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.

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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])

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.

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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])

On April 20, 2026 Orion Corporation (Orion Pharma) reported that its investigational drug ODM-212 has received Orphan Drug Designation (ODD) from the US Food and Drug Administration (FDA) for the treatment of mesothelioma, which is a rare and difficult to treat cancer. The FDA grants orphan drug designation to investigational therapies addressing rare diseases or conditions that affect fewer than 200,000 people in the US.

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ODM-212 is an oral small-molecule pan-TEAD (Transcriptional Enhanced Associate Domain) inhibitor being tested in a Phase 2 clinical study (TEADES) for the treatment of malignant pleural mesothelioma (MPM), epithelioid hemangioendothelioma (EHE) and other solid tumors with dysfunction in Hippo pathway. The trial includes patients who have progressed after receiving standard treatments and have no further treatment options. The primary endpoints of the study are safety and tolerability with secondary endpoints including Overall Response Rate, Progression Free Survival and Overall Survival. This is a global trial conducted at leading oncology centers in the US and Europe.

"Receiving orphan drug designation for mesothelioma is an important milestone for the ODM-212 program. It underscores the importance of developing urgently needed innovative therapies for patients living with mesothelioma" said Praveen Aanur, MD, MPH, MBA, Chief Medical Officer, Oncology Therapy Area, Orion Pharma.

About Orphan Drug Designation
Orphan Drug Designation is granted by FDA to therapies intended to prevent, diagnose, or treat rare diseases or conditions. With this designation for ODM-212, Orion Pharma, the sponsor, is now qualified for incentives including tax credits, exepmption from user fees, and eligibility for a 7-year period of market exclusivity following approval. Orphan Drug Designation neither shortens the development time or regulatory review time of a drug nor gives the drug any advantage in the regulatory review or approval process.

About ODM-212
ODM-212 is an oral small-molecule pan-TEAD (Transcriptional Enhanced Associate Domain) inhibitor developed by Orion Pharma. It targets the Hippo signaling pathway, which regulates cell growth and organ size. Dysregulation of this pathway—particularly through YAP/TAZ activation—can lead to uncontrolled tumor growth and resistance to cancer therapies. ODM-212 works by blocking TEAD transcription factors, disrupting YAP-TEAD protein-protein interactions, and inhibiting TEAD auto-palmitoylation, which is essential for TEAD activity.

(Press release, Orion, APR 20, 2026, View Source [SID1234664582])

On April 20, 2026 Lirum Therapeutics, Inc. ("Lirum"), an innovative clinical-stage biopharmaceutical company focused on the treatment of debilitating diseases, reported that new LX-101 data in Ewing sarcoma has been selected for presentation at the 2026 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, being held from April 17-22 in San Diego. LX-101 is a novel clinical-stage payload-bearing targeted therapy directed to the insulin-like growth factor 1 receptor (IGF-1R), currently being developed in oncology and autoimmune indications.

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These new data demonstrated LX-101’s potent antitumor activity as a single agent in patient-derived xenograft (PDX) models of Ewing sarcoma, with additional activity, including synergy, when used in combination with PI3K or mTOR inhibition. The presentation concluded that LX-101 demonstrated improved preclinical activity relative to previously reported IGF-1R-targeting approaches. The observed single-agent activity and synergy with PI3K and mTOR inhibitors support further clinical development of LX-101 and LX-101-based combination strategies. The results will be presented by Roberto Cardenas-Zuniga, a member of the research team in the lab of Joseph Ludwig, M.D., at The University of Texas MD Anderson Cancer Center, Lirum’s collaborator on this project.

