On June 3, 2026 Cardiff Oncology presented its corporate presentation.

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(Presentation, Cardiff Oncology, JUN 3, 2026, View Source [SID1234666405])

On June 2, 2026 Telix Pharmaceuticals Limited (ASX: TLX, NASDAQ: TLX, "Telix") and United Imaging Healthcare North America, Inc. ("United Imaging") reported the signing of a Memorandum of Understanding (MOU) to evaluate a strategic research collaboration in the United States (U.S.) focused on advancing integrated theranostics solutions.

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The companies will evaluate the combination of United Imaging’s scanner platforms, software, connectivity and AI capabilities with Telix’s molecular imaging portfolio and validated clinical protocols. The collaboration will explore how a unified approach can drive theranostic workflow efficiencies and standardization by:

Enhancing integration between imaging systems and radiopharmaceutical workflows.
Enabling consistent, protocol-driven imaging performance across systems and sites.
Supporting treatment planning, monitoring, and longitudinal patient management.
Advancing data-driven and AI-enabled clinical decision support tools.
Jeffrey M. Bundy, Ph.D., President & Chief Commercial Officer, United Imaging Healthcare North America, said: "Theranostics represents a fundamental shift toward more integrated and personalized cancer care. Through this collaboration with Telix, we aim to explore how deeply integrated imaging, AI, and radiopharmaceutical workflows can be combined to support routine clinical use at scale."

Kevin Richardson, CEO, Telix Precision Medicine, added, "Realizing the full potential of theranostics requires close alignment between state-of-the-art scanners, integrated software solutions, and radiopharmaceutical innovation. By working with United Imaging, we are exploring new ways to deliver more seamless, data-driven workflow solutions that can support clinicians in their decision making, leading to better patient outcomes."

The collaboration will initially focus on TLX101-Px (Pixclara1, Floretyrosine F 18) in the U.S, with potential expansion into additional markets, and other Telix products and product candidates, subject to mutual agreement. Early efforts will include scanning protocol optimization, workflow support tools development and validation, and launching pilot programs aligned with high-impact clinical applications.

About TLX101-Px

TLX101-Px is a PET imaging candidate, which has been granted Fast Track and Orphan Drug designations by the FDA for the characterization of recurrent or progressive glioma from treatment related changes. In April 2026, the U.S. Food and Drug Administration (FDA) accepted Telix’s New Drug Application (NDA) for review, and assigned a PDUFA2 goal date of September 11, 2026.

TLX101-Px targets membrane transport proteins known as L-type amino acid transporters 1 and 2 (LAT1 and LAT2). This enables TLX101-Px to be potentially utilized as a patient selection and response assessment tool for Telix’s LAT1-targeting therapy candidate TLX101-Tx (131I-iodofalan), currently under investigation in the pivotal IPAX-BrIGHT trial in patients with recurrent glioblastoma3. TLX101-Px has not received a marketing authorization in any jurisdiction.

(Press release, Telix Pharmaceuticals, JUN 2, 2026, View Source [SID1234666403])

On June 2, 2026 Legend Biotech Corporation (NASDAQ: LEGN) (Legend Biotech or the Company), a global leader in cell therapy, reported that promising preliminary clinical data for LB2501, its investigational in vivo CD19/CD20 dual-targeting CAR-T cell therapy, in patients with relapsed/refractory B-cell non-Hodgkin lymphoma (R/R B-NHL), will be presented during a late-breaking session at the European Hematology Association (EHA) (Free EHA Whitepaper) 2026 Congress, taking place June 11-14, 2026, in Stockholm, Sweden.

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"The upcoming presentation of Phase 1 LB2501 data in patients with B-cell malignancies represents an important step in advancing in vivo CAR-T approaches," said Ying Huang, Ph.D., Chief Executive Officer of Legend Biotech. "By generating CAR-T cells directly within the patient, this approach has the potential to simplify treatment delivery and expand access for patients who may not be able to receive traditional CAR-T cell therapies. LB2501 is built on the TaVec platform, which is a proprietary lentiviral vector engineered to enhance T-cell specificity, transduction efficiency, and safety, while restricting transduction of non-T cells."

LB2501: Promising Phase 1 Trial of In Vivo CAR-T Data Demonstrate High Response Rates in B-cell Malignancies

Data from 12 patients across two dose cohorts in an ongoing Phase 1 study evaluating LB2501 in patients with R/R B-NHL provide early clinical evidence supporting the potential of an in vivo CAR-T approach in B-cell malignancies. LB2501 is designed to generate CAR-T cells directly within the patient following a single intravenous infusion, eliminating the need for cell manufacturing and lymphodepletion.

