD-L1 positive TMFCs in their blood had significantly improved progression free survival. Monitoring PD-L1 in TMFCs may serve as a real-time biomarker to better indicate ICI response and further studies into the role of TMFC PD-L1 in predicting therapeutic response are ongoing.

Following the presentation, copies of the posters will be made available at View Source

(Press release, BriaCell Therapeutics, APR 20, 2026, View Source [SID1234664585])

Calidi Biotherapeutics Presents New Data on Its Differentiated Approach to In Situ T-Cell Engagers Including a New Candidate Targeting TROP-2 at the AACR Annual Meeting in April 2026

On April 20, 2026 Calidi Biotherapeutics, Inc. (NYSE American: CLDI) ("Calidi" or the "Company"), a biotechnology company pioneering the development of targeted genetic medicines, reported new data at the American Association of Cancer Research (AACR) (Free AACR Whitepaper) annual meeting in San Diego, California on April 19, 2026. The Company demonstrated new data on its approach of simultaneously activating T-cells while inducing the expression of T-cell engagers specifically in situ in the tumor microenvironment ("TME"). The poster is available here.

RedTail is Calidi’s systemically delivered virotherapy platform designed to selectively target tumors, remodel the TME, and enable high-level expression of therapeutic genetic payloads directly at the tumor site while limiting peripheral exposure. CLD-401, the lead candidate derived from the RedTail platform, is engineered to express high levels of IL-15 superagonist ("IL-15 SA"), a known CD8⁺ T-cell, NK cell, and gamma delta (γδ) T-cell activator, in the TME. The Company expects to file an IND for CLD-401 by the end of 2026.

Data presented at the AACR (Free AACR Whitepaper) meeting showcased RedTail viruses that can express both a functional T-cell engager, capable of binding targeted solid tumor cells, and IL-15 SA at high concentrations, allowing for simultaneous T-cell activation and high expression in situ of a T-cell engager. T-cell engagers have shown exceptional efficacy in hematological malignancies but have failed to show clinical benefit in solid tumors where the TME inhibits immune cell infiltration and T-cell activity. By remodeling the TME and driving T-cell activation in concert with expression of a T-cell engager, RedTail is designed to overcome these historical limitations.

The Company is developing CLD-501, a lead candidate targeting TROP2, a cell-surface glycoprotein. TROP2 expression in normal tissue and the high potential for off-tumor / on-target toxicity has made it a difficult target for T-cell engagers. The RedTail approach confines expression of the T-cell engager to the TME, limiting off-tumor interactions. The Company is pursuing additional T-cell engager targets like EGFR, EpCAM, and Nectin-4.

"Data presented at AACR (Free AACR Whitepaper) show the advances we have made with the RedTail platform, our first lead, CLD-401, and our progress in addressing a central challenge in immuno-oncology: how to deliver tumor-specific T-cell engagers effectively in solid tumors" said Eric Poma, PhD, Chief Executive Officer of Calidi. "We believe RedTail represents a major breakthrough in the ability to deliver genetic payloads, including in situ T-cell engagers in a targeted fashion to distal sites of disease through systemic administration."

"The data we presented at AACR (Free AACR Whitepaper) highlight the ability of the RedTail platform to functionally overexpress complex biologics including cytokines and T-cell engagers, and profoundly alter the tumor microenvironment" said Antonio F. Santidrian, PhD, Chief Scientific Officer and Head of Technical Operations at Calidi. "This tumor-restricted approach enables targeting of antigens such as TROP2, something that has not been effectively accomplished with existing T-cell engager therapies.

The Company continues to expand the functionality of the RedTail platform and is also actively pursuing strategic partnerships to accelerate clinical development and broaden the impact of its RedTail platform.

(Press release, Calidi Biotherapeutics, APR 20, 2026, View Source [SID1234664584])

CytoDyn Presents New Leronlimab Data in Metastatic Triple-Negative Breast Cancer at AACR Annual Meeting 2026

On April 20, 2026 CytoDyn Inc. (OTCQB: CYDY) ("CytoDyn" or the "Company"), a clinical-stage oncology company advancing leronlimab, a first-in-class humanized monoclonal antibody targeting the CCR5 receptor with therapeutic potential across multiple indications, including metastatic triple-negative breast cancer ("mTNBC") and colorectal cancer ("mCRC"), reported that new clinical and translational data in metastatic triple-negative breast cancer (mTNBC) were presented at the AACR (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17–22, 2026, at the San Diego Convention Center.

The presentation highlighted emerging evidence supporting CCR5 inhibition with leronlimab as a strategy to modulate the tumor microenvironment, enhance immune responsiveness, and improve outcomes in metastatic triple-negative breast cancer (mTNBC).

Metastatic triple-negative breast cancer remains an aggressive disease with limited treatment options and poor long-term survival. While immune checkpoint inhibitors (ICIs) have demonstrated benefit in select patients, many tumors exhibit low PD-L1 expression and resistance to immunotherapy. Preclinical and clinical findings presented at AACR (Free AACR Whitepaper) show that CCR5 inhibition with leronlimab modulates immune checkpoint signaling, potentially sensitizing tumors to immune checkpoint inhibitor therapy.

"Our findings suggest that CCR5 plays a key role in immune exhaustion and therapy resistance pathways in TNBC," said Richard G. Pestell, M.D., Ph.D., FRCP, AO, Lead Consultant in Preclinical and Clinical Oncology at CytoDyn. "Induction of PD-L1 predicts response to immune checkpoint therapy. Leronlimab-mediated CCR5 inhibition induced PD-L1 expression and reduced key mediators of immune suppression, including sB7-H3 and sTyro3 signaling. These data support the hypothesis that leronlimab may help prime tumors for immune checkpoint therapy and improve clinical outcomes in patients with otherwise limited therapeutic options."

Key findings from baseline tumor biology and leronlimab treatment analysis in TNBC include:

Across breast cancer cohorts (N=1,096), CCR5 expression correlated with gene signatures of T-cell immune exhaustion and immune infiltration.
CCR5 expression was enriched in TNBC subtypes associated with immune modulation, including mesenchymal-like immune-altered (MLIA) and immunomodulatory (IM) subtypes.
In TNBC cell models, CCR5 inhibition with leronlimab increased PD-L1 expression, suggesting a potential mechanism to enhance responsiveness to PD-L1-targeted therapies.
Proteomic analyses demonstrated that CCR5 activity promotes expression of immune checkpoint mediators, including sB7-H3 (CD276) and Tyro3 signaling, both associated with resistance to ICIs; these effects were attenuated with leronlimab.
In a retrospective analysis of 28 patients with mTNBC, leronlimab treatment was associated with induction of PD-L1 in circulating tumor cells (CTCs) and cancer-associated macrophage-like cells (CAMLs).
Higher leronlimab dose, PD-L1 induction, and use in combination or sequence with ICIs were associated with improved patient survival outcomes.
Notably, 17.9% (5/28) of heavily pretreated patients remain alive after more than 60 months of follow-up.

"These results reinforce the potential role of CCR5 as a critical regulator of the tumor microenvironment in TNBC," said Jacob P. Lalezari, M.D., Chief Executive Officer of CytoDyn. "The observed induction of PD-L1 and association with long-term survival in mTNBC support continued clinical development of leronlimab in combination approaches designed to enhance immune response and overcome treatment resistance."

Dr Pestell is the first author of the poster presentation titled "Leronlimab induces PD-L1 expression and is associated with long term survival with an ICI in PD-L1 low metastatic TNBC" on April 19, 2026, from 2:00 p.m. – 5:00 p.m. PT (Poster #1033). A copy of the poster will be made available on CytoDyn’s website under the Publications & Posters section.

(Press release, CytoDyn, APR 20, 2026, View Source [SID1234664583])