On June 29, 2026 Ipsen (Euronext: IPN; ADR: IPSEY) and Kartos Therapeutics, reported they have entered into a definitive merger agreement under which Ipsen has agreed to acquire Kartos Therapeutics. The acquisition adds navtemadlin, an investigational MDM2 inhibitor designed to restore the natural tumor-suppressing function of p53, a critical tumor-suppressor in myelofibrosis. Data show strong therapeutic potential of navtemadlin for intermediate and high-risk TP53 wild-type (wt) myelofibrosis as an add-on treatment for patients with a suboptimal response to standard of care ruxolitinib.

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"This acquisition further strengthens our late-stage oncology pipeline and reflects our continued focus on bringing transformational treatments to people living with cancer," said David Loew, CEO, Ipsen. "We are excited by the potential of navtemadlin to define a new treatment paradigm for patients with myelofibrosis who have a suboptimal response to current standard of care, addressing a critical care gap and offering the potential for a new therapeutic option as early as 2028."

Current standard of care ruxolitinib improves splenomegaly and myelofibrosis-related symptoms. However, a significant proportion of patients experience a suboptimal response to ruxolitinib, resulting in treatment discontinuation. Patient outcomes after ruxolitinib discontinuation are dismal, with a median overall survival of approximately 1-2 years. Navtemadlin is currently being evaluated in the global Phase III trial POIESIS designed to enroll >600 patients across >250 sites, as an add-on therapy to standard of care ruxolitinib in patients with intermediate and high-risk TP53wt myelofibrosis who have a suboptimal response to ruxolitinib. The trial builds on earlier clinical evidence, including a Phase Ib/II trial (KRT-232-109) in which add-on navtemadlin demonstrated clinically meaningful and disease-modifying activity in myelofibrosis patients who had a suboptimal response to standard of care ruxolitinib. Data presented at the European Hematology Association (EHA) (Free EHA Whitepaper) Congress in 2023 showed that at Week 24, in patients with a suboptimal response to ruxolitinib (n=19), 42% achieved at least a 25% reduction in spleen volume, 32% achieved at least a 35% reduction in spleen volume, and 32% achieved a total symptom score improvement of at least 50%. These data also showed potential disease modification activity of navtemadlin, as evidenced by 71% of evaluable patients (n=7) achieving a ≥20% reduction of driver variant allele frequency and 57% showing an improvement in bone marrow fibrosis by Central Review of ≥1 Grade by Week 24.

Srdan Verstovsek, MD, PhD, Chief Medical Officer of Kartos Therapeutics, commented, "As a treating clinician who cared for more than a thousand patients with myelofibrosis, I have seen first-hand the significant care gap for patients with myelofibrosis who remain symptomatic or have persistent splenomegaly despite ruxolitinib treatment. Navtemadlin has the potential to enhance the existing standard of care through an add-on approach designed to move patients with a suboptimal response into a clinical responder group by optimizing their care. We believe this innovative treatment paradigm could meaningfully improve outcomes for patients while avoiding unnecessary over-treatment of those already responding well."

"Myelofibrosis remains a serious and rare blood cancer associated with a substantial symptom burden and progressive splenomegaly that significantly impact quality of life," said John Mascarenhas, Professor of Medicine at the Icahn School of Medicine at Mount Sinai and Director of the Center of Excellence for Blood Cancers and Myeloid Disorders. "The clinical rationale for combining navtemadlin with ruxolitinib is very compelling, and the emerging data suggest the synergistic potential to deepen responses and address the underlying biology of the disease."

"The Phase III POIESIS trial has the potential to redefine how we treat patients with myelofibrosis," said Dr Pankit Vachhani, Associate Professor of Medicine and Director of Clinical Research Unit at the University of Alabama at Birmingham, and Global Principal Investigator of POIESIS. "It is the largest trial conducted in this disease and uniquely designed to reflect real-world clinical practice. The trial evaluates how adding navtemadlin can deliver more clinically meaningful and durable responses, thereby addressing a critical unmet need. I am excited by the prospect of navtemadlin delivering disease modifying benefits, ushering an era of rational combination therapies for those with suboptimal response to standard therapy, and targeting complementary disease pathways beyond JAK inhibition alone in myelofibrosis."

Transaction details
Under the terms of the agreement and plan of merger, Ipsen through a fully-owned subsidiary, will pay $450 million upfront at closing. Kartos Therapeutics shareholders are also eligible to receive additional milestone payments of up to $1.3 billion including a significant regulatory approval milestone and sales-based milestones.

This late-stage transaction is expected to be accretive to Ipsen’s core operating income from 2029, with limited dilution to 2026 full-year guidance. The transaction is anticipated to close by the end of Q3 2026, subject to fulfilment of customary closing conditions including the expiration of the waiting period under the Hart-Scott-Rodino Antitrust Improvements Act.