As of April 1, 2026, 12 patients with R/R B-NHL were treated across two dose levels (DL1 and DL2). Additional details will be presented at EHA (Free EHA Whitepaper) 2026. Key findings from the abstract include:

Efficacy Results

At DL2 (median follow-up for DL2 was 2.2 months [range, 2.0 to 3.8])
Objective response rate (ORR): 100% (6/6)
Complete response rate (CR): 83.3% (5/6)
All responses were ongoing at data cutoff

Pharmacokinetics

Dose-dependent in vivo CAR-T expansion observed
CAR-T cells detected in peripheral blood for up to 116 days

Safety Results

No dose-limiting toxicities (DLTs), serious adverse events (SAEs), or deaths were observed
Infusion-related reactions occurred in 75% of patients, all of which were ≤ Grade 2
Cytokine release syndrome (CRS) occurred in 66.7% of patients, all of which were ≤ Grade 2
No immune effector cell-associated neurotoxicity syndrome (ICANS) was reported
Grade ≥3 lentiviral vector-related and CAR-T-related adverse events were limited to decreased lymphocyte count and decreased neutrophil count

EHA Presentation (June 11-14, 2026)

Abstract No. Title Information
Abstract #LB5006
Late-Breaking Oral Presentation First-in-human trial of LB2501, an in vivo CD19/CD20 dual targeting CAR-T therapy, in relapsed/refractory B-Cell NHL

Session ID: s204
Date/Time: Sunday, June 14, 2026, 9:15-10:45 AM CEST
Location: Nobel Hall

ABOUT LB2501
LB2501 is an investigational, potential first-in-class CD19/CD20 dual-targeting in vivo CAR-T therapy designed to generate CAR-T cells directly within the patient following a single intravenous infusion. It is being evaluated in an ongoing Phase 1, open-label study NCT07002112) in patients with relapsed/refractory B-cell malignancies to assess safety, tolerability, and preliminary efficacy.i

ABOUT B-CELL NON-HODGKIN LYMPHOMA
Non-Hodgkin lymphoma (NHL) is a group of cancers that originate in lymphocytes, a type of white blood cell that plays a key role in the body’s immune system.ii B-cell lymphomas account for approximately 85% of NHL cases and arise from abnormal growth of B lymphocytes (B cells), which are responsible for producing antibodies. These malignancies include a range of subtypes that vary in aggressiveness, from slow-growing to highly aggressive disease.

(Press release, Legend Biotech, JUN 2, 2026, View Source [SID1234666402])

On June 2, 2026 Greywolf Therapeutics, a clinical-stage biotech company advancing novel antigen modulation treatments for cancer and autoimmune diseases, reported clinical and translational results from six completed Phase 1b expansion cohorts of the EMITT-1 trial (NCT06923761) evaluating GRWD5769, a first-in-class oral ERAP1 inhibitor, in combination with cemiplimab in patients with secondary anti-PD-1 resistance or microsatellite stable colorectal cancer without liver metastases (MSS-CRC NLM).

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Data were presented in an oral session at the 2026 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting by Professor Fiona Thistlethwaite, Consultant Medical Oncologist at The Christie NHS Foundation Trust and Medical Director of the National Institute for Health and Care Research (NIHR) Manchester Clinical Research Facility at The Christie, and Principal Investigator of the EMITT-1 trial.

Professor Fiona Thistlethwaite, Consultant Medical Oncologist at The Christie NHS Foundation Trust and Medical Director of the National Institute for Health and Care Research (NIHR) Manchester Clinical Research Facility at The Christie said:

"What excites me about this trial is the combination of what we’re seeing – strong signals of efficacy across six tumor types that have shown great resistance to immunotherapy, with very few side effects. That’s unusual at such an early stage."

Highlights from the Phase 1b data

Objective Response Rates (ORR) of 13–36% across all six cohorts in patients with a median of 2 prior lines of therapy and documented secondary anti-PD-1 resistance (except MSS-CRC (NLM) where this therapy is not effective)
Durable Clinical Benefit of 18–55% across all cohorts (DCB — defined as complete response, partial response, or stable disease lasting ≥6 months) and Progression Free Survival duration of 33 wks in NSCLC, 16 wks in HCC and 33 wks in MSS-CRC (NLM) (with 8.8 months median follow-up and still maturing). These data are very encouraging in a setting where durable benefit is exceptionally rare.
GRWD5769 is well tolerated in cemiplimab combination, with no safety signals and most adverse events being Grade 1

