On June 15, 2026 Sumitomo Pharma America, Inc. (SMPA) reported the presentation of new clinical and translational research at the European Hematology Association (EHA) (Free EHA Whitepaper) 2026 Congress, held from June 11-14, 2026, in Stockholm, Sweden.

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Among the data is the first-ever disclosure of preliminary clinical data for the investigational PIM1 inhibitor nuvisertib in combination with momelotinib (MMB) for patients with myelofibrosis (MF), and new translational research into the mechanistic basis for hemoglobin improvement observed in patients with MF in an ongoing Phase 1/2 study with nuvisertib. Alongside these findings, SMPA is also sharing new data gathered around acquired resistance patterns observed with enzomenib in acute leukemia.

"We are excited to present the preliminary data for our investigational combination of nuvisertib and momelotinib at EHA (Free EHA Whitepaper) 2026, while also sharing learnings from our ongoing translational research of nuvisertib and enzomenib," said Tsutomu Nakagawa, Ph.D., President and Chief Executive Officer of SMPA. "We appreciate this opportunity to share the latest data for these two programs with the oncology community, and these results reinforce our commitment to developing multi-faceted therapeutic approaches that address the most persistent challenges in treating hematologic malignancies."

Promising clinical response with nuvisertib and momelotinib in myelofibrosis
James McCloskey, M.D., Interim Chief of the Division of Leukemia, John Theurer Cancer Center, Hackensack, USA, presented preliminary clinical data from the ongoing global Phase 1/2 study (NCT04176198). As of December 6, 2025, a total of 26 patients with relapsed/refractory (R/R) MF and anemia were enrolled across four dose levels of nuvisertib (240, 360, 480, and 720 mg twice daily under fed condition) in combination with the approved dose of momelotinib in MF (200 mg once daily). This study population was particularly challenging to treat as every patient had previously received at least one approved Janus Kinase (JAK) inhibitor and 41% of patients carried high molecular risk (HMR) mutations. Despite these complexities, the combination appeared well tolerated with no dose-limiting toxicities (DLTs) observed. The most common treatment-related adverse events occurring in ≥20% patients were diarrhea, nausea, and thrombocytopenia. The most frequent treatment-related Grade 3 adverse event was thrombocytopenia without bleeding, which occurred in three patients. Of note, mean hemoglobin and platelet count levels remained stable throughout the 24-week treatment period.

Among the efficacy evaluable patients who completed at least 12 weeks of treatment (n=15), the combination of nuvisertib and momelotinib demonstrated evidence of clinical activity. Spleen volume reduction of at least 25% (SVR25) was achieved by 73% of patients at Week 12 and reached 100% at Week 24 (n=5). Similarly, 53% of patients achieved a total symptom score reduction of at least 50% percent (TSS50) at Week 12 that further improved to 60% of patients at Week 24 (n=5). Anemia response by IWG ELN2024 criteria was observed in 50% of patients at any time. Most significantly, 60% of patients achieved a triple response at the Week 24 mark, meeting concurrent criteria for symptom reduction, spleen volume reduction, and anemia improvement.

The development of nuvisertib and momelotinib combination therapy was driven by the need to address the pathways that drive MF progression more comprehensively. While standard treatments focus on inhibiting the JAK signaling pathway, research has shown that PIM1 expression is often upregulated in MF and can be driven by JAK-independent compensatory pathways, such as Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-kB) and Ets Related Gene (ERG). These secondary pathways can allow the disease to survive and progress even during JAK inhibitor therapy. By combining nuvisertib with the JAK/Activin A Receptor Type 1 (ACVR1) inhibitor momelotinib, researchers aim to shut down these escape routes, potentially leading to deeper and more durable clinical responses for patients.

New Nuvisertib translational research presented in MF
Joseph M Scandura, M.D., Ph.D., Division of Hematology and Medical Oncology, Weill/Cornell Leukemia Program, New York, USA, presented translational research further elucidating the proposed mechanism of action of nuvisertib. In addition to its primary activity as a PIM1 inhibitor, in vitro and biochemical data demonstrated that nuvisertib also binds to and inhibits ACVR1, resulting in reduced hepcidin mRNA expression, a central regulator of iron homeostasis. Consistent with these findings, preliminary clinical data from a Phase 1/2 study of nuvisertib monotherapy showed reduced hepcidin levels in patients with R/R MF, providing a potential mechanistic explanation for the hemoglobin stability and improvement observed in patients with MF treated with nuvisertib.