Advisors
Orrick Herrington & Sutcliffe LLP (DC office) is acting as legal counsel to Ipsen. Goldman Sachs & Co. LLC and PJT Partners (UK) Ltd are serving as financial advisors to KARTOS THERAPEUTICS. DLA Piper LLP (NY office) is serving as legal counsel to KARTOS THERAPEUTICS.

About navtemadlin
Navtemadlin is an investigational oral MDM2 inhibitor being developed as an add-on therapy to ruxolitinib for patients with myelofibrosis who have a suboptimal response to ruxolitinib. The Phase III POIESIS study is evaluating whether the addition of navtemadlin could improve clinical outcomes compared with ruxolitinib alone in this patient population. Early clinical data demonstrate navtemadlin has the potential to transform suboptimal responses to standard of care ruxolitinib into clinically meaningful responses in patients with intermediate and high risk TP53wt myelofibrosis, to provide both enhanced clinical outcomes and potential disease-modifying benefit.

About myelofibrosis
Myelofibrosis is a myeloproliferative neoplasm, frequently linked to alterations in the JAK/STAT pathway, in which patients develop bone marrow fibrosis due to the abnormal proliferation of hematopoietic stem cells and secretion of fibrogenic cytokines. As marrow function declines, blood production shifts to other organs, most often the spleen, leading to splenomegaly. Myelofibrosis is characterized by bone marrow failure, fibrosis, splenomegaly and a high symptom burden that can significantly affect quality of life, including fatigue, night sweats and other progressive symptoms. It also carries a risk of transformation to acute myeloid leukemia. The median age at diagnosis is approximately 67–69 years and the condition affects around 1.5 per 100,000 people in the U.S. and Europe. Approximately 75–89% of patients are intermediate- or high-risk at diagnosis and more than 95% are TP53wt. Ruxolitinib, a JAK inhibitor, is the first-line standard of care; however, it is estimated that a significant proportion of patients have an initial suboptimal response and approximately 50%-75% discontinue treatment after three years. Median overall survival is typically one to two years after treatment discontinuation, underscoring the need for new strategies that can increase the number of patients that can achieve optimal clinical outcomes.

(Press release, Ipsen, JUN 29, 2026, View Source [SID1234668991])

On June 29, 2026 Genmab A/S (Nasdaq: GMAB) reported topline results from the Phase 3 EPCORE DLBCL-4 trial evaluating the combination of fixed duration epcoritamab, a T-cell engaging bispecific antibody administered subcutaneously, and lenalidomide, compared to standard-of-care, rituximab plus gemcitabine plus oxaliplatin (R-GemOx), in adult patients with relapsed or refractory (R/R) diffuse large B-cell lymphoma (DLBCL) who received at least one prior line of treatment. Based on topline results, the trial met its primary objective, demonstrating statistically significant and clinically meaningful improvement in progression-free survival (PFS). The risk of disease progression and death was reduced by 60% (HR 0.40 [95% CI 0.30, 0.55]; p value < 0.0001) and 56% (HR 0.44 [95% CI 0.33, 0.60]; p value < 0.0001), based on different censoring rules in the U.S. and outside the U.S., respectively. The safety profile of epcoritamab when administered in combination with lenalidomide was consistent with the previously reported safety profiles of the individual agents (epcoritamab or lenalidomide).

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"These topline results add to the growing evidence supporting the versatility of epcoritamab-based combinations, including fixed-duration epcoritamab, across lines of therapy for patients with relapsed or refractory large B-cell lymphoma who received at least one prior treatment," said Jan van de Winkel, Ph.D., Chief Executive Officer of Genmab. "With each new combination and treatment setting, we are building on our vision for epcoritamab as a core therapy across B-cell malignancies. We look forward to engaging with regulatory authorities as we continue to advance this program."

Genmab and AbbVie will engage global regulatory authorities. Data will be submitted for presentation at a future medical meeting.

About the EPCORE DLBCL-4 Trial
EPCORE DLBCL-4 (NCT06508658) is a global Phase 3 open label, multi-center, randomized trial to evaluate the efficacy of epcoritamab (GEN3013, DuoBody-CD3xCD20) in combination with lenalidomide compared to chemoimmunotherapy, rituximab plus gemcitabine plus oxaliplatin (R-GemOx), in adult patients with relapsed or refractory large B-cell lymphoma (LBCL), including patients with diffuse large B-cell lymphoma, not otherwise specified (DLBCL, NOS), high-grade B-Cell lymphoma (HGBL) with MYC and B-cell /lymphoma 2 (BCL2) and/or BCL6 rearrangements, follicular lymphoma grade 3B (FL3B), T-cell/histiocyte-rich large B-Cell lymphoma (TCHR LBLC), and Epstein-Barr Virus-positive diffuse large B-cell lymphoma (EBV+ DLBCL). Patients in the trial were previously treated with at least one line of systemic antineoplastic therapy including anti-CD20 mAb-containing combination chemotherapy, and failed or relapsed after, or were not a candidate for autologous stem cell transplantation (ASCT) and ineligible for or unable to receive CAR-T since DLBCL diagnosis. The trial started on August 13, 2024, and is ongoing.