Evaluable*
(n) Partial response(s) Overall response rate
(%) Durable clinical benefit
(%) Progression-free survival
(wks)
Urothelial carcinoma 14 5 36 36 8
Non-small cell lung cancer 14 3 21 55 33
Hepatocellular carcinoma (liver cancer) 14 2 14 32 16
Microsatellite stable colorectal cancer (no liver metastases) 12 2 17 51 33
Cervical 14 2 14 18 9
Head and neck squamous cell carcinoma 8 1 13 38 14

Tom Lillie, Chief Medical Officer of Greywolf Therapeutics, said:

"Seeing the combination of strong durable clinical benefit rates and sustained PFS in a population that had already failed anti-PD-1 therapy, and in MSS-CRC where it isn’t licensed, is a clinically meaningful signal. Critically, we’re seeing this alongside a tolerability profile that enables patients to remain on treatment for extended periods, providing excellent potential for GRWD5769 to be used in other combination therapies."

Peter Joyce, CEO and Co-founder of Greywolf Therapeutics, said:

"EMITT-1 has validated a mechanism that the field has long recognized as scientifically compelling but clinically unproven. We are now advancing into Stage 2 cohort expansions to inform a randomized Phase 2 study, and we believe this data positions GRWD5769 as a genuinely differentiated approach to two of the largest unmet needs in oncology — T cell exhaustion and tumor visibility to the immune system."

About GRWD5769

GRWD5769 is a first-in-class oral small molecule inhibitor of Endoplasmic Reticulum Aminopeptidase 1 (ERAP1), an enzyme that regulates tumor antigen presentation on MHC-I. By inhibiting ERAP1 on a cyclical Q3W on/off schedule, GRWD5769 aims to generate alternating antigenic repertoires to broaden T cell responses and prevent T cell exhaustion driven by chronic antigen exposure. The drug is administered as an oral capsule in combination with cemiplimab, an approved anti-PD-1 therapy.

About the EMITT-1 trial

EMITT-1 (NCT06923761) is a global Phase 1/2 study evaluating GRWD5769 in combination with cemiplimab across multiple solid tumor types. The Phase 1b expansion enrolled patients across six cohorts: non-small cell lung cancer (NSCLC), urothelial carcinoma (UC), hepatocellular carcinoma (HCC), MSS-CRC (without liver metastases), squamous cell carcinoma of the head and neck (SCCHN), and cervical cancer. All patients had secondary resistance to prior anti-PD-1 therapy, except for the MSS-CRC NLM cohort. The trial is ongoing across 28 centers in Australia, France, Spain, and the United Kingdom.

(Press release, Grey Wolf Therapeutics, JUN 2, 2026, View Source [SID1234666401])

On June 2, 2026 SEED Therapeutics, Inc. ("SEED"), a clinical-stage biotechnology company pioneering rationally designed molecular glue degraders, reported the presentation of a trial-in-progress poster at the 2026 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting highlighting the first-in-human Phase 1 study of ST-01156, SEED’s oral, selective RBM39 molecular glue degrader. The presentation underscores SEED’s transition from platform validation to clinical execution, with ST-01156 advancing across multiple RBM39-dependent cancers, with development informed by mechanism-based preclinical data and real-time pharmacokinetic and pharmacodynamic assessments.

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ST-01156 is designed to degrade RNA-binding motif protein 39 (RBM39), a regulator of RNA splicing programs that govern oncogenes essential for tumor survival. The ASCO (Free ASCO Whitepaper) poster outlines the scientific rationale, Phase 1 dose-escalation design, and planned expansion strategy for ST-01156which is currently being evaluated in a first-in-human Phase 1 dose-escalation study (NCT07197554) in patients with advanced solid malignancies.

Highlights At A Glance

Clinical-stage lead asset: ST-01156 is currently being evaluated in an open-label Phase 1 study in patients with advanced solid malignancies.
Oral, brain-penetrant molecular glue degrader: ST-01156 was rationally optimized for selective RBM39 degradation, potency, metabolic stability, and drug-like properties.
Integrated biomarker and dose-selection strategy: The study incorporates real-time RBM39 target engagement in peripheral blood mononuclear cells (PBMCs), together with safety and pharmacokinetics, to support recommended Phase 2 dose (RP2D) selection.
Broad oncology expansion potential: Planned expansion cohorts include Ewing sarcoma, advanced hepatocellular carcinoma, KRAS-mutant cancers, and other RBM39-dependent tumors, including biliary tract carcinoma, endometrial carcinoma, and DNA damage repair–aberrant cancers.
Preclinical proof-of-concept across multiple models: SEED has demonstrated preclinical antitumor activity in response to RBM39 degradation, including tumor regression, with complete regression observed in Ewing sarcoma, neuroblastoma, and KRAS-mutant colorectal cancer models.

Together, these findings support SEED’s strategy to advance ST-01156 from dose escalation into patient-enriched expansion cohorts where emerging RBM39 biology informs indication selection and clinical proof-of-concept.

