Imara to Present Clinical and Preclinical Data at the American Society of Hematology (ASH) Annual Meeting 2021

Tovinontrine (IMR-687) VOC data in patients with sickle cell disease from ongoing Phase 2a open-label extension study and preclinical models of beta-thalassemia to be presented

Oral presentation provides first look at IMR-261, a novel oral Nrf2 activator shown to reactivate fetal hemoglobin and reduce VOCs in preclinical models of sickle cell disease and increase hemoglobin in a preclinical model of beta-thalassemia

BOSTON, Nov. 04, 2021 (GLOBE NEWSWIRE) -- Imara Inc. (Nasdaq: IMRA), a clinical-stage biopharmaceutical company dedicated to developing and commercializing novel therapeutics to treat patients suffering from rare inherited genetic disorders of hemoglobin and other serious diseases, today announced that it will present clinical and preclinical data at the American Society of Hematology (ASH) Annual Meeting to be held December 11-14, 2021.

“We look forward to reporting updated 12-month VOC data from our Phase 2a open label extension trial of tovinontrine (IMR-687) in adults with sickle cell disease as well as data in preclinical models of beta-thalassemia,” said Rahul Ballal, Ph.D., President and Chief Executive Officer of Imara. “In addition, we are excited to share this first look at IMR-261, a new asset in our development pipeline. IMR-261 is a clinic-ready oral activator of nuclear factor erythroid 2–related factor 2, or Nrf2. In pre-clinical models of SCD, IMR-261 was observed to reactivate fetal hemoglobin and reduce vaso-occlusive crises. Furthermore, in a preclinical model of beta-thalassemia, IMR-261 was observed to increase hemoglobin and enhance red blood cell maturation. We have initiated work towards drug product manufacturing for IMR-261, as we explore potential clinical development paths.”

IMR-261, formerly known as CXA-10, was acquired by Imara and was previously evaluated by Complexa, Inc. in Phase 2 clinical trials in focal segmental glomerulosclerosis (FSGS) and pulmonary arterial hypertension (PAH). Independent medical literature suggests potential promise in a broad array of red cell diseases, including disorders of hemoglobin.

The accepted abstracts are listed below and are available online on the ASH meeting library website.

Title: PDE9 Inhibition By IMR-687 Improves Markers of Beta-Thalassemia in the Hbb ^th1/th1 Experimental Mouse Model
Live Q&A Session Date and Time: Saturday, December 11, 2021, 5:30 PM - 7:30 PM ET
Poster Abstract Session: Thalassemia and Globin Gene Regulation: Poster I
Abstract: #945
Presenter: Jennifer O’Cain, Ph.D., Imara Inc.

Title: Treatment with IMR-687, a Highly Selective PDE9 Inhibitor, Increases HbF and Reduces VOCs in Adults with Sickle Cell Disease in a Long-Term, Phase 2a, Open-Label Extension Study
Live Q&A Session Date and Time: Sunday, December 12, 2021, 6:00 PM - 8:00 PM ET
Poster Abstract Session: Hemoglobinopathies, Excluding Thalassemia: Clinical and Epidemiological: Poster II
Abstract: #2046
Presenter: Biree Andemariam, M.D., Associate Professor at UConn School of Medicine and Director of the New England Sickle Cell Institute at UConn Health

Title: IMR-261, a Novel Oral Nrf2 Activator, Induces Fetal Hemoglobin in Human Erythroblasts, Reduces VOCs, and Ameliorates Ineffective Erythropoiesis in Experimental Mouse Models of Sickle Cell Disease and Beta-Thalassemia
Live Q&A Session Date and Time: Monday, December 13, 2021, 6:15 PM - 7:45 PM ET
Oral Abstract Session: Hemoglobinopathies, Excluding Thalassemia: Basic and Translational: Emerging Strategies to Identify and Prevent Sickle Cell Disease Pathology
Abstract: #853
Presenter: Thiago Trovati Maciel, Ph.D., INSERM, France

About tovinontrine (IMR-687)
Tovinontrine is a highly selective and potent small molecule inhibitor of PDE9. PDE9 uniquely degrades cyclic guanosine monophosphate (cGMP), an active signaling molecule that plays a role in vascular biology. Lower levels of cGMP are often found in people with sickle cell disease and beta-thalassemia and are associated with impaired blood flow, increased inflammation, greater cell adhesion and reduced nitric oxide-mediated vasodilation.

Blocking PDE9 acts to increase cGMP levels, which are associated with reactivation of fetal hemoglobin, or HbF, a natural hemoglobin produced during fetal development. Increased levels of HbF in red blood cells have been demonstrated to improve symptomology and lower disease burden in patients with sickle cell disease and patients with beta-thalassemia. Tovinontrine is designed to have a multimodal mechanism of action that acts on red blood cells, white blood cells, adhesion mediators, and other cell types.

About IMR-261
IMR-261 (formerly CXA-10) is an activator of nuclear factor erythroid 2–related factor 2, or Nrf2. Nrf2 coordinates the expression of antioxidant genes in response to oxidative stress, regulates inflammation, inhibits the NF-kB pathway, and reactivates fetal hemoglobin, or HbF. In preclinical sickle cell disease models, IMR-261 significantly increased HbF and F-cells, improved hemolytic markers, and decreased vaso-occlusive crises. In a preclinical beta-thalassemia model, IMR-261 increased hemoglobin and enabled RBC maturation. Imara has initiated work on drug product manufacturing for IMR-261, as it explores potential clinical development paths.

About Imara
Imara Inc. is a clinical-stage biotechnology company dedicated to developing and commercializing novel therapeutics to treat patients suffering from rare inherited genetic disorders of hemoglobin and other serious diseases. Imara is advancing tovinontrine (IMR-687), a highly selective, potent small molecule inhibitor of PDE9 that is an oral, potentially disease-modifying treatment currently in clinical development for sickle cell disease and beta-thalassemia and preclinical development for HFpEF. Imara is also advancing IMR-261, an oral activator of nuclear factor erythroid 2–related factor 2 (Nrf2). For more information, please visit www.imaratx.com.

Cautionary Note Regarding Forward-Looking Statements
Statements in this press release about future expectations, plans and prospects, as well as any other statements regarding matters that are not historical facts, may constitute “forward-looking statements” within the meaning of The Private Securities Litigation Reform Act of 1995. These statements include, but are not limited to, statements relating to the Company’s (i) plans to present preclinical and clinical data on tovinontrine (IMR-687) and IMR-261 at the ASH Annual Meeting and the quality of such data and (ii) beliefs regarding the therapeutic potential of tovinontrine and IMR-261. The words “anticipate,” “believe,” “continue,” “could,” “estimate,” “expect,” “intend,” “may,” “plan,” “potential,” “predict,” “project,” “should,” “target,” “will,” “would” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Actual results may differ materially from those indicated by such forward-looking statements as a result of various important factors, including: the impact of extraordinary external events, such as the risks and uncertainties resulting from the impact of the COVID-19 pandemic on the Company’s business, operations, strategy, goals and anticipated milestones, and other factors discussed in the “Risk Factors” section of the Company’s most recent Quarterly Report on Form 10-Q, which is on file with the Securities and Exchange Commission and in other filings that the Company makes with the Securities and Exchange Commission in the future. Any forward-looking statements contained in this press release speak only as of the date hereof, and the Company expressly disclaims any obligation to update any forward-looking statement, whether as a result of new information, future events or otherwise.

Media Contact:
Marin Bergman
Ten Bridge Communications
818-516-2746
Marin@tenbridgecommunications.com

Investor Contact:
Michael Gray
617-835-4061
mgray@imaratx.com