More information on this trial can be found at View Source (NCT: NCT06508658).

About Diffuse Large B-Cell Lymphoma
Diffuse large B-cell lymphoma (DLBCL) DLBCL is the most common type of non-Hodgkin lymphoma (NHL) worldwide, accounting for approximately 25-30 percent of all NHL cases.[i],[ii] In the U.S., there are approximately 25,000 new cases of DLBCL diagnosed each year.[iii] DLBCL can arise in lymph nodes as well as in organs outside of the lymphatic system, occurs more commonly in the elderly and is slightly more prevalent in men.[iv],[v] DLBCL is a fast-growing type of NHL, a cancer that develops in the lymphatic system and affects B-cell lymphocytes, a type of white blood cell. For many people living with DLBCL, their cancer either relapses, which means it may return after treatment, or becomes refractory, meaning it does not respond to treatment. Although new therapies have become available, treatment management can remain a challenge.iv,[vi]

About Epcoritamab
Epcoritamab is an IgG1-bispecific antibody created using Genmab’s proprietary DuoBody technology and administered subcutaneously. Genmab’s DuoBody-CD3 technology is designed to direct cytotoxic T cells selectively to elicit an immune response toward target cell types. Epcoritamab is designed to simultaneously bind to CD3 on T cells and CD20 on B cells and induces T-cell-mediated killing of CD20+ cells.[vii]

Epcoritamab (approved under the brand name EPKINLY in the U.S. and Japan, and TEPKINLY in the EU) has received regulatory approval in certain lymphoma indications in more than 65 territories. Where approved, epcoritamab is a readily accessible therapy. Epcoritamab is being co-developed by Genmab and AbbVie as part of the companies’ oncology collaboration. The companies will share commercial responsibilities in the U.S. and Japan, with AbbVie responsible for further global commercialization. Both companies will pursue additional international regulatory approvals for R/R FL indication and additional approvals for the R/R DLBCL indication.

Genmab and AbbVie continue to evaluate epcoritamab as a monotherapy, and in combination, across lines of therapy in a range of hematologic malignancies. This includes several ongoing Phase 3, open-label, randomized trials, among them a trial evaluating epcoritamab in combination with R-CHOP in adult patients with newly diagnosed DLBCL (NCT05578976) and a trial evaluating epcoritamab in combination with lenalidomide and rituximab (R2) compared to chemoimmunotherapy in patients with previously untreated FL (NCT06191744). The safety and efficacy of epcoritamab have not been established for these investigational uses. Please visit www.clinicaltrials.gov for more information.

Please see local country prescribing information for all labeled indication and safety information.

(Press release, Genmab, JUN 29, 2026, View Source [SID1234668990])

On June 29, 2026 Akari Therapeutics, Plc (Nasdaq: AKTX), an oncology biotechnology company developing antibody drug conjugates (ADCs) with novel RNA splicing modulator payloads, reported the completion of its previously announced PIPE through the consolidation of the remaining scheduled investment closings into a single funding event. Combined with warrant exercises completed in May, the Company received approximately $8.3 million in total capital during Q2 2026.

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"We appreciate the decision of our investor group to complete the remaining funding earlier than originally scheduled, and for some of these investors to further increase their commitment through warrant exercises." said Abizer Gaslightwala, President and Chief Executive Officer of Akari Therapeutics. "This additional capital is expected to provide added financial flexibility as we advance AKTX-101 towards a Phase 1 first-in-human clinical trial while advancing our proprietary PH1 RNA splicing modulator ADC payload through potential strategic partnerships."

As previously announced, Akari entered into a securities purchase agreement with certain existing investors pursuant to which the Company agreed to sell and issue in a private placement an aggregate of 1,470,588 ADSs or prefunded warrants to purchase ADSs together with Series H warrants, Series I warrants and Series J warrants to each purchase 1,470,588 ADSs.

Under the purchase agreement, the $5.5 million gross proceeds of the offering were to be funded in three separate tranches, the first of which occurred at the end of May 2026, and the second and third closings of which were supposed to occur during June and July 2026, respectively. Subsequently, the parties agreed to consolidate the second and third closings into one final closing, which occurred on June 26, 2026. The issuance of the associated Series H, Series I and Series J warrants remains subject to shareholder approval at the Company’s Annual General Meeting scheduled for June 30, 2026.

Separately, during May 2026 the Company received approximately $2.8 million in additional proceeds from the exercise of warrants by some of the investors who participated in the PIPE.

(Press release, Akari Therapeutics, JUN 29, 2026, View Source [SID1234668989])

On June 29, 2026 AB Science SA (Euronext – FR0010557264 – AB) reported an update on the Phase 1 study of the molecule AB8939 and the completion of Step 3, evaluating the combination of AB8939 + venetoclax in patients with acute myeloid leukemia (AML) associated with a very unfavorable genetic profile.

