On December 2, 2024 Omeros Corporation (Nasdaq: OMER) reported that two abstracts directed to zaltenibart (OMS906), Omeros’ investigational inhibitor of MASP-3, the key activator of the alternative pathway of complement, will be presented at the 66th Annual Meeting of the American Society of Hematology (ASH) (Free ASH Whitepaper), to be held December 7-10, 2024 in San Diego (Press release, Omeros, DEC 2, 2024, View Source [SID1234648739]). The zaltenibart abstracts are directed to the treatment of paroxysmal nocturnal hemoglobinuria (PNH), a rare, life-threatening hematological disorder. Enrollment for the zaltenibart Phase 3 clinical trials in PNH is expected to open in early 2025.

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Both abstracts are available on the ASH (Free ASH Whitepaper) website at www.hematology.org. Details of the congress presentations and direct links to the abstracts are found below.

Monotherapy Treatment with Zaltenibart (OMS906), an Alternative Pathway Masp-3 Inhibitor, Improved Key Hematologic Parameters in Patients with PNH with a Suboptimal Response to Ravulizumab: Interim Results from a Phase 2 Proof-of-Concept Study
Abstract Number / Link: 4072
Session: 508. Bone Marrow Failure: Acquired: Poster III
Presentation Time: Monday, December 9, 2024, 6:00 PM-8:00 PM
Location: San Diego Convention Center, Halls G-H
Presenting Author: Morag Griffin, MBChB, MRCP

Population Pharmacokinetics/Pharmacodynamics and Clinical Pharmacology of Zaltenibart (OMS906) in Healthy Subjects and Patients with PNH
Abstract Number / Link: 4081
Session: 508. Bone Marrow Failure: Acquired: Poster III
Presentation Time: Monday, December 9, 2024, 6:00 PM-8:00 PM
Location: San Diego Convention Center, Halls G-H
Presenting Author: William Pullman, BMedSc, MBBS, PhD, FRACP

The presentation materials associated with each abstract will be made available on Omeros’ website at www.omeros.com following the congress presentations.

About OMS906

OMS906 is an investigational human monoclonal antibody targeting mannan-binding lectin-associated serine protease-3 (MASP-3), the key and most proximal activator of the complement system’s alternative pathway. The complement system is a critical part of innate immunity and plays a central role in host homeostasis and defense against pathogens. Responsible for the conversion of pro-complement factor D to complement factor D, MASP-3 is believed to be the premier target in the alternative pathway – it has the lowest native circulating level and low relative clearance compared to the other alternative pathway proteins and, unlike C5 and C3 blockers, MASP-3 inhibition leaves intact the lytic arm of the classical pathway, important for fighting infection. Also, unlike other components of the alternative pathway, MASP-3 is believed not to be an acute phase reactant, which could provide a significant advantage to MASP-3 inhibitors, like OMS906, over other alternative pathway inhibitors. MASP-3 inhibitors are thought to have preventive or therapeutic effects across a broad range of diseases including paroxysmal nocturnal hemoglobinuria (PNH), hemolytic uremic syndrome (HUS), atypical HUS, traumatic brain injury, arthritis, geographic atrophy or "dry" macular degeneration, ischemia-reperfusion injury, transplant-related complications and other immune-related disorders.

On December 2, 2024 Mission Bio, a leader in single-cell multiomics solutions for precision medicine, reported a collaboration with Dr. C. Ola Landgren, MD, PhD, head of one of the world’s leading myeloma computational and translational research laboratories (Press release, Mission Bio, DEC 2, 2024, View Source [SID1234648738]). Dr. Landgren’s team, including Dr. David Coffey and Dr. Benjamin Diamond, at the University of Miami’s Sylvester Comprehensive Cancer Center, will work together to generate clinical data sets using Mission Bio’s Tapestri Single-cell DNA Multiple Myeloma Panel to examine Multiple Myeloma (MM) at an unprecedented level of clonal detail, promising to reveal new insights that may potentially improve outcomes for MM patients.

