On June 2, 2026 Kazia Therapeutics Limited (NASDAQ: KZIA) ("Kazia," "Kazia Therapeutics" or the "Company"), a clinical-stage oncology company advancing therapies designed to reprogram cancer biology and overcome treatment resistance, reported the appointment of James Levine as Chief Financial Officer, effective June 1, 2026. Mr. Levine brings more than two decades of experience across investment banking, executive and financial leadership at publicly traded biotech companies.

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"James has built an impressive career leading financial strategy, strategic transactions and major pharmaceutical collaborations, following an extensive career in investment banking," said Dr. John Friend, CEO, Kazia Therapeutics. "As we advance paxalisib and progress our pipeline, James’ expertise will be central to helping us capitalize on that momentum and continue building long-term value for patients and shareholders."

Most recently, Mr. Levine served as Chief Financial Officer of Cardiff Oncology, a clinical-stage oncology company developing a PLK1 inhibitor therapy for solid tumors. Prior to Cardiff Oncology, Mr. Levine served as CFO of Cidara Therapeutics, an antifungal and antiviral biotech company, where he led the financial structuring of a $568 million licensing collaboration with Mundipharma and a $780 million global partnership with Janssen Pharmaceuticals (Johnson & Johnson). He also served as CEO of Verenium Corporation, an industrial biotech company, where he executed major asset sales for total proceeds of approximately $200 million, as well as Sapphire Energy, a human nutrition-focused biotech.

Earlier in his career, Mr. Levine spent 12 years at Goldman Sachs & Co. as a Managing Director advising pharmaceutical and biotech clients across the U.S. and Europe on financings, mergers and acquisitions and strategic transactions, including landmark deals such as the Glaxo Wellcome and SmithKline Beecham merger. Mr. Levine holds a Master of Business Administration degree from The Wharton School at the University of Pennsylvania.

"I am very excited to be joining Kazia as the Company advances paxalisib across multiple indications and builds out a promising pipeline targeting novel mechanisms of treatment resistance," added Mr. Levine. "I look forward to working closely with the management team to help translate Kazia’s scientific progress into strategic and financial outcomes as we approach what we expect to be a period of meaningful clinical and strategic milestones for the Company."

(Press release, Kazia Therapeutics, JUN 2, 2026, View Source [SID1234666368])

On June 2, 2026 AvenCell Therapeutics, a clinical-stage cell therapy company developing switchable CAR-T therapies for cancer, reported that data from the completed Phase 1a portion of the RevSTAR-123 study, evaluating AvenCell’s investigational switchable allogeneic CAR-T candidate (AVC-201) in patients with CD123-positive relapsed/refractory (r/r) or minimal residual disease (MRD) positive acute myeloid leukemia (AML), will be presented in a late-breaking oral presentation in the plenary session at the 2026 European Hematology Association (EHA) (Free EHA Whitepaper) Congress, taking place June 11-14 in Stockholm, Sweden. The study is registered at ClinicalTrials.gov as NCT05949125.

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EHA 2026 Abstract Details

Abstract number

EHA-7241

Title

First-in-class Switchable Allogeneic CAR-T therapy for
CD123+ AML – Results from the Phase Ia RevSTAR-
123 (AVC-201-01) Study

Topic

Gene therapy, cellular immunotherapy and vaccination
– Clinical

Presenter

Martin Wermke, University Hospital Carl Gustav Carus
Dresden

Presentation details

Plenary Abstracts Session on Saturday, June 13, 12:00
– 13:30 CEST

(Press release, AvenCell Therapeutics, JUN 2, 2026, View Source [SID1234666384])

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])

On June 2, 2026 Kura Oncology, Inc. (Nasdaq: KURA, "Kura") and Kyowa Kirin Co., Ltd. (TSE: 4151, "Kyowa Kirin") reported the publication in Blood of updated results from the relapsed/refractory (R/R) NPM1-mutated acute myeloid leukemia (NPM1-m AML) cohort of KOMET-007, a Phase 1a/b trial evaluating ziftomenib in combination with venetoclax and azacitidine (ven/aza). The publication reports nearly two-thirds of patients experienced clinically meaningful, deep and durable responses with a well-tolerated safety profile in adults with R/R NPM1-m AML.