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Step 3 evaluated the combination of AB8939 plus venetoclax administered over a 14-day cycle. A total of six patients were treated across two dose levels of AB8939 (16 mg/m² and 21.3 mg/m²), each in combination with venetoclax. The combination was well-tolerated, with no dose-limiting toxicity (DLT) and no hematological toxicity observed at either dose level, allowing selection of the recommended Phase 2 dose (RP2D).

Encouraging preliminary signs of efficacy were observed. Of the six patients treated, four achieved an objective response (one complete remission with incomplete hematologic recovery and three partial responses), corresponding to a 67% overall response rate (ORR). The two remaining patients achieved stable disease, resulting in a 100% disease control rate (CDR). These responses were achieved after a single cycle of treatment (14 days) in heavily pre-treated patients receiving second- to fourth-line therapy. Notably, two of the responding patients had previously progressed on venetoclax in combination with other chemotherapies.

The patients treated all have very difficult to treat cytogenetic profiles, including complex karyotype, TP53 mutation, NRAS mutation, monosomy 5 and 7 and MECOM-rearrangement, that typically have a poor prognosis due to their aggressive disease course and treatment resistance

This is a high response rate in a population where standard-of-care therapies achieve ORR of 10–30% in adverse-risk, multiply pre-treated AML (Gill H, et al. Cancer Med. 2020;9(10):3371-3382).

Response after the first 14 days cycle in the six patients treated in Step 3 (AB8939 + venetoclax)

Patient AB8939 dose Line of therapy Key adverse genetics Best response
Patient 1 16 mg/m² 2nd RUNX1 and NRAS mutations CRi
Patient 2 16 mg/m² 2nd MECOM-rearrangement, complex karyotype, monosomy 5 and 7 PR
Patient 3 16 mg/m² 4th TP53 mutation, complex karyotype, monosomy 5 and 7 PR
Patient 4 21.3 mg/m² 3rd TP53 mutation, complex karyotype, monosomy 5 and 7 PR
Patient 5 21.3 mg/m² 2nd TP53 mutation SD
Patient 6 21.3 mg/m² 2nd TP53 mutation (very high-risk MDS) SD
Complete remission (CRc) is defined as CRc = CR + CRh + CRi + CRp

CR=Bone marrow blasts <5%; of circulating blasts; low level (<5%); extramedullary disease; ANC ≥1.0 x 109/L (1000/μL); platelet count ≥100 x 109/L (100 000/μL).
CRh =ANC ≥ 0.5 × 109/L (500/μL) and platelet count ≥ 50 × 109/L (50 000/μL), otherwise all other CR criteria met
CRi =All CR criteria except for residual neutropenia (<1.0 x 109/L [1000/μL]) or thrombocytopenia (<100 x 109/L [100 000/μL]).
CRp =All CR criteria except platelet count < 100 × 109/L (100 000/μL)
Partial remission (PR) requires bone marrow response of at least 50% with a residual % between 5% and 25%.
Progressive disease (PD): > 50% increase in marrow blasts over baseline (a minimum 15% increase is required in cases <30% blasts at baseline).

This diversity of responsive patients appears to corroborate the mechanism of action of AB8939, which is capable of destabilizing microtubules while evading multi-drug resistance and also targeting cancer stem cells without eliminating non tumoral stem cells

These results corroborate the positioning of AB8939 in patients with adverse genetics, complex karyotypes, TP53 mutations, NRAS and KRAS mutations, monosomy 5 and 7, and MECOM-rearrangement, which represents the highest unmet medical need.

Nicholas J. Short, MD, Associate Professor and Co-Lead of the Section of Developmental Therapeutics, Department of Leukemia, MD Anderson Cancer Center, said, "This new data is very encouraging, particularly considering the very adverse risk profile of this patient’s leukemia. These early efficacy and safety data suggest that AB8939 can be combined with venetoclax and could have significant activity in the highest-risk subtypes of AML. There is a strong interest in continuing the development of this combination in patients whose AML has high-risk features that are expected to lead to resistance to venetoclax + azacitidine."

Professor Olivier Hermine, MD, President of the Scientific Committee of AB Science and member of the Académie des Sciences in France, said, "There is a strong rationale to combine AB8939 and venetoclax as both molecules have low hematologic toxicity and complementary mode of actions. These first results are supportive of this rationale."

With Step 3 completed, the next step is Step 4, evaluating the triple combination of AB8939 + venetoclax + azacitidine.

About AB8939

AB8939 is a drug candidate that targets (i) cancer cells by destabilizing microtubules (essential for cell division) and (ii) cancer stem cells by inhibiting ALDH1A1 and ALDH2 (enzymes essential for maintaining their physiological state and survival).

AB8939 has shown in vitro activity in Ara-C (cytarabine, which is one of the standards of care) resistant patient cell lines, including adverse genetic MECOM and TP53 mutations.
Analysis of cell lines responsive to AB8939 showed that AB8939 is effective in cell lines with TP53 mutations, MECOM, and complex karyotypes, whereas ARAC and azacitidine are not effective.
AB8939 increased survival and had an additive effect in combination with venetoclax (another standard of care) in vivo in a MECOM-grafted PDX mouse model.
AB8939 increased survival and had an additive effect in combination with Vidaza (azacitidine, another standard of care) in vivo in the MECOM PDX#C1005 mouse model of leukemia.
AB8939 eradicated Leukemia Cancer Stem Cells in vivo in a human PDX AML mouse model, which is compatible with targeting stem cells via ALDH.