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MM is a challenging and incurable blood cancer that afflicts around 230,000 people worldwide. Relapse is a particular problem for many of these patients — as many as 50% experience relapse within the first year of frontline treatments, and only 20% of relapse victims survive for five years with current standard therapies.

The key to controlling relapse in MM patients lies in better understanding of resistant clones: cells that have developed mutations or alterations that help them evade treatment. However, current tools inadequately profile the disease from the initial emergence of clones to full-blown myeloma. Using clinical samples from University of Miami, the goal of the collaboration is to help predict which patients are at higher risk of relapse, and, in the event of relapse, whether it can inform and guide subsequent treatment decisions. In addition, the project will determine if blood can be used as an alternative sample for patient testing instead of bone marrow samples. The utilization of blood would vastly improve sample accessibility and alleviate the invasive patient experience.

"We recognize that Multiple Myeloma is a genetically complex disease that hasn’t been easy to comprehend fully using existing methods, particularly when it comes to the crucial questions of when patients might experience relapse and what clinicians should do next when relapse occurs," said Dr. Landgren. "Our aim is to utilize Tapestri to better understand Multiple Myeloma disease heterogeneity, which in turn will allow us to detect and treat relapse faster. Ultimately, we hope to demonstrate the clinical feasibility of the Multiple Myeloma assay and to facilitate the establishment of Tapestri to advance outcomes for patients."

"Our partners and customers continue to push the boundaries of single-cell DNA and multiomic analysis in new and inspiring ways," said Brian Kim, CEO of Mission Bio. "The work being done by Dr. Landgren and his team promises to unearth critical insights that will not only be able to help predict relapse in Multiple Myeloma patients, but also inform more effective, personalized treatment strategies in the future."

On December 2, 2024 Ajax Therapeutics, Inc., a biopharmaceutical company developing next generation JAK inhibitors for patients with myeloproliferative neoplasms (MPNs), reported that an overview of the company’s ongoing first-in-human study with its next generation Type II JAK2 inhibitor, AJ1-11095, has been selected for presentation in a poster session on December 8, 2024 at the 66th American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting and Exposition in San Diego (Press release, Ajax Therapeutics, DEC 2, 2024, View Source [SID1234648737]).

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The poster, entitled "A Multicenter, Open-Label, Phase 1 Clinical Trial of AJ1-11095 Administered As Oral Monotherapy in Patients with Primary Myelofibrosis (PMF), Post-Polycythemia Vera Myelofibrosis (PPV-MF), or Post-Essential Thrombocythemia Myelofibrosis (PET-MF) Who Have Been Failed By a Type I JAK2 Inhibitor (JAK2i)," will be presented by John Mascarenhas, MD, Professor of Medicine, Icahn School of Medicine at Mt. Sinai and Director, Center of Excellence in Blood Cancers and Myeloid Disorders at Tisch Cancer Institute and principal investigator of the Phase 1 Study. Further details about the study can be found at www.clinicaltrials.gov under the NCT identifier: NCT06343805.

Details of the poster session are as follows:

Session Name: 631. Myeloproliferative Syndromes and Chronic Myeloid Leukemia: Basic and Translational: Poster II
Session Date and Time: Sunday, December 8, 2024, 6:00 – 8:00 p.m. PT
Location: San Diego Convention Center, Halls G-H
Publication Number: 3147.1

About AJ1-11095

AJ1-11095 was designed by Ajax Therapeutics, through an exclusive collaboration with Schrödinger, using structure-based drug design and computational methods at scale to selectively bind the Type II conformation of the JAK2 kinase in order to provide greater efficacy with disease modification compared to all currently approved JAK2 inhibitors, including ruxolitinib, which bind the Type I conformation of JAK2. AJ1-11095 has been shown in preclinical studies to reverse marrow fibrosis, reduce mutant allele burden, and maintain efficacy against MPN cells that become resistant to chronic Type I JAK2 inhibition.