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KOMZIFTI (ziftomenib) is approved by the U.S. Food and Drug Administration as monotherapy for adult patients with relapsed or refractory AML with a susceptible NPM1 mutation who have no satisfactory alternative treatment options. Ziftomenib in combination with ven/aza is investigational and has not been approved by the FDA.

"This analysis provides a more mature evaluation of ziftomenib in combination with venetoclax and azacitidine in patients with NPM1-mutated AML," said Eunice S. Wang, M.D., Chief of Leukemia, Roswell Park Comprehensive Cancer Center, and co-first senior author of the publication. "In the relapsed/refractory setting, outcomes with venetoclax-based regimens in patients with NPM1-mutant AML remain suboptimal, highlighting the substantial need for more effective therapies. These KOMET-007 results are notable for the depth and durability of response observed with the investigational three-drug combination. The favorable safety profile also supports the continued evaluation of this combination in a setting where better treatment options are urgently needed."

"As combination approaches become increasingly important in this setting, the data highlighted in this publication strengthen the case for ziftomenib as a backbone in NPM1-mutant AML," said Mollie Leoni, M.D., Chief Medical Officer of Kura Oncology. "Ziftomenib combined with ven/aza demonstrated deep molecular responses, durable remissions, and a generally manageable safety profile in R/R NPM1-m AML. These findings support our ongoing efforts to evaluate ziftomenib-based combinations across the treatment continuum, including in randomized studies designed to define the potential of ziftomenib in newly diagnosed disease."

KOMET-007 Results in R/R NPM1-m AML

The data include 64 response-evaluable patients with R/R NPM1-m AML from the ongoing KOMET-007 Phase 1a/b trial (NCT05735184), 27 of whom were treated in phase 1a dose escalation and 37 of whom were treated in phase 1b expansion, as of the January 16, 2026 data cutoff date. Patients had received 1 to 8 prior lines of therapy (median of 1), and 37 patients (55%) had prior venetoclax exposure.

Robust clinical activity was observed in patients with R/R NPM1-m AML across all ziftomenib dose levels, with nearly two-thirds of all patients experiencing clinically meaningful, deep, and durable responses. In addition, rapid responses were observed, with a median time to composite complete remission (CRc) of 3.9 weeks.

Venetoclax-Naïve Population (600 mg ziftomenib)

70% CRc rate (16/23) with 75% (9/12) central measurable residual disease (MRD) negativity (<0.01% threshold), demonstrating deep molecular responses
87% objective response rate (ORR) (20/23)
Median duration of CRc response of 9.2 months (95% CI, 5.8-NE)
Median overall survival (OS) not reached after median follow-up of 10.7 months (N=25)
Venetoclax-Experienced Population (600 mg ziftomenib)

24% CRc rate (6/25) with 50% (3/6) central MRD negativity (<0.01% threshold)
48% ORR (12/25)
Median duration of CRc response of 8.6 months (95% CI, 1.6-NE)
Median OS of 7.4 months after median follow-up of 9.9 months (N=26)
Safety in Both Populations at All Dose Levels (N=67)

The triplet combination was well tolerated, with a safety profile consistent with that reported for ven/aza alone
Low rates of differentiation syndrome (3%, 2/67) observed with the protocol-specified staggered dosing schedule of ven/aza before menin inhibition; both events resolved with protocol-specified mitigation
One case of ziftomenib-related QTc; the event resolved without dose interruption or dose change
Median time to neutrophil and platelet recovery were similar to ven-based regimens alone, supporting feasibility in combination regimens
"For people living with relapsed or refractory NPM1-mutated AML, the need for new treatment regimens remains significant," said Yoshifumi Torii, Ph.D., Chief Medical Officer of Kyowa Kirin. "These published findings in the journal Blood add to our understanding of ziftomenib in combination with venetoclax and azacitidine and reinforce our shared commitment with Kura Oncology to advancing this program with urgency and rigor for patients who may benefit."

