Today, the Lasker Foundation announced its 2026 winners in three categories: the Basic Medical Research Award, the Clinical Medical Research Award, and the Public Service Award. The awards were first founded back in 1942 by biomedical philanthropists Albert and Mary Lasker in an effort to recognize and celebrate scientific advancements that improve human health, and garner public support for science. This year’s awards will be formally presented as part of a ceremony in New York City on September 17th.
Albert Lasker Basic Medical Research Award
In August, the FDA approved Takeda’s Orzeyful (oveporexton) tablets to treat narcolepsy type 1 (NT1) in adults. The drug is the first approved treatment for NT1 designed to address the full spectrum of symptoms and the first to directly target the loss of orexin signaling that causes the disorder.
Now, nearly three decades after they independently discovered orexin, Emmanuel Mignot and Masashi Yanagisawa have been awarded the 2026 Albert Lasker Basic Medical Research Award for uncovering the neuropeptide’s role in maintaining wakefulness and showing that its absence causes narcolepsy.
Despite both revealing key insights into orexin, Mignot and Yanagisawa approached the discovery from very different directions. Yanagisawa was not originally looking for the biological basis of sleep. His team was searching for molecules that activate orphan receptors in the brain — receptors whose natural binding partners had not yet been identified. The first ligand they discovered was orexin.
The researchers initially thought orexin was involved in appetite regulation. But when they created mice lacking the peptide, the expected changes in feeding and body weight did not materialize. Instead, when observed at night, the animals displayed behavior resembling human narcolepsy.
At roughly the same time, Mignot was investigating narcolepsy from a completely different direction, studying inherited disease in dogs. His team identified mutations in the gene encoding orexin receptor 2, connecting the receptor to narcolepsy.
The two lines of research converged on the same conclusion: Orexin is a critical component of the brain's wakefulness machinery. The discovery changed sleep biology.
“Until our discovery of orexin and its connection to narcolepsy, sleep biology was largely studied through classical physiology and anatomy,” Yanagisawa told DDN. The discovery gave researchers a way to understand sleep and wakefulness in terms of genes, molecules, and neural circuits.
For Yanagisawa, seeing the work become medicine demonstrates the value of exploratory research and following unexpected findings rather than abandoning an experiment when an initial hypothesis fails. “Our initial hypothesis turned out to be wrong,” he said. “But it became an unexpectedly great discovery.”
Thirty years on, the researchers are still pushing the boundaries of what sleep can reveal about biology. Mignot’s Stanford Medicine team developed SleepFM, a foundation model trained on more than 585,000 hours of polysomnography data from more than 65,000 participants. The model extracts subtle physiological signals from brain activity, breathing, and cardiac data, and uses these signals to predict disease risk across a wide range of conditions, including neurological and cardiovascular diseases.
Meanwhile, Yanagisawa is currently the Director of the International Institute for Integrative Sleep Medicine at the University of Tsukuba, where he encourages young researchers to follow their curiosity and pursue unexpected findings wherever the data leads. He told DDN that he is still focused on some of sleep biology's most fundamental questions — including what sleepiness physically represents in the brain, how the brain keeps track of accumulated wakefulness and sleep, and why animals need to sleep at all.
The discovery of orexin may have explained an important part of how the brain maintains wakefulness. But there is still plenty more to find out.
Lasker~DeBakey Clinical Medical Research Award
Today, treatment for hemophilia A looks much different than it did just ten years ago. Patients with this more common type of hemophilia — who lack the clotting protein factor VIII — used to have to replace the missing factor with frequent intravenous doses. Over time, some patients develop immune responses that stop the treatment from working.
In 2017, the FDA approved the first non-factor medicine for hemophilia A to prevent uncontrolled bleeding: the bispecific antibody drug known as Hemlibra from Genentech. The drug was hailed as a game-changer by many physicians in the years following. “It’s an amazing time to be a hemophilia provider,” said Alice Ma, a hematologist at the University of North Carolina at Chapel Hill in a 2022 interview. Ma described a patient who was initially hesitant to try Hemlibra but then said “it has made his hemophilia recede into the background of his life, which is pretty, pretty nice.”
To honor the science that ultimately led to such meaningful changes for patients, the 2026 Lasker~DeBakey Clinical Medical Research Award goes to three scientists at Chugai Pharmaceuticals at the time of the discoveries: Kunihiro Hattori, Takehisa Kitazawa, and Tomoyuki Igawa.