Scientific Rationale and ASCO (Free ASCO Whitepaper) Poster Takeaways

RBM39 is an RNA-binding protein that regulates cancer-relevant RNA splicing programs, including pathways involved in tumor proliferation, survival, DNA damage response, and oncogenic fusion proteins. ST-01156 is designed to act as a molecular glue degrader by recruiting RBM39 to DCAF15, an E3 ligase adapter, leading to RBM39 degradation through the ubiquitin-proteasome system. By eliminating RBM39, ST-01156 has the potential to disrupt multiple cancer-driving pathways that are difficult to address with conventional targeted therapies.

The ASCO (Free ASCO Whitepaper) poster highlights preclinical and clinical-development findings supporting SEED’s strategy:

Ewing sarcoma rationale: ST-01156 demonstrated tumor regression in an A673 Ewing sarcoma xenograft model, with complete regression at higher dose levels. Separately, treatment with ST-00937, a non-deuterated precursor of ST-01156, showed complete elimination of RBM39 and the EWS-FLI1 fusion protein in tumor lysates.
Neuroblastoma and KRAS-mutant cancer activity: ST-01156 produced complete tumor regression in an SH-SY5Y neuroblastoma xenograft model, while ST-00937 demonstrated complete regression in an HCT-116 KRAS G13D-mutant colorectal cancer xenograft model.
Mechanism-based expansion strategy: The clinical development plan includes expansion cohorts in Ewing sarcoma, advanced hepatocellular carcinoma, KRAS-mutant cancers, and other RBM39-dependent tumors, including biliary tract carcinoma, endometrial carcinoma, and tumors with DNA damage repair aberrations.
Integrated dose-selection approach: The Phase 1 study is designed to determine the optimal dose and recommended Phase 2 dose using safety, pharmacokinetic, and pharmacodynamic data, including real-time measurement of RBM39 target engagement in PBMCs.

"ST-01156 is designed to address a biologically important and difficult-to-drug target through selective RBM39 degradation. The ASCO (Free ASCO Whitepaper) presentation highlights a disciplined clinical strategy that integrates safety, pharmacokinetics, and real-time target engagement to guide dose selection and expansion into cancers with strong mechanistic rationale. We believe this approach positions ST-01156 to generate early meaningful clinical proof-of-concept across multiple RBM39-dependent tumor types," said Dr. James Tonra, PhD, President, and Chief Scientific Officer of SEED.

"The advancement of ST-01156 into first-in-human clinical evaluation is an important milestone for SEED and a validation of our RITE3 technology. Our goal is not only to discover molecular glues, but to rationally design degraders with clear target biology, translational biomarkers, and a defined clinical development path. ST-01156 reflects that strategy and represents a meaningful step toward unlocking disease drivers that have historically been considered undruggable," said Dr. Lan Huang, PhD, Co-Founder, Chairman, and Chief Executive Officer of SEED.

Clinical Development Status

ST-01156 is being evaluated in an ongoing, open-label Phase 1 multiple ascending dose (MAD) study in patients with advanced solid malignancies. The study is designed to enroll approximately 30 to 50 patients, with ST-01156 administered orally once daily for five days every seven days, with the option to adapt to a continuous once-daily schedule based on emerging data.

The primary objectives are to characterize safety and tolerability and determine the optimal dose and recommended Phase 2 dose. Secondary objectives include pharmacokinetics, RBM39 target engagement in PBMCs, and preliminary antitumor activity. Per protocol, SEED plans to evaluate ST-01156 in mechanism-based back-fill cohorts within this MAD study, including Ewing sarcoma, advanced hepatocellular carcinoma, KRAS-mutant cancers, and other RBM39-dependent tumors. Data from these cohorts are intended to inform the design of the protocol’s subsequent Phase 1 expansion phase.

ASCO 2026 Poster Presentation Details:

Title: First-in-Human Clinical Evaluation of ST-01156, an Optimized and Selective Degrader of RNA-Binding Motif 39 (RBM39): A Phase 1 Study in Advanced Solid Malignancies with a Focus on RBM39-Dependent Cancers
Presenter/Authors: Eric K. Rowinsky, Gregory M. Cote, George D. Demetri, Robert G. Maki, Suzanne George, Daneng Li, Alain C. Mita, Monica M. Mita, Jordi Rodon Ahnert, Dan Lu, Dong Liu, Lan Huang, James Tonra
Session: Developmental Therapeutics—Molecularly Targeted Agents and Tumor Biology
Abstract Number: TPS3164

(Press release, Seed Therapeutics, JUN 2, 2026, View Source [SID1234666400])