On April 27, 2026 MediciNova, Inc., a biopharmaceutical company traded on the NASDAQ Global Market (NASDAQ: MNOV) and the Standard Market of the Tokyo Stock Exchange (Code Number: 4875), reported that a study conducted by researchers at the Spanish National Cancer Research Centre (CNIO) has identified macrophage migration inhibitory factor (MIF)–mediated reprogramming of CD74‑positive microglia and macrophages as a central vulnerability in brain metastasis. The research, recently published in the peer‑reviewed journal "Cancer Research" (March 2026), demonstrates pharmacological modulation of this pathway using the brain‑penetrant small molecule ibudilast.

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The work, led by Manuel Valiente PhD, head of CNIO Brain Metastasis group, and colleagues at CNIO, shows that tumor‑derived MIF alters the functional state of microglia and infiltrating macrophages in the brain, converting them from a potentially protective role into a pro‑metastatic one. In multiple experimental models and fresh patient‑derived brain metastasis samples, inhibition of the MIF–CD74 signaling axis significantly reduced metastatic progression. Importantly, the investigators also identified secreted MIF as a candidate liquid biopsy biomarker detectable in cerebrospinal fluid, supporting a translational, biomarker‑guided clinical strategy.

The study further demonstrates that ibudilast can effectively block MIF–CD74 signaling, reverse pro‑metastatic immune reprogramming, and suppress brain metastasis growth in preclinical systems. In addition, transcriptomic analyses define predictive biomarker signatures associated with treatment response, reinforcing the potential for patient stratification in future clinical studies. The findings suggest translational potential for MN-166 (ibudilast), the company’s leading product, in future therapeutic strategies for brain metastasis within neuro-oncology.

MediciNova plans to collaborate with Dr. Valiente and CNIO on future clinical research aimed at patients with solid tumors having brain metastases.

Dr. Valiente commented on the findings, "Brain metastases develop in up to 30% of patients with advanced solid tumors, most commonly arising from lung cancer, breast cancer, melanoma, and colorectal cancer, and remain an area of substantial unmet medical need. Despite recent advances in systemic therapies, patients with brain metastases have historically been excluded from many clinical trials, limiting progress in the development of targeted treatments. By focusing on brain‑specific immune–microenvironment interactions rather than tumor‑intrinsic alterations alone, the CNIO findings open a new therapeutic avenue that may be applicable across multiple primary tumor types."

"Brain metastasis represents one of the most urgent and challenging frontiers in oncology," said Dr. Kazuko Matsuda, Chief Medical Officer. "The publication of this work in Cancer Research provides strong mechanistic and translational rationale to pursue biomarker‑driven clinical strategies. We hold granted patents covering MN‑166 for preventing and minimizing cancer metastasis across multiple solid tumor types, including pancreatic, lung, breast, colorectal and ovarian cancers, as well as melanoma. Our focus is now on advancing future clinical investigations and responsibly translating these insights into studies designed for patients with brain metastases."

The full study, "MIF‑Induced CD74+ Microglia and Macrophages Promote Progression of Brain Metastasis and Are Clinically Relevant Across Central Nervous System Disorders," is available online in Cancer Research. (View Source )

(Press release, MediciNova, APR 27, 2026, View Source [SID1234664821])

On April 27, 2026 Janux Therapeutics, Inc. (Nasdaq: JANX) ("Janux"), a clinical-stage biopharmaceutical company developing a broad pipeline of novel immunotherapies, reported that it will discontinue further clinical development of JANX008, its EGFR-targeted Tumor Activated T Cell Engager (TRACTr) program.

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Following completion of the Phase 1a portion of the study, which included dose escalation and expansion cohorts across multiple solid tumor indications, and an internal review of the data, the Company has determined to prioritize development resources toward other pipeline opportunities. The decision to discontinue JANX008 is program-specific and does not impact the Company’s broader TRACTr platform strategy. As part of its disciplined portfolio prioritization process, the Company evaluated the JANX008 dataset against predefined development criteria. While durable responses were observed in select patients through extended follow-up, the overall magnitude and consistency of activity were not sufficient to support continued development relative to other pipeline programs.

The study also generated insights relevant to the broader TRACTr platform. The occurrence of cytokine release syndrome (CRS) was infrequent and primarily limited to Grade 1, enabling Safety Review Committee approval for outpatient dosing. In addition, JANX008 demonstrated a differentiated tolerability profile relative to conventional EGFR-targeted therapies, with minimal gastrointestinal, dermatologic, and subcutaneous adverse events typically associated with EGFR antibodies and tyrosine kinase inhibitors. These findings, together with the ability to dose beyond the limitations of conventional T cell engagers, support the potential of the TRACTr platform to improve safety. While musculoskeletal adverse events were dose-limiting, reflecting constraints associated with the EGFR target, the TRACTr format enabled a sufficient therapeutic window to assess clinical activity across a range of doses.