AB8939 is currently being evaluated in a Phase 1 clinical trial (study AB18001, NCT05211570) in patients with refractory and relapsed AML.

The Phase 1 clinical trial of AB8939 has completed its first three steps. The first two steps determined the maximum tolerated dose (MTD) after 3 and 14 consecutive days of monotherapy. In both cases, the MTD was 21.3 mg/m².

The third step, now completed, evaluated the combination of AB8939 and venetoclax. Six patients were treated across two dose levels (AB8939 14 days at a dose of 16 mg/m² + venetoclax 14 days, then AB8939 14 days at a dose of 21.3 mg/m² + venetoclax 14 days), with no dose-limiting toxicity observed, supporting selection of the recommended Phase 2 dose. The next step (Step 4) will evaluate the triple combination of AB8939 + venetoclax + azacitidine.

Medical need in AML and AB8939 mechanism of action

Although several drugs have been registered for AML, 70% of patients still relapse and die, creating a persistent unmet medical need for effective treatments. Acute myeloid leukemia remains the most lethal form of leukemia in humans.

AML is a heterogeneous disease, and its outcome is highly dependent on genetic factors. TP53 mutation has a very poor prognosis, with a median overall survival (OS) of 5.5 months. NRAS and KRAS mutants have a poor prognosis, with a median OS of 12.1 months. MECOM also has a very poor prognosis in AML, with a median OS of 5.5 months in relapsed or refractory settings.

The challenge in AML is the recurrence of tumors due to a combination of two factors: the resistance of cancer cells to chemotherapy and relapse due to the persistence of cancer stem cells. This challenge may be overcome by AB8939’s dual mechanism of action.

First, AB8939 blocks the proliferation of leukemia cells through microtubule disruption. It is not subject to multi-drug resistance as it does not bind to PgP, which is responsible for efflux outside the cells, and is not degraded by myeloperoxidase.
Second, AB8939 targets leukemia cancer stem cells by inhibiting ALDH and promotes bone marrow repopulation of normal progenitors.
AB8939 + venetoclax combination

There is a strong rationale to combine AB8939 with venetoclax

Both molecules exhibit low hematologic toxicity. This combination is expected to be less toxic than azacitidine + venetoclax as first-line treatment for AML
These molecules have different and complementary targets in cancer cells. There is an additive, even synergistic, efficacy potential for the combination, with three mechanisms of action in a single treatment.
Venetoclax’s mechanism of action inhibits the BCL2 pathway, a protein that prevents apoptosis (programmed cell death) in cancer cells. BCL2 is a key factor in AML resistance, as it allows cancer cells to survive despite treatment
AB8939 is pro-apoptotic, destabilizing microtubules, and would benefit from BCL2 inhibition to optimize apoptosis
In addition, AB8939 specifically targets cancer stem cells by inhibiting ALDH, reducing resistance to treatment and limiting the risk of relapse

Next steps

Following completion of Step 3, the next step is to initiate Step 4, evaluating the triple combination of AB8939 + venetoclax + azacitidine, and to launch an expansion study in approximately 15 AML patients eligible for AB8939 + venetoclax at the appropriate dose. The expansion phase is expected to generate robust preliminary evidence of efficacy in the AML label, sufficient to support the clinical development plan and a beneficial partnership agreement.

AB Science has started to discuss three possibilities for registration studies, which are not mutually exclusive, with the European Medicines Agency (EMA) and US Food and Drug Administration (FDA):

AB8939 + venetoclax as first-line treatment, with aged patients and/or patients with adverse genetics (complex karyotypes, TP53 mutations, NRAS and KRAS mutations, monosomy 5 and 7, and MECOM-rearrangement)
AB8939 + venetoclax as a second- or third-line treatment, in all patients or patients with adverse genetics
AB8939 as a single agent in MECOM as a second or third-line treatment.

Addressable market with AB8939 in relapsed/refractory AML

Treatments for relapsed or refractory AML represent an estimated market size potential of greater than EUR 2 billion per annum.