About Myelofibrosis

Myelofibrosis (MF) is a rare blood cancer that affects approximately 20,000 patients in the United States. The disease is characterized by spleen enlargement, scarring (fibrosis) in the bone marrow, progressive anemia, and debilitating symptoms, such as fatigue, night sweats, itching, and abdominal discomfort, which can impair a patient’s quality of life. The most widely used treatment for MF patients are Type I JAK2 inhibitors which can reduce spleen size and provide symptomatic improvement but have little effect on the underlying cause of disease. Over time, most MF patients stop Type I JAK2 inhibitor therapy. The most common causes for treatment discontinuation include a lack of benefit or loss of response, adverse events, and disease progression, leaving significant unmet treatment needs for these patients.

On December 2, 2024 IDEAYA Biosciences, Inc. (NASDAQ: IDYA), a precision medicine oncology company committed to the discovery and development of targeted therapeutics, reported its participation in upcoming investor relations events (Press release, Ideaya Biosciences, DEC 2, 2024, View Source [SID1234648735]).

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Citi’s 2024 Global Healthcare Conference
Tuesday, December 3rd, 2024 at 8:00 AM ET

Fireside chat with Yujiro S. Hata, President and Chief Executive Officer, hosted by Yigal D. Nochomovitz, Ph.D., Director, SMid Cap Biotech Analyst
7th Annual Evercore HealthCONx Conference
Wednesday, December 4th, 2024 at 1:20 PM ET

Fireside chat with Yujiro S. Hata, President and Chief Executive Officer, hosted by Jonathan Miller, Managing Director, Biotech and Pharma Equity Research
A live audio webcast of the conference event, as permitted by the conference host, will be available at the "Investors/Events" section of the IDEAYA website at View Source and/or through the conference host. A replay of the webcast will be accessible for 30 days following the live event.

On December 2, 2024 Solu Therapeutics ("Solu Therapeutics" or "Solu"), a biotechnology company pioneering novel therapies to eliminate disease-driving cells in cancer, immunology, and other therapeutic areas, reported that it will present the first preclinical data on STX-0712, its novel CCR2-CyTAC (Chemokine Receptor Type 2 Cytotoxicity Targeting Chimera) for the treatment of chronic myelomonocytic leukemia (CMML) and acute myeloid leukemia (AML) (Press release, Solu Therapeutics, DEC 2, 2024, View Source [SID1234648734]). The data will be featured in two poster presentations at the American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting, being held December 7-10, 2024, in San Diego, California.

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STX-0712 is a CyTAC targeting the G-Protein Coupled Receptor (GPCR) CCR2, a selective marker expressed at high levels on malignant monocytes in these indications, which are key drivers in certain hematologic cancers. By targeting CCR2, STX-0712 is designed to selectively eliminate these malignant cells.

ASH Poster Presentation Details:

Abstract Title: Ex-Vivo Evaluation of STX-0712, a CCR2 Cytotoxicity Targeting Chimera (CCR2-CyTAC) for the treatment of Acute Myeloid Leukemia
Date: Saturday, December 7, 2024
Time: 5:30 PM-7:30 PM PT
Location: San Diego Convention Center, Halls G-H
Session: 604. Molecular Pharmacology and Drug Resistance: Myeloid Neoplasms: Poster I
Abstract Number: 1380

Abstract Title: Preclinical Evaluation of STX-0712, a CCR2 Cytotoxicity Targeting Chimera (CCR2-CyTAC) for the treatment of Chronic Myelomonocytic Leukemia
Date: Sunday, December 8, 2024
Time: 6:00 PM-8:00 PM PT
Location: San Diego Convention Center, Halls G-H
Session: 604. Molecular Pharmacology and Drug Resistance: Myeloid Neoplasms: Poster II
Abstract Number: 2771