"Our decision to discontinue JANX008 reflects the disciplined approach we take to advancing our pipeline," said David Campbell, Ph.D., President and Chief Executive Officer of Janux. "We evaluate each program against a high bar for safety, activity, and differentiated profile. We prioritize resources toward programs that meet these criteria and offer opportunities to deliver best-in-class outcomes."

"The JANX008 study enabled a rigorous evaluation of activity for this EGFR-targeted TRACTr construct," said William Go, M.D., Ph.D., Chief Medical Officer of Janux. "We observed objective responses and disease control across treated patients. These findings provide important insight into how target biology and masking strategy define the therapeutic window and inform the continued advancement of our pipeline."

(Press release, Janux Therapeutics, APR 27, 2026, View Source [SID1234664820])

On April 27, 2026 Dispatch Bio, a biotech company engineering a universal treatment across solid tumors leveraging its first-in-class Flare platform, reported the presentation of new preclinical data supporting its SEND (Synthetic Efficacy eNableD) T cell armoring strategy at the American Society of Gene & Cell Therapy (ASGCT) (Free ASGCT Whitepaper) 2026 Annual Meeting, taking place May 11–15, 2026, in Boston. The data will be presented in a poster entitled, "SEND – A T cell armoring strategy that incorporates simultaneous signaling through multiple pathways for optimized safety and efficacy via novel cell state," during a poster session on Thursday, May 14, from 5:00–6:30 p.m.

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SEND is a novel T cell armoring strategy designed to overcome the limitations of supportive cytokine signals in the tumor microenvironment by utilizing a synthetic cytokine receptor to simultaneously activate multiple pathways required for optimal T cell function. Preclinical data show that SEND outperforms current benchmarks for armored T cell performance in high bar solid tumor models and has the potential to optimize safety and efficacy profiles of a multitude of immunotherapy treatments.

"Engineering T cells with a single cytokine signal often forces a tradeoff between proliferation, persistence, and effector function in engineered T cells," said Lex Johnson, Ph.D., Co-Founder and Chief Platform Officer. "SEND is designed to eliminate those compromises by coordinating multiple signaling pathways within the same cell, resulting in a fundamentally new T cell state with the potential for best-in-class performance. We look forward to sharing our findings at the upcoming ASGCT (Free ASGCT Whitepaper) conference."

"Based on these data, we believe SEND could have broad applicability across engineered T cell approaches, including autologous CAR T therapies, in vivo CAR T approaches, and TCR-based therapies, amongst others," said Barbra Sasu, Ph.D., Chief Scientific Officer. "We are advancing SEND as a foundational T cell armoring strategy, as we continue to work toward a world in which all people with cancer can be cured."

SEND-armored CAR T cells demonstrated robust anti-tumor activity in vivo, achieving tumor clearance at low doses, while remaining well tolerated at all doses tested with a 200X+ therapeutic window. Moreover, this activity was observed with or without lymphodepleting chemotherapy, which has the potential to significantly improve patient treatment options in the clinic. Single-cell RNA sequencing of tumor-infiltrating CAR T cells armored with SEND revealed, for the first time in published literature, simultaneous enrichment of effector and memory gene programs within the same cell, demonstrating robust expansion without exhaustion and contraction following tumor clearance, supporting controlled, antigen-dependent activity and a favorable safety profile.

(Press release, Dispatch Bio, APR 27, 2026, View Source [SID1234664818])

On April 27, 2026 Taiho Oncology, Inc., Taiho Pharmaceutical Co., Ltd., and Araris Biotech AG ("Araris") reported that the U.S. Food and Drug Administration (FDA) has completed its Investigational New Drug (IND) review period for ARC-02, an antibody-drug conjugate (ADC) being developed for the treatment of non-Hodgkin lymphoma, enabling Taiho Oncology to initiate a Phase 1 dose-escalation clinical trial of ARC-02.

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Taiho Pharmaceutical acquired Araris Biotech in March 2025, expanding Taiho group’s capabilities in biologics and ADC research and development. Araris is a spin-off of the Paul Scherrer Institute and ETH in Switzerland focused on the development of antibody-drug conjugates (ADCs). Central to Araris’ approach is its proprietary AraLinQ ADC technology, which enables the creation of stable and site-specific ADCs using standard antibodies with scalable manufacturing processes. ARC-02 is a CD79b-protein-targeting ADC based on Araris’ proprietary AraLinQTM technology using monomethyl auristatin E (MMAE) as payload, designed for selective targeting and killing of B-cell malignancies.