"Preliminary clinical data suggests that the combination of nuvisertib and momelotinib may provide a more comprehensive suppression of the disease pathways driving myelofibrosis," said Raajit Rampal, M.D. Ph.D., Director of the Myeloproliferative Neoplasms Program at the Memorial Sloan Kettering Cancer Centre, New York, USA. "The promising symptom, spleen and anemia responses, coupled with the new nonclinical data on potential dual PIM1 and ACVR1 inhibitory activity by nuvisertib, suggest that this combination therapy may potentially offer meaningful clinical benefits for patients with myelofibrosis."

Translational research in leukemia and menin inhibition identifies E368K mutation as key resistance signature at relapse
Also, during the conference, translational research in leukemia and menin inhibition was shared by Jevon Cutler, PhD, Assistant Professor of Cell, Developmental and Cancer Biology at the Oregon Health Sciences University School of Medicine, that identified distinct MEN1 mutational signatures associated with acquired resistance to the menin inhibitor (MI) enzomenib in patients with acute leukemia. Serial molecular profiling revealed that the E368K mutation was the predominant resistance signature identified at relapse, appearing in 53% of patients who relapsed after an initial response. Preclinical work predicted the E368K mutation to be the primary resistance mutation and that this mutation may not affect the other menin inhibitors; these findings support the further exploration of rational, sequential MI therapy to improve clinical outcomes for patients with acute leukemia.

Presentation Details

Abstract title

Lead Author

Investigational PIM1 Inhibitor Nuvisertib in Combination with Momelotinib Showed Promising Clinical Activity in Patients with Myelofibrosis and Anemia: Data from an Ongoing Global Phase 1/2 Study

James McCloskey, MD

Preclinical Evidence of Targeting ACVR1/Hepcidin by Nuvisertib, an Oral Investigational PIM1 Kinase Inhibitor, Suggests Potential Mechanistic Basis for Hemoglobin Benefit in Myelofibrosis

Joseph M Scandura, MD, PhD

Distinct MEN1 Mutational Signatures Are Associated with Acquired Resistance During MENIN-KMT2A Inhibition in a Phase 1 Enzomenib Trial

Jevon Cutler, PhD

(Press release, Sumitomo Dainippon Pharma, JUN 15, 2026, View Source [SID1234668746])

On June 15, 2026 NeoGenomics, Inc. (NASDAQ: NEO), a leading provider of oncology diagnostic solutions that enable precision medicine, reported that it has commenced a private offering of $275 million aggregate principal amount of convertible senior notes due 2032 (the "notes") to persons reasonably believed to be qualified institutional buyers pursuant to Rule 144A under the Securities Act of 1933, as amended (the "Securities Act"). In connection with this offering, NeoGenomics expects to grant the initial purchasers of the notes an option to purchase, for settlement within a 13-day period beginning on, and including, the date on which the notes are first issued, up to an additional $41.25 million aggregate principal amount of the notes. The offering of the notes is subject to market and other conditions and there can be no assurance as to whether or when the offering may be completed, or as to the actual size or terms of the offering.

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The notes will be senior, unsecured obligations of NeoGenomics, will accrue interest payable semi-annually in arrears and will mature on July 1, 2032, unless earlier converted, redeemed or repurchased. Noteholders will have the right to convert their notes in certain circumstances and during specified periods. NeoGenomics will settle conversions by paying or delivering, as applicable, cash, shares of its common stock, par value $0.001 per share ("common stock"), or a combination of cash and shares of its common stock, at NeoGenomics’ election. The notes will be redeemable, in whole or in part (subject to certain limitations), for cash at NeoGenomics’ option at any time, and from time to time, on or after July 6, 2029 and on or before the 51st scheduled trading day immediately preceding the maturity date, if the last reported sale price per share of NeoGenomics’ common stock equals or exceeds 130% of the conversion price for a specified period of time. The redemption price will be equal to the principal amount of the notes to be redeemed, plus accrued and unpaid interest, if any, to, but excluding, the redemption date. In addition, the notes will be redeemable at any time if the aggregate principal amount of the notes that remains outstanding is less than 15% of the aggregate principal amount of the notes initially issued in the offering and certain other conditions are satisfied. The interest rate, initial conversion rate and other terms of the notes will be determined at the pricing of the offering.

In connection with the pricing of the notes, NeoGenomics expects to enter into privately negotiated capped call transactions with one or more of the initial purchasers or their respective affiliates or other financial institutions (the "option counterparties"). The capped call transactions are expected generally to reduce potential dilution to NeoGenomics’ common stock upon conversion of any notes and/or offset any potential cash payments NeoGenomics is required to make in excess of the principal amount of converted notes, as the case may be, with such reduction and/or offset subject to a cap.