Region Incidence Case
(1) % Relapse or Refractory (2,3) % Insured Patients (4) Drug Price (€) Market Size
(per in Mio EUR)
USA / CANADA 23,700 50%

90% 100,000(5) 1 000 000
EUROPE 27,600 90% 60,000 770 000
APAC 27,800 30% 60,000 250 000
INDIA 11,000 30% 60,000 100,000
LATAM 7,200 30% 60,000 65 000
MENA 3,900 30% 60,000 35 000
TOTAL 90,200 2 200 000
EUROPE = EU27 + Norway + United Kingdom + Switzerland ; APAC = Australia, People’s Republic of China , Japan, New Zealand, Singapore, Taiwan ; LATAM = Argentina, Brazil, Chile, Colombia, Costa Rica, Mexico ; MENA = Algeria, Bahrain, Egypt, Israel, Kuwait, Morocco, Oman, Qatar, Saudi Arabia, Tunisia, United Arab Emirates
(1) Zhou, Y et al. Global, regional, and national burden of acute myeloid leukemia, 1990–2021: a systematic analysis for the global burden of disease study 2021. Biomark Res 12, 101 (2024).
(2) Ravandi F. Relapsed acute myeloid leukemia: Why is there no standard of care Best Pract Res Clin Haematol. 2013;26(3):253-9
(3) Walter RB et al. Resistance prediction in AML: analysis of 4601 patients from MRC/NCRI, HOVON/SAKK, SWOG and MD Anderson Cancer Center. Leukemia (2015) 29:312–20. .
(4) Estimated
(5) Choi M. et al. Costs per patient achieving remission with venetoclax-based combinations in newly diagnosed patients with acute myeloid leukemia ineligible for intensive induction chemotherapy. Journal of Managed Care & Specialty Pharmacy Volume 28, Number 9. View Source

Intellectual property

AB8939 intellectual property rights in AML are secured until 2036 through a ‘composition of matter’ patent and potentially until 2041 with a 5 years extension. Two additional ‘second medical use’ patent applications have been filed to protect the use of AB8939 in the treatment of AML with specific chromosomal abnormalities. If these applications are accepted, the protection for AB8939 will be extended until 2044 and 2046 for these AML subpopulations.

AB8939 has also received orphan drug designation for AML by both the EMA and FDA. This orphan drug designation confers 10 and 7 years of marketing exclusivity in Europe and the US, respectively, from the date of product registration.

AB Science is the sole proprietary holder of AB8939 and its family of compounds.

(Press release, AB Science, JUN 29, 2026, View Source [SID1234668988])

On June 29, 2026 Clarity Pharmaceuticals (ASX: CU6) ("Clarity" or "Company"), a clinical-stage radiopharmaceutical company with a mission to develop next-generation products that improve treatment outcomes for patients with cancer, reported the acceptance of data on 64Cu-SAR-bisPSMA and 67Cu-SAR-bisPSMA for presentation at the European Association of Nuclear Medicine (EANM) Annual Congress 2026, to be held on October 17-21 in Vienna, Austria. These include:

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Top Rated Oral Presentation of data from the Co-PSMA investigator-initiated trial (IIT) with 64Cu-SAR-bisPSMA, led by Prof Louise Emmett at St Vincent’s Hospital, Sydney.
Three-patient case report on detection of prostate cancer recurrence using 64Cu-SAR-bisPSMA following negative standard-of-care (SOC) prostate-specific membrane antigen (PSMA) positron emission tomography (PET) scan on Siemens Biograph Vision Quadra.
Case reports from the theranostic Phase I/IIa SECuRE trial1 on two participants with metastatic castration-resistant prostate cancer (mCRPC) who achieved undetectable disease following 67Cu-SAR-bisPSMA treatment as reported this year.
EANM 2026 Annual Congress is one of the world’s leading nuclear medicine conferences and the acceptance of these abstracts is testament to the strength of the data generated by Clarity’s products and the promising prospects for SAR-bisPSMA to change the paradigm in the diagnosis and treatment of prostate cancer.

64Cu-SAR-bisPSMA

Prof Emmett’s Co-PSMA trial compared 64Cu-SAR-bisPSMA head-to-head with the current SOC 68Ga-PSMA-11 PET/computed tomography (CT) in patients in biochemical recurrence (BCR) of prostate cancer with low PSA, following radical prostatectomy. The study demonstrated improved diagnostic performance of 64Cu-SAR-bisPSMA next-day imaging vs. 68Ga-PSMA-11 across all key parameters assessed, including mean number of lesions per participant (1.26 vs. 0.48, p<0.0001), total number of lesions (63 vs. 24), true positive rate (71% vs. 29%) and proportion of participants with a positive scan (78% vs. 36%, respectively)2.

In addition to the Co-PSMA presentation, 64Cu-SAR-bisPSMA is also being highlighted through real-world case profiles. The case study abstract reports on three patients with BCR of prostate cancer who were negative on SOC PSMA PET/CT (68Ga-PSMA-11 and/or 18F-DCFPyL) using Siemens Biograph Vision Quadra, but positive with subsequent 64Cu-SAR-bisPSMA PET/CT in all three cases. Baseline prostate-specific antigen (PSA) in the 3 patients ranged from 1.4–21.0 ng/mL. Next-day imaging (24 hours post-injection) detected a 2.25-fold increase in lesions (nine versus four) compared with same-day (1 hour post-injection) imaging, with additional lesions identified in the prostate bed and lymph nodes. For the lesions visible at both 64Cu-SAR-bisPSMA imaging timepoints, mean maximum standardised uptake value (SUVmax) increased from 3.5 to 6.1, a 1.8-fold increase in tracer uptake.