The trial represents the first clinical trial of a product candidate developed using the AraLinQ ADC technology and marks Taiho’s expansion into the clinical development of ADCs for oncology.

"Advancing our first ADC into the clinic represents an important milestone for our pipeline and reflects the continued expansion of Taiho group’s oncology development capabilities," said Fabio Benedetti, MD, Global Chief Medical Officer, Taiho Pharmaceutical. "This initial clinical study will allow us to evaluate ARC-02 in patients and generate data to inform both the continued development of ARC-02 and our ADC platform. We look forward to advancing this program as part of our broader efforts to deliver innovative therapies to people living with cancer."

About AraLinQ

AraLinQTM is Araris’ ADC technology, which enables site-specific payload attachment to a privileged attachment site on a specific amino acid residue (Q295) within the native antibody Fc framework. Preclinical data demonstrate that when a payload is attached to this site using Araris’ proprietary linkers, the antibody maintains nearly identical performance (e.g. pharmacokinetics and effector functions) to the unconjugated, original antibody. Furthermore, the linker-payload is connected to the antibody through a very strong isopeptide bond resulting in exceptional stability. Once entering a cancer cell via antibody-mediated internalization, the linker can be easily broken to release the payload. All three of these properties are key factors to enable efficient payload delivery and maximize ADC efficacy. AraLinQTM linkers are hydrophilic, rendering them soluble and avoiding their clumping in water-based solutions like blood. In addition, this linker can have unique branching structures that make it possible to create ADCs that carry multiple payloads of different types. AraLinQ allows for the generation of ADCs in one step using "off-the-shelf," antibodies that are native or engineered. The process is fast, cost-efficient and can be easily upscaled without the need for custom antibody synthesis.

(Press release, Taiho, APR 27, 2026, View Source [SID1234664817])

On April 27, 2026 Strand Therapeutics, a clinical-stage biotechnology company pioneering programmable mRNA medicines, reported it will present preclinical data from its in vivo CAR-T program at the 2026 American Society of Gene & Cell Therapy (ASGCT) (Free ASGCT Whitepaper) Annual Meeting, taking place May 11-15 in Boston.

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Ashlesha Odak, PhD, Principal Scientist of Advanced Cell Engineering, will present findings addressing a central challenge in the field: generating CAR-T cells directly in the body without ex vivo cell engineering. The data demonstrate that Strand’s programmable EverScript circular RNA (circRNA), combined with a targeted lipid nanoparticle (LNP) delivery approach, can generate functional CAR-T cells in vivo following intravenous administration, achieving robust target cell elimination across humanized mouse models and non-human primates.

Strand Signal Stack technology integrates an optimized EverScript circRNA backbone, enhanced CAR architecture, and a targeted LNP delivery approach capable of reaching T cells systemically without the manufacturing complexity of conventional ex vivo CAR-T approaches. The broader Strand Signal Stack technology also includes SignalLock, Strand’s proprietary microRNA (miRNA)-responsive regulatory sequences designed to modulate CAR protein expression in off-target cell types, thereby building safety controls directly into the construct while minimizing unintended immune activation and helping to support repeat dosing.

Together, these advances establish a programmable circRNA platform with the potential to enable scalable in vivo CAR-T therapies across cancer, autoimmune diseases, and beyond.

"Generating functional CAR-T cells inside the body has been a long-standing goal for the field, and the data show we can do it with delivery precision and programmable safety controls it requires," said Jake Becraft, PhD, Co-founder and Chief Executive Officer of Strand Therapeutics. "In vivo CAR-T is a natural extension of what we have been building, and the NHP data is exactly the kind of validation that moves this program forward."

"These results reflect years of work optimizing every layer of this platform, from the circRNA backbone and CAR architecture to the microRNA targeting system and built-in safety controls," said Tasuku Kitada, PhD, MBA, Co-founder, President, and Head of R&D of Strand Therapeutics. "What excites us is the breadth of what this unlocks. The same programmable architecture driving CAR-T activity in oncology has clear implications for autoimmune disease and beyond, and this data moves us meaningfully closer to both."

Abstract Title: Programmable circRNA-tLNP platform enables efficient in vivo CAR-T cell programming and robust activity in a NHP model
Session Type: Oral
Session Name: LNPs for in vivo CAR-T applications
Date and Time: Tuesday, May 12, 2026, at 9:00-9:15 am ET
Location: MCEC Room 210 ABC (Level 2)

Full abstract details are available on the ASGCT (Free ASGCT Whitepaper) Annual Meeting website.

(Press release, Strand Therapeutics, APR 27, 2026, View Source [SID1234664816])