Patients diagnosed with myeloproliferative neoplasm, a group of blood cancers in which the body overproduces red or white blood cells, don’t have great options. Treatment tends to be palliative, without changing the course of disease. Enter Imago BioSciences, which is working on a treatment that shuts down an enzyme important to cancer growth.
The company reeled in $80 million in series C funding to get that drug, bomedemstat, through the clinic in two indications, with a phase 3 study on deck for the most promising one next year. Farallon Capital Management led the round, with T. Rowe Price Associates, Blackrock Advisors, Surveyor Capital, Irving Investors and Kingdon Capital Management also chipping in.
“We’ve got some pretty exciting results, and I think it was those results that really drove the recent financing event,” Imago CEO Hugh Rienhoff Jr., said of the phase 2b studies the company has completed so far.
Imago is focusing on two of the three myeloproliferative neoplasms: myelofibrosis, in which bone marrow is replaced by scar tissue, and essential thrombocythemia, caused by elevated platelets, which allow blood clotting. The drug has picked up fast-track and orphan-drug tags from the FDA in both indications.
Imago hopes bomedemstat will stave off disease progression and—in the case of myelofibrosis—prevent the condition from becoming a deadlier form of cancer, acute myeloid leukemia (AML). Unlike the JAK inhibitors approved for these diseases, bomedemstat blocks lysine-specific demethylase 1 (LSD1 or KDM1A), an enzyme important in cancer stem cells.
Incyte’s Jakafi and Bristol-Myers Squibb’s Inrebic target JAK2, which plays a role in controlling blood cell production, while bomedemstat’s target, LSD1, regulates the “ability of malignant stem cells to perpetuate forever, to be able to divide forever,” Rienhoff said.
Because malignant stem cells are often “the reservoir of relapse,” Rienhoff said, “you can kill all the cells that are dividing rapidly, but these guys sort of lie in the weeds and divide slowly and have kind of a different biology. So LSD1 is part of how those cells are able to survive in the face of standard chemotherapy.”
These cancer stem cells also cause the overproduction of megakaryocytes, or the cells that enable blood clotting. An overabundance of megakaryocytes is what causes myelofibrosis and AML, so by inhibiting LSD1, the drug is both reducing the number of megakaryocytes and the number of malignant stem cells. And eliminating that reservoir of cancer stem cells could mean wiping out the disease entirely, Rienhoff said.
Beyond trials in bomedemstat’s first two indications, the new funding will bankroll a clinical study in the third cancer under the myeloproliferative neoplasm umbrella—polycythemia vera—and advance solid tumor and sickle cell programs into phase 1. It will also support a combination trial.
“Because this drug we believe is extremely safe, we can add it on top of the two already approved drugs that work through same mechanism,” Ed Baracchini, Ph.D., Imago’s chief business officer, said. “When these patients do start to fail through the current approved therapies we’ll be in a position to be either a monotherapy or in combination with the current JAK inhibitors.”