NeoGenomics has been advised that, in connection with establishing their initial hedges of the capped call transactions, the option counterparties or their respective affiliates expect to purchase shares of NeoGenomics’ common stock and/or enter into various derivative transactions with respect to NeoGenomics’ common stock concurrently with or shortly after the pricing of the notes. This activity could increase (or reduce the size of any decrease in) the market price of NeoGenomics’ common stock or the notes at that time. In addition, the option counterparties and/or their respective affiliates may modify their hedge positions by entering into or unwinding various derivatives with respect to NeoGenomics’ common stock and/or purchasing or selling NeoGenomics’ common stock or other securities of NeoGenomics in secondary market transactions following the pricing of the notes and prior to the maturity of the notes (and are likely to do so during any observation period related to a conversion of notes or following certain repurchases or redemptions of the notes). This activity could cause or avoid an increase or a decrease in the market price of NeoGenomics’ common stock or the notes, which could affect the ability of holders to convert the notes and, to the extent the activity occurs following conversion or during any observation period related to a conversion of notes, it could affect the amount and value of the consideration that holders will receive upon conversion of such notes.

NeoGenomics intends to use a portion of the net proceeds from the offering to pay the cost of the capped call transactions. If the initial purchasers exercise their option to purchase additional notes, NeoGenomics expects to use a portion of the net proceeds from the sale of the additional notes to enter into additional capped call transactions. In addition, NeoGenomics intends to use a portion of the remaining net proceeds from the offering, together with cash on hand, to repurchase a portion of NeoGenomics’ 0.25% convertible senior notes due 2028 (the "existing notes") through privately negotiated transactions entered into concurrently with the pricing of the notes effected through one or more of the initial purchasers or their affiliates as our agents, and a portion of the remaining net proceeds from the offering, if any, together with cash on hand, to repurchase up to $25 million of shares of our outstanding common stock from certain purchasers of the notes in privately negotiated transactions, effected through one or more of the initial purchasers or their respective affiliates as our agent, entered into concurrently with the pricing of this offering, and the remainder of the net proceeds, if any, for general corporate purposes.

The concurrent repurchases of the existing notes and shares of Company’s common stock described above may result in the Company’s common stock trading at prices that are higher than would be the case in the absence of these repurchases, which may result in a higher initial conversion price for the notes to be offered.

NeoGenomics expects to repurchase for cash a portion of the existing notes through privately negotiated transactions (the "note repurchase transactions") entered into concurrently with the pricing of the notes. The terms of each note repurchase transaction will depend on a variety of factors, including the market price of NeoGenomics’ common stock and the trading price of the existing notes at the time of the note repurchase transactions. No assurance can be given as to how much, if any, of the existing notes will be repurchased or the terms on which they will be repurchased. This press release is not an offer to repurchase the existing notes, and the offering of the notes is not contingent upon the repurchase of the existing notes.

In connection with the note repurchase transactions, NeoGenomics expects that holders of the existing notes who agree to have their existing notes repurchased and who have hedged their equity price risk with respect to such existing notes (the "hedged holders") will unwind all or part of their hedge positions by buying NeoGenomics’ common stock and/or entering into or unwinding various derivative transactions with respect to NeoGenomics’ common stock. The amount of NeoGenomics’ common stock to be purchased by the hedged holders or the notional number of shares of NeoGenomics’ common stock underlying such derivative transactions may be substantial in relation to the historic average daily trading volume of NeoGenomics’ common stock. This activity by the hedged holders could increase (or reduce the size of any decrease in) the market price of NeoGenomics’ common stock, including concurrently with the pricing of the notes, resulting in a higher effective conversion price of the notes. NeoGenomics cannot predict the magnitude of such market activity or the overall effect it will have on the price of the notes or NeoGenomics’ common stock and the corresponding effect on the initial conversion price of the notes.

The notes will be offered only to persons reasonably believed to be qualified institutional buyers pursuant to Rule 144A under the Securities Act. The offer and sale of the notes and any shares of common stock issuable upon conversion of the notes have not been, and will not be, registered under the Securities Act or any other securities laws, and the notes and any such shares cannot be offered or sold absent registration or except pursuant to an applicable exemption from, or in a transaction not subject to, the registration requirements of the Securities Act and any other applicable securities laws.

This press release does not constitute an offer to sell, or the solicitation of an offer to buy, the notes or any shares of common stock issuable upon conversion of the notes, nor will there be any sale of the notes or any such shares, in any state or other jurisdiction in which such offer, sale or solicitation would be unlawful.