Importantly, 64Cu-SAR-bisPSMA imaging changed planned clinical management in all three patients. In one patient this enabled targeted radiotherapy to 64Cu-SAR-bisPSMA-positive lesions and allowed androgen deprivation therapy (ADT) to be deferred over a 3-year period while achieving PSA responses, a patient-centric relevant outcome given the side-effect burden of ADT2.

The patient described above, Steve Hunter, who received 64Cu-SAR-bisPSMA under compassionate use, commented, "I was diagnosed with prostate cancer in 2016 and initially had the usual treatment of a prostatectomy and radiation therapy. Although initially quite successful, in 2023 my blood PSA indicated that my cancer was returning, doubling every six months. With SOC PSMA imaging currently available, no lesions were detectable. I was informed by more than one doctor that what I had was a micro-metastatic version of prostate cancer; that is, I had a large number of cancers too small to be detected, and worse, my only option was ADT and the significant side effects I would suffer.

"My recent career has been dedicated to the area of advanced medical imaging utilising PET, single-photon emission computed tomography (SPECT) and magnetic resonance imaging (MRI). I have also worked in the past in oncology research. My experiences led me to believe that what I really had were a small number of tumours that were undetectable by the current SOC PSMA PET/CT imaging even on a state-of-the-art PET/CT system. I contacted Dr Alan Taylor in 2023 and asked if there was any possibility of being tested using their next-day imaging, knowing that this would significantly enhance the chance of finding these tumours. The results were beyond my expectations. Three tumours were found and I underwent targeted external beam radiation. Since then, I have repeated this process with Clarity and Alan’s support a few times to scan, find and subsequently treat the ensuant small number of tumours that arise, with stereotactic radiation therapy.

"I am so grateful to Clarity in making these scans available. This approach has proven to be highly successful by allowing me to obtain clear information about my disease and defer requiring ADT therapy and all the associated side effects with this treatment. I am currently symptom-free and hope to remain like this for a long time. It certainly demonstrates the importance of this agent for patients like me."

67Cu-SAR-bisPSMA

The therapeutic potential of 67Cu-SAR-bisPSMA is also being showcased at the EANM 2026 Annual Congress through a case study of the two participants from Clarity’s Phase I/IIa SECuRE trial1, a theranostic study in mCRPC that Clarity reported earlier this year. Both participants had Stage IV mCRPC at study entry. Participant A (64 years old, baseline PSA: 6.06 ng/mL with metastatic bone disease) received prior definitive radiotherapy and ADT, docetaxel for metastatic hormone-sensitive disease and enzalutamide for mCRPC with additional palliative stereotactic body radiotherapy. He went on to receive four cycles of 67Cu-SAR-bisPSMA across 5 months. His PSA declined by 95.7% to 0.26 ng/mL within 4 weeks of first cycle and became undetectable (limit of detection 0.02 ng/mL) after the third cycle, remaining undetectable at 33 weeks (last follow-up). No metastatic disease was detected on follow-up bone scan and 64Cu-SAR-bisPSMA PET/CT following treatment with 67Cu-SAR-bisPSMA.

Patient A: Lesion uptake of 64Cu-SAR-bisPSMA PET at baseline (left), following two cycles of 67Cu-SAR-bisPSMA (8 GBq each; centre) and following four cycles of 67Cu-SAR-bisPSMA (right). Coloured arrows indicate metastatic bone lesions within each region: red – skull; blue – ribs and sternum; orange – spine; green – pelvis.​ No detectable disease was observed on the post-treatment PET. Images are shown as maximum intensity projections. SUV: standardised uptake value.

Participant B (76 years old, baseline PSA: 3.25 ng/mL with nodal metastases) had undergone salvage prostate fossa radiotherapy with ADT and later progressed to mCRPC treated with abiraterone and ongoing ADT. He received two cycles of 67Cu-SAR-bisPSMA across 2 months, with concomitant enzalutamide. His PSA declined by 94.2% to 0.19 ng/mL within 4 weeks of first cycle and was undetectable at 8 weeks, remaining undetectable at 16 weeks (last follow-up), with a complete response per Response Evaluation Criteria in Solid Tumors v1.1 (RECIST) and undetectable disease on 64Cu-SAR-bisPSMA PET/CT after two cycles of treatment.

Patient B: Lesion uptake of 64Cu-SAR-bisPSMA PET at baseline (left images) and following two cycles of 67Cu-SAR-bisPSMA (8 GBq each; right images). PET images on the right were acquired 1 month after the second cycle and show no lesion uptake of 64Cu-SAR-bisPSMA compared to baseline. Red arrows indicate metastatic nodal lesions. Top images: maximum intensity projections. Bottom images: coronal sections of the corresponding insets. SUV: standardised uptake value.

Both participants experienced mostly mild and transient 67Cu-SAR-bisPSMA-related adverse events, with Participant A reporting Grade 1 nausea, vomiting, flu-like symptoms (all resolved) and Participant B having Grade 1 altered taste, dry eyes, eye pain, fatigue, salivary gland soreness (all resolved) as well as Grade 2 anaemia (ongoing at the last assessment).

