On Sept. 9, 2026, the Albert Lasker~DeBakey Clinical Medical Research Award honored three scientists for inventing a bispecific antibody that joins blood clotting Factors IX and X. With this breakthrough, Kunihiro Hattori (formerly at Chugai Pharmaceutical), Takehisa Kitazawa (Chugai Pharmaceutical), and Tomoyuki Igawa (Chugai Pharmaceutical) restored deficient Factor VIII activity in hemophilia A, thus preventing the severe bleeding that characterizes this genetic disorder. Hattori launched the enterprise with inspired vision, and Kitazawa and Igawa brought it to fruition through their synergistic pharmacological and chemical-engineering expertise. Fueled by imagination and tenacity, these investigators have transformed quality of life for people with this debilitating disease.

As a liquid, blood serves essential functions, transporting oxygen and nutrients, removing waste, and delivering infection fighters. But after injury, this vital substance must solidify to seal ruptured vessels. Cell fragments called platelets gather at the fissure to provide a platform for coagulation, and the vascular damage spurs a sequential set of reactions that culminates in a clot. A protein called Factor VIII (F-VIII) plays a crucial role in this pathway. It grabs two other proteins, Factor IXa (F-IXa) and Factor X (F-X). Once F-VIII has brought them together, F-IXa cleaves F-X, converting it into its active form, F-Xa, which drives the process forward.

A deficiency of F-VIII causes hemophilia A. This disease is commonly inherited, and because the F-VIII gene lies on the X chromosome, it afflicts mostly males—about one in 4000. Severity varies, but affected individuals clot poorly and can bleed uncontrollably even in the absence of trauma. Blood frequently pools spontaneously in the joints, which causes chronic pain and impairs mobility. Symptoms interfere with social and leisure pursuits as well as school and work, compromising well being, especially for children and their caregivers.

After initial studies established acceptable safety in humans, the drug’s efficacy was assessed. In 2016, Midori Shima at Nara Medical University and his colleagues at other Japanese institutions published results from a trial on 18 people with severe hemophilia A. Weekly subcutaneous administration of emicizumab deflated annualized bleeding rates relative to what they were in the six months before this treatment, even in individuals with inhibitors.

The next year, Shima reported data from a multi-center, international clinical investigation on 109 people with inhibitors. The therapy slashed annualized bleeding rates from 23.3 with treatment to 2.9 without, an 87% drop. Sixty-three percent of the participants had no bleeds in at least 24 weeks compared with 6% in the group that was treated only with standard therapies, not with emicuzumab.

These results, along with similar ones from a study on children under 12 years old, led to expedited approval by the U.S. Food and Drug Administration in 2017, which was extended to people without inhibitors in 2018. More than 100 countries have followed suit. The drug’s half-life is about 29 days, which has allowed many individuals to deploy a dosing frequency of once every four weeks. The real-world impact has been profound, especially on children, who can participate more fully in normal play now that mobility impairment and pain do not bedevil their joints, and the risk of a life-threatening bleed from a jungle-gym tumble has plunged. Emicizumab’s safety profile has remained favorable, with the most frequent side effect being injection-site reactions. In phase 3 clinical studies, no serious events have occurred in patients who have received emicizumab alone or in combination with F-VIII or another factor, but dangerous clots that obstruct a blood vessel have been reported in several patients when a medicine called activated prothrombin complex concentrate was repeatedly given in combination with emicizumab.

Hattori, Igawa, and Kitazawa have touched not only the 30,000 individuals across the globe who have received emicizumab (marketed as Hemlibra®). They have also expanded the possibilities of therapeutic antibody design more widely, opening avenues toward bispecific antibodies that target diverse pathological processes. Since emicizumab arrived, 14 additional bispecifics have been approved, 11 of which aim to kill cancers. Most target T cells along with a specific molecule on the surface of lymphoma, myeloma, or other tumor cells. To date, emicizumab is the only bispecific that bypasses a molecular deficiency and restores its function. Its uniqueness underscores the scientists’ ingenuity, pluck, and dedication.