(Press release, NeoGenomics Laboratories, JUN 15, 2026, View Source [SID1234668745])

On June 15, 2026 Rznomics Inc., a biopharmaceutical company specializing in the development of RNA-based gene therapies, reported that the Phase 1/2a interim clinical results for ‘RZ-001 (Taspitimagene advec)’, its RNA editing-based anticancer gene therapy for recurrent glioblastoma (rGBM), were presented on June 13th at the Asian Society for Neuro-Oncology Annual Meeting (ASNO 2026) held in Kanazawa, Japan.

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The presentation was delivered by Dr. Chae-Yong Kim, a professor of the Department of Neurosurgery at Seoul National University Bundang Hospital, highlighting the safety and preliminary efficacy data from the ongoing clinical trial.

RZ-001 is an innovative anticancer gene therapy utilizing Rznomics’ proprietary RNA trans-splicing ribozyme platform, engineered to express a therapeutic gene specifically inside tumor cells to induce cancer cell death. According to the presentation, 20 patients have completed screening to date, with 10 patients officially enrolled and treated in the trial.

The interim analysis revealed that no new or unexpected treatment-related safety concerns have been identified. No dose-limiting toxicity (DLT) was reported, and no treatment-related Grade 4 or higher adverse events were observed. Most reported adverse events were deemed to be disease-related or associated with underlying conditions typical of glioblastoma patients. Furthermore, several patients demonstrated prolonged tumor recurrence inhibition and disease control exceeding six months.

Recurrent glioblastoma is one of the most aggressive and intractable malignant brain tumors, notorious for high recurrence rates and an extremely poor prognosis even after standard-of-care treatments. With currently approved treatment options showing limited efficacy and conventional immuno-oncology therapies repeatedly facing clinical failures, rGBM represents an area with immense unmet medical needs for novel therapeutic mechanisms.

"The secured data demonstrate a manageable safety profile for RZ-001 alongside encouraging preliminary signs of clinical activity," explained Dr. Chae-Yong Kim. "Given that recurrent glioblastoma typically recurs within two to four months, the data from patients showing long-term recurrence inhibition—particularly that of extending past nine months—is highly encouraging. We look forward to further clarifying its full clinical value through additional patient enrollment and long-term follow-up observations."

Meanwhile, RZ-001 is currently undergoing clinical development for both recurrent glioblastoma and hepatocellular carcinoma (HCC). The HCC program recently achieved a significant milestone by receiving Regenerative Medicine Advanced Therapy (RMAT) designation from the U.S. FDA this past May.

(Press release, Rznomics, JUN 15, 2026, View Source [SID1234668744])

On June 15, 2026 Akeso, Inc. (HKEX: 9926) reported that the first patient has been enrolled in the Phase Ib/II clinical study (AK138D1-202) evaluating its internally developed next-generation HER3 antibody-drug conjugate (ADC), AK138D1, as either monotherapy or in combination with ivonescimab for the treatment of advanced breast cancer.

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HER3 is broadly expressed across various solid tumors, including breast, ovarian, colon, gastric, lung, skin, and pancreatic cancers, affecting millions of patients globally. While traditional HER3-targeted ADCs have demonstrated therapeutic potential in combination settings, their clinical utility has historically been constrained by dose-limiting toxicities.

AK138D1 is a next-generation, differentiated HER3-targeting ADC developed in-house by Akeso. Leveraging a unique, innovative design, AK138D1 is engineered to reduce uptake in normal tissues, thereby minimizing off-target toxicities and widening the therapeutic window. Furthermore, its design prevents the clustering of ADC molecules on the tumor surface, enhancing deep tissue penetration and uniform distribution to overcome the "binding site barrier". Early-stage clinical studies conducted in China and Australia have demonstrated that AK138D1 exhibits robust anti-tumor activity in solid tumors and breast cancer, coupled with an excellent safety profile, notably characterized by low hematologic toxicity and the absence of interstitial lung disease (ILD). This compelling balance of efficacy and safety overcomes common limitations of conventional ADCs, establishing a foundation for AK138D1 to be explored in diverse combination therapeutic regimens.

The AK138D1-202 study focuses on the two major breast cancer subtypes with the greatest unmet need: hormone receptor-positive, HER2-negative (HR+/HER2-) disease, which accounts for approximately 65% of all breast cancers, and triple-negative breast cancer (TNBC), which represents 10-20% of cases. The trial enrolls patients across multiple treatment lines from treatment-naïve to heavily pretreated, and includes diverse PD-L1 expression levels. Breast cancer remains the most common cancer among women worldwide, with an estimated 2.3 million new cases diagnosed annually. Substantial unmet needs persist in both first-line and later-line settings for HR+/HER2- breast cancer and TNBC.