Dr Alan Taylor, Executive Chairperson of Clarity Pharmaceuticals, commented, "The EANM Annual Congress is a conference focused specifically in our area of nuclear medicine, and we are very pleased to see Professor Louise Emmett and her team receive yet another Top Rated Oral Presentation for her excellent work on the Co-PSMA trial, which corroborated previously reported improvement in diagnostic performance of 64Cu-SAR bisPSMA over SOC PSMA imaging in BCR patients3. The Co-PSMA data has already been published in a high impact factor journal, European Urology2, and presented at the European Association of Urology 2026 conference. This additional recognition from EANM is testament to the high quality and clinical relevance of this head-to-head trial.

"Data from trials with 64Cu-SAR-bisPSMA to date2,3,4 provide an early view of what is expected to be the largest single body of work ever undertaken on PSMA imaging agents comparing same-day and next-day imaging in the pre-prostatectomy and BCR spaces, supporting our two ongoing registrational Phase III clinical trials5,6. Furthermore, we have now generated head-to-head data in a range of clinical trials where 64Cu-SAR-bisPSMA has always outperformed SOC imaging under multiple conditions. As part of this commitment to the highest standard of clinical validation and rigor, we have also continued to generate data under the Special Access Scheme (SAS) in Australia and Expanded Access Program (EAP) in the US, building a growing body of real-world evidence that complements and confirms the findings of clinical trial data generated to date, which we will continue to release to the market in preparation for commercialisation. This body of knowledge is now in the range of 700-800 patients dosed with 64Cu-SAR-bisPSMA and imaged on a wide range of different cameras, spanning multiple geographies and numerous clinical settings. Beyond the data, what drives our team in the development of this product is the effect it can have on patients’ lives and the positive feedback we continue to receive from clinicians and patients. The ability to detect lesions where other products cannot and have a real, positive impact on a cancer journey of men and their families battling this disease is what unites and motivates our team and collaborators to persevere and work harder towards our mutual goal.

"We recognise that there is significant interest in this product, which is expected, given its potential to change the diagnostic field and reshape treatment pathways in prostate cancer management. This is why we continue to design and support robust clinical trials with rigorous methodologies and work directly with clinicians through SAS and EAP programs, including head-to-head studies against SOC imaging and investigating same-day versus next-day imaging. We will continue to release these data, all in preparation to enter the large and growing market of PSMA PET imaging with our continued audacious goal of taking a product from the Australian benchtop to blockbuster status. In the entire history of Australian life sciences, this has only been achieved by a number of pharmaceutical products you can count on one hand, the most widely recocognised of which is Gardasil. At Clarity, with clinical trials on track and our regulatory, manufacturing, medical, clinical and commercial teams in place, we are entirely committed to this goal, especially for our fellow teammates, our shareholders and the patients we serve. This is a truly Australian story, with the potential to deliver meaningful impact for patients around the world.

"At Clarity, this does not stop at diagnostic products, and our core mission continues to be to improve treatment outcomes for patients with cancer. 67Cu-SAR-bisPSMA represents a key asset within our therapeutic portfolio for achieving this goal. The continued encouraging results from the SECuRE trial, together with the two most recently announced cases where participants achieved undetectable disease, further build on a growing body of evidence supporting the clinical potential of 67Cu-SAR-bisPSMA to make a difference in the lives of prostate cancer patients. In the two mCRPC patients, 67Cu-SAR-bisPSMA demonstrated marked anti-tumour activity with only three or fewer cycles, leading to undetectable disease by PSA and imaging, with most adverse events being mild and transient. These findings reinforce the potential role of 67Cu-SAR-bisPSMA in addressing a significant unmet need in mCRPC treatment."

Product Abstract Title
64Cu-SAR-bisPSMA Top Rated Oral Presentation: #1803
Prospective Comparison of 64Copper[64Cu]SAR-bisPSMA vs 68Gallium[68Ga] PSMA-11 PET/CT for Biochemical Recurrence of Prostate Cancer Following Radical Prostatectomy (Co-PSMA Trial)Session Date: Monday, October 19 2026
Session Time: 8:00AM – 9:30AM
64Cu-SAR-bisPSMA E-Poster: #296
Real-world Detection of Prostate Cancer Recurrence With 64Cu-SAR-bisPSMA Imaging Following Negative Standard-Of-Care PSMA PET: A Three-Patient Case Report
67Cu-SAR-bisPSMA E-Poster: #1786
67Cu-SAR-bisPSMA leads to Undetectable Disease in Metastatic Castration-Resistant Prostate Cancer Patients: Two Case Reports From The Phase I/IIa SECuRE Trial

Presentations will be available on Clarity’s official website after the EANM 2026 Congress: claritypharmaceuticals.com/pipeline/scientific_presentations

(Press release, Clarity Pharmaceuticals, JUN 29, 2026, View Source [SID1234668987])