The ongoing KOMET-007 Phase 1a/1b trial (NCT05735184) is evaluating ziftomenib in combination with ven/aza in multiple cohorts of newly diagnosed chemotherapy-ineligible AML and relapsed/refractory AML. The trial is also evaluating ziftomenib in combination with cytarabine plus daunorubicin (7+3) in patients with newly diagnosed NPM1-m or KMT2A-rearranged (KMT2A-r) AML, as well as ziftomenib combined with quizartinib plus 7+3 intensive chemotherapy in patients with newly diagnosed AML harboring FLT3-ITD/NPM1-m co-mutations.

Kura and Kyowa Kirin are continuing to evaluate ziftomenib across multiple combination regimens and treatment settings, including in the ongoing pivotal KOMET-017 Phase 3 trials in newly diagnosed NPM1-m and KMT2A-r AML.

(Press release, Kura Oncology, JUN 2, 2026, View Source [SID1234666369])

On June 2, 2026 3H Pharmaceuticals reported new clinical data for its wholly owned candidate, 3HP-2827 at the 2026 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting. The ongoing study focuses on patients with advanced cholangiocarcinoma (CCA) and other solid tumors carrying FGFR2 alterations—an area of persistent and significant unmet need. The data showed that 3HP-2827, a highly selective FGFR2 inhibitor, demonstrated encouraging anti-tumor activity in patients with advanced CCA driven by FGFR2 fusions or rearrangements, as well as notable tumor shrinkage in FGFR2-mutated solid tumors. On May 31 in Chicago, on the sidelines of the ASCO (Free ASCO Whitepaper) meeting, eChinaHealth spoke with Academician Zhou Jian, President of Zhongshan Hospital, Fudan University. He shared his views on the current treatment landscape for FGFR2-altered CCA, the clinical profile and future potential of 3HP-2827, and the prospects for further advances in the field.

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Academician Zhou noted that CCA is a highly aggressive cancer, with incidence rising in both China and worldwide. For patients with advanced disease, the prognosis is extremely poor—even worse than for hepatocellular carcinoma. Currently, the standard first-line treatment for advanced CCA remains chemotherapy plus immunotherapy. In recent years, however, a growing number of new approaches have emerged. Drugs targeting IDH1 and FGFR, for instance, have already received approval. At this year’s ASCO (Free ASCO Whitepaper) Annual Meeting alone, more than 80 abstracts on CCA were presented, with FGFR2-targeted therapy emerging as a particularly active area of research. Earlier studies have validated the efficacy of FGFR2 inhibition in CCA, and as these targeted agents are refined, the efficacy data continue to improve. Looking ahead, FGFR2-directed therapy is expected to play a larger role in the treatment of advanced CCA, offering patients more precise and effective options.

3HP-2827, a novel and highly selective FGFR2 inhibitor, is being evaluated in a multicenter clinical study in China led by Academician Fan Jia and Professor Shen Lin, with RLY-4008 as the active comparator. To date, the efficacy of 3HP-2827 appears comparable to the early-stage clinical results reported for RLY-4008, and both agents have shown superior efficacy compared with pan-FGFR inhibitors. In addition, 3HP-2827 has demonstrated a favorable safety profile. Of note, the patient population in the current study was more heavily pretreated: 80% of patients had previously received an immune checkpoint inhibitor (ICI) in combination with chemotherapy, and 60% had undergone prior anti-angiogenic therapy. Additional clinical data will be important to further evaluate the potential of this approach.