Early data from AK138D1 studies have already shown meaningful efficacy and a strong safety profile in breast cancer. Concurrently, a Phase III study of ivonescimab-based combination therapy in first-line TNBC is ongoing. The combination of AK138D1 and ivonescimab is poised to emerge as a highly differentiated "IO2.0 + ADC2.0" therapeutic strategy for advanced breast cancer.

As IO+ADC combinations become a cornerstone of global oncology research, Akeso is strategically and efficiently building a comprehensive global portfolio of these next-generation therapies, leveraging its proprietary leadership in bispecific and multispecific antibody platforms.

On the IO front, Akeso stands as the only company globally with two approved bispecific antibodies for oncology, spearheading the advancement of IO2.0 therapies. Regarding its ADC pipeline, Akeso’s development of AK146D1 (a Trop2/Nectin4 bispecific ADC) and AK138D1, among other innovations, aims to resolve the toxicity-related limitations of current ADCs and propel the field into the "ADC2.0" era.

About AK138D1

Injectable AK138D1 is a HER3-targeted antibody-drug conjugate (ADC), with a fully humanized anti-HER3 IgG1 antibody, patritumab. It is conjugated to the topoisomerase I inhibitor DXd through a cleavable linker, MC-AAA (maleimide-alanine-alanine-alanine). After binding to HER3 on tumor cells, the ADC is internalized into the tumor cells, where the linker is cleaved, releasing the membrane-permeable DXd. This leads to DNA damage and subsequent cell apoptosis. Early study results have shown that AK138D1 possesses potent biological activity and a favorable safety profile. A phase II clinical trial is currently ongoing to investigate AK138D1 combined with cadonilimab and ivonescimab in patients with solid tumors. This regimen is a critical part of Akeso’s IO2.0 + ADC 2.0 combination approach.

(Press release, Akeso Biopharma, JUN 15, 2026, View Source;adc2-0-strategy-302800044.html [SID1234668743])

On June 15, 2026 IDEAYA Biosciences, Inc. (NASDAQ: IDYA), a leading precision medicine oncology company, reported that the first patient has been enrolled in its Phase 1 clinical trial evaluating IDE892, a potential best-in-class methylthioadenosine (MTA)-cooperative inhibitor of PRMT5, in combination with IDE397, a potential first-in-class and best-in-class inhibitor of MAT2A, in MTAP-deleted solid tumors, with a focus on NSCLC and pancreatic cancer. In preclinical studies, dual inhibition of PRMT5 and MAT2A with the combination of IDE892 and IDE397 resulted in potent anti-tumor activity in MTAP-deleted tumor models, including complete and durable responses at well-tolerated doses below those required for monotherapy activity.

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"We are excited to begin enrolling this Phase 1 combination trial evaluating IDE892 in MTAP-deleted pancreatic cancer and non-small cell lung cancer. We designed IDE892 with potential best-in-class properties, including approximately 1,400-fold selective MTA-PRMT5 cooperative binding versus SAM-PRMT5 cooperative binding intended to maximize its therapeutic window and favorable drug-like properties to enable rational combinations with IDE397 and pan-RAS inhibitors. This trial exemplifies our clinical development strategy of enabling rational combinations to deliver deeper and more durable responses for MTAP-deleted pancreatic cancer and lung cancer patients where there are currently no approved treatment options," said Yujiro S. Hata, President and Chief Executive Officer, IDEAYA Biosciences.

Loss of MTAP leads to the accumulation of MTA and increased dependence on PRMT5 and MAT2A, two key enzymes involved in methylation and RNA splicing. In MTAP-deleted tumors, this biology establishes a robust synthetic lethal vulnerability that underpins the mechanistic rationale for combining IDE892 and IDE397. IDEAYA also entered into a clinical collaboration with Roche evaluating IDE892 in combination with RG6505, Roche’s Phase 1 pan-RAS inhibitor, in MTAP-deleted pancreatic ductal adenocarcinoma (PDAC) to target the genetic co-alterations of MTAP and KRAS in this indication. Next, IDEAYA is advancing a third proprietary program for MTAP-deleted solid tumors targeting CDKN2A, the most common co-alteration of MTAP, through ongoing preclinical toxicology studies to support an investigational new drug (IND) application in the first half of 2027.

MTAP deletion is estimated to occur in approximately 15% of all solid tumors, including 15-20% of NSCLC and up to 40% of pancreatic cancer. There are no approved therapies for MTAP-deleted cancers, highlighting the significant unmet need and opportunity for new precision therapies for these patients.

(Press release, Ideaya Biosciences, JUN 15, 2026, View Source [SID1234668742])