About Us

Our scientific efforts are aimed at developing drugs that improve the management of proliferative diseases of the bone marrow. Our clinical focus is on acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), polycythemia vera (PV), myelofibrosis (MF) and essential thrombocythemia (ET) – diseases sharing several features. These diseases are caused by acquired mutations in blood stem cells. These mutations drive excessive growth and alter the function of specific bone marrow cells. In the case of myelofibrosis, mutant megakaryocytes, the cells that make platelets, are a central cell type driving disease. It is the altered function of these mutant bone marrow cells that is responsible for the signs and symptoms of myelofibrosis. For example, myelofibrosis can be viewed as a chronic inflammatory disorder in which inflammatory cytokines and growth factors released by mutant bone marrow cells cause both the characteristic symptoms of myelofibrosis and the destruction of bone marrow.

Bomedemstat (IMG-7289) and LSD1 Inhibition

Bomedemstat is a small molecule discovered by Imago that inhibits lysine-specific demethylase 1 (LSD1), an enzyme active in hematopoiesis. Among its functions, LSD1 is essential for the maturation and normal activity of megakaryocytes, and for the self-renewal of malignant hematopoietic stem/progenitor cells. It is widely appreciated that megakaryocytes are a primary source of the growth factors and cytokines that drive the pathogenesis of MF, supporting the hypothesis of the ongoing Phase 2b study in patients with MF.

Given the distinct mechanism of action of bomedemstat, the supporting pre-clinical data and the current clinical data in ruxolitinib-refractory patients, bomedemstat is well suited for once-daily monotherapy for the treatment of MF and other MPNs. Future studies may prove that bomedemstat combined with ruxolitinib, in those patients with a sub-optimal response to ruxolitinib, provides additional clinical benefit.

Bomedemstat has also been studied clinically in high-risk acute myeloid leukemia and high-risk myelodysplastic syndrome. In pre-clinical mouse models of solid tumors, combinations of bomedemstat with other agents show activity against these neoplasms. Finally, LSD1 inhibition induces fetal hemoglobin (HbF) production, which may offer therapeutic opportunities in thalassemia intermedia and sickle cell disease.

Imago BioSciences is based in South San Francisco.

Contact us for more information about the company, or to discuss research and corporate development opportunities.

415-529-5055

329 Oyster Point Blvd.
3rd Floor
South San Francisco, CA 94080

Our name, Imago, (pron. i-mắ-go), invokes the final and fully developed stage of an insect after its metamorphosis. In this process of growth and development, the imago refers to the fully formed adult, one that has completed its transformation and, for a butterfly, has taken flight. In our view, the full maturation of a scientific idea or observation in medical research is when new treatments prove their worth in clinical studies. To patients, anything less is to miss the mark.

Imago’s Name