Based on available data, both RLY-4008 and Pemigatinib have shown greater efficacy in the first-line treatment of advanced CCA than in the second-line setting. The latest data for single-agent RLY-4008 show an objective response rate (ORR) of 46.5% among 144 second-line patients, while the ORR reached 63.6% in a small cohort of 11 first-line patients—though the limited sample size in the first-line group requires cautious interpretation and further validation. For Pemigatinib, prior phase II and the most recent phase III data report an ORR of 35.5% in 146 second-line patients and 47.0% in 83 first-line patients. To date, 3HP-2827 has generated preliminary efficacy evidence in the second-line setting. Evaluating its single-agent activity in the first-line setting to pursue a first-line indication represents an important next step.

Academician Zhou said he expects the future first-line treatment paradigm for CCA to shift toward a multi-drug, multi-modality combination approach integrating chemotherapy, immunotherapy and targeted therapy. Such a strategy, he noted, is scientifically sound and could improve both treatment efficacy and patient outcomes. From a safety perspective, the main adverse reactions linked to 3HP-2827 are FGFR2-related toxicities affecting the skin and mucosa — a profile distinct from that of chemotherapy or immunotherapy. That difference suggests a low risk of overlapping toxicity when used in combination, supporting the potential for 3HP-2827 to be added to existing regimens. In addition, among patients with FGFR2 fusion- or rearrangement-driven CCA treated with 3HP-2827, two achieved complete disappearance of target lesions, and the majority experienced substantial tumor shrinkage. Because most CCA patients are no longer candidates for surgery at initial diagnosis, the pronounced tumor-shrinking effect of 3HP-2827 opens the door to exploring conversion therapy in the future — using preoperative single-agent treatment to downstage tumors and expand the pool of patients eligible for curative resection.

Currently, most FGFR2-targeted agents in clinical development are aimed at CCA patients with FGFR2 fusions or rearrangements. In contrast, patients with FGFR2-mutated solid tumors have few options, with no approved therapies to date. FGFR2 mutations occur across a wide range of solid tumors — including biliary tract cancers, gynecologic malignancies, melanoma, colorectal cancer, lung cancer, gastric cancer and urothelial carcinoma — representing a patient population larger than that of FGFR2 fusions or rearrangements. The longstanding lack of a targeted treatment for this group highlights a significant unmet medical need. The activity observed with 3HP-2827 suggests a potential new treatment approach for these patients.

The clinical data released by 3H Pharmaceuticals at the meeting showed that among patients with FGFR2-mutated solid tumors, 3HP-2827 achieved a best objective response rate (ORR) of 57.1% and a disease control rate (DCR) of 100%. Although the number of enrolled patients remains small at this stage, the cohort already includes multiple clinically relevant FGFR2 mutation sites, including N549K, Y375C, C382R and F276C. Looking ahead, the clinical development program for 3HP-2827 should continue to gather additional data in FGFR2-mutated solid tumors and initiate a multi-histology basket trial, with the goal of further evaluating its potential in this patient population.

In the interview, Academician Zhou Jian of Zhongshan Hospital, Fudan University, discussed the latest clinical data on 3HP-2827, a highly selective FGFR2 inhibitor, in patients with FGFR2-altered advanced CCA and other solid tumors. He noted that while chemotherapy plus immunotherapy remains the current standard first-line treatment for advanced CCA, FGFR2-targeted therapy is emerging as an important precision medicine approach. Looking ahead, Zhou recommended pursuing first-line treatment studies, combination therapy regimens and basket trials targeting FGFR2 mutations — strategies that could further expand the reach of precision oncology.

Note: 3HP-2827 is a highly selective FGFR2 inhibitor independently developed by 3H Pharmaceuticals. It works by specifically inhibiting FGFR2 phosphorylation, blocking the FGFR2 signaling pathway and producing anti-tumor activity. The drug is designed to offer a more effective and better-tolerated treatment option for patients with FGFR2 alterations, especially those who have developed resistance to prior therapies.

(Press release, 3H Pharmaceuticals, JUN 2, 2026, View Source [SID1234666385])