The bispecific antibody, known as emicizumab, replaces the need for factor VIII in the blood entirely by binding activated factor IX with one arm and factor X with the other, acting as a molecular bridge. Hattori came up with the creative solution back in 2000, but turning it into a manufacturable drug that worked as intended took over a decade, with many setbacks along the way.
“When the idea was first proposed, some within the company said it was “absolutely impossible,” and we were unable to secure sufficient personnel. Even so, we kept firmly in mind the urgent challenges faced by people with hemophilia A and their families. United by our determination to develop a medicine that could ease their burden, we embarked on this challenge with a small team,” said Hattori, Kitazawa, and Igawa in a joint statement to DDN.
The team first identified a bispecific antibody that worked only weakly, and it was shelved in 2006. Then, after exhaustively assessing 40,000 antibody variants, the scientists identified a second bispecific antibody and focused on optimizing its activity, safety, immunogenicity, and convenience for patients — while at the same time investing in fine-tune engineering that allowed the removal of byproduct impurities for large-scale manufacturing. Fortunately, this drug became emicizumab.
Clinical trials of emicizumab resulted in a massive 87 percent reduction of serious bleeding episodes in patients. Even better, patients were able to inject themselves under the skin, a major step up compared to the intravenous infusions of factor concentrate.
The FDA’s approval in 2017 ushered in a new era of hemophilia treatment that has now allowed more than 30,000 patients to receive the treatment all over the world.
“The greatest reward has been seeing firsthand how this medicine has truly changed the lives of people with hemophilia A and their families,” said the Lasker~DeBakey Clinical Medical Research Awardees in the statement to DDN. They described receiving letters of gratitude, video messages, and stories shared by physicians, including patients in wheelchairs who were able to walk again.
Their work is not done, however. Hattori, Kitazawa, and Igawa noted that “while emicizumab has brought significant advances in the treatment of hemophilia A, important unmet medical needs remain. We continue to pursue drug discovery research aimed at addressing these needs.” Specifically, their team is investigating a next-generation bispecific antibody in Phase 3 trials.
The researchers also emphasized the potential for this novel molecular bridge approach to improve treatments for a range of other conditions, too. “We hope that numerous bispecific antibody therapeutics with diverse functions will be generated and developed across a wide range of diseases, ultimately reaching and helping patients,” they said.
Lasker~Bloomberg Public Service Award
At age 29, Michael J. Fox woke up to a twitching finger. He was diagnosed with early-onset Parkinson's disease soon after, a condition that affects only 10 to 20 percent of patients before age 50. Fox hid his tremors for seven years before going public with his diagnosis in 1998, then spent the next three decades sharing the course of his disease on-screen and off, giving a face and a voice to Parkinson's patients worldwide.
Now, Fox has been awarded the 2026 Lasker~Bloomberg Public Service Award for founding The Michael J. Fox Foundation for Parkinson's Research and building it into the world's largest nonprofit funder of Parkinson's science.
Since 2000, the Foundation has funneled more than $3 billion into Parkinson's research globally, including work supported in partnership with the Aligning Science Across Parkinson's initiative. According to Brian Fiske, chief scientist at MJFF, the Foundation was built around a strategic research agenda that follows the science and identifies the key barriers standing between the field and a cure, rather than restricting itself to a single stage of the drug development pipeline.
"We support the tools, biomarkers and therapeutic programs needed to better understand Parkinson's biology, de-risk promising targets and treatments, and make clinical trials more efficient and informative," Fiske said.
That mandate has shifted as the field has matured. Early Parkinson's drug development focused mainly on replacing dopamine and managing symptoms. Fiske said the therapeutic pipeline has since expanded toward treatments designed to slow or stop disease progression altogether, a shift that has pushed the Foundation to invest more heavily in biomarkers capable of detecting and quantifying disease biology.
Fiske described the Foundation's role as filling a specific gap in the drug discovery ecosystem: the space between a promising scientific finding and evidence robust enough for industry to confidently pursue.
"That's where MJFF can play an important role," Fiske said. "We can support work around scientifically risky early ideas — validating targets, generating evidence in human samples, developing biomarkers and research tools, and supporting early therapeutic development — to build greater confidence around promising approaches and de-risk larger investment."
The Foundation also funds shared infrastructure that would be