Presentation Details

Abstract#: 7873
Title: In Vivo Preclinical Efficacy of a Novel "Payload-Bearing" Peptide LX-101 Targeting IGF-1R in Ewing Sarcoma
Date/Time: April 22, 2026 – 9:00 AM – 12:00 PM PT
Session Title: PO.CL06.03 – Targeted Therapies, Predispositions, and Survivorship in Pediatric Cancers
Lirum also recently announced a "Study May Proceed" letter from the FDA enabling the inclusion of LX-101 in the RAPID platform clinical trial. RAPID (Rapidly Assess Promising Innovative Drugs) is a patient-centric, multicenter, open-label platform trial led by Joseph Ludwig, M.D., professor at The University of Texas MD Anderson Cancer Center. RAPID employs a master protocol that enables the study of both single-agent and novel drug combinations in patients with relapsed/refractory Ewing sarcoma and desmoplastic small round cell tumor (DSRCT).

About Ewing Sarcoma
Ewing sarcoma is an aggressive cancer that primarily develops in the bones or surrounding soft tissues, most commonly affecting children, adolescents and young adults. ES is the second most common bone cancer in children in the US. Notably, Ewing sarcoma has strong ties to IGF-1R signaling pathway, including DNA-level gene fusions (i.e., EWSR1-FLI1) that affect IGF-1R signaling, providing a strong scientific and clinical rationale for LX-101 in this indication. Current treatments are limited to a combination of chemotherapy, surgical removal of the tumors and sometimes radiation therapy.

(Press release, Lirum Therapeutics, APR 20, 2026, View Source [SID1234664581])

On April 20, 2026 BridgeBio Oncology Therapeutics, Inc. ("BBOT") (Nasdaq: BBOT), a clinical-stage biopharmaceutical company focused on RAS-pathway malignancies, reported that the U.S. Food and Drug Administration (FDA) has granted Fast Track designation to BBO-11818 for the treatment of adult patients with advanced KRAS-mutant pancreatic ductal adenocarcinoma.

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"Receiving Fast Track designation from the FDA for BBO-11818 in KRAS-mutant pancreatic ductal adenocarcinoma reflects the importance and urgency of accelerating the development of our pan-KRAS inhibitor in this serious disease," said Yong Ben, MD, Chief Medical and Development Officer of BBOT. "Pancreatic cancer remains one of the most difficult-to-treat malignancies. KRAS mutations are present in the vast majority of cases, yet patients have had few targeted options. This designation will help us collaborate closely with the FDA to advance BBO-11818 as efficiently as possible for patients who need new options."

This designation follows preliminary data, first released in January 2026, in which BBO-11818 monotherapy demonstrated a confirmed partial response in pancreatic cancer. In addition, anti-tumor activity was observed across dose levels and tumor types with tumor reductions at higher dose levels with a generally favorable, differentiated safety profile in dose escalation.

While KRASG12C inhibitors have demonstrated promising clinical efficacy, there remains a clear unmet medical need for therapies targeting cancers that carry other KRAS mutations, such as KRASG12D and KRASG12V. BBO-11818 was developed to address this gap and is specifically designed as a potent pan-KRAS inhibitor with strong binding affinity for KRAS, high selectivity over HRAS and NRAS, and the ability to achieve high levels of KRAS inhibition in both the ON and OFF states. BBO-11818 is being evaluated as monotherapy, in combination with standard-of-care therapies, or alongside BBOT’s RAS:PI3Kα breaker, BBO-10203.

Fast Track designation is intended to help rapidly advance the development and review process for promising therapeutic candidates for serious conditions that may fill an unmet medical need.

About BBO-11818
BBO-11818 is a selective, orally bioavailable non-covalent inhibitor that targets KRAS in both the ON and OFF states, has high selectivity over HRAS and NRAS, and displays strong activity in KRAS-mutant preclinical models, including KRASG12D and KRASG12V. In addition, it potently suppresses MAPK signaling and inhibits cell proliferation in KRAS-mutant cell lines. BBO-11818 is currently being evaluated in the Phase 1 KONQUER-101 trial in subjects with locally advanced unresectable or metastatic KRAS-mutant solid tumors.

(Press release, BridgeBio Oncology Therapeutics, APR 20, 2026, View Source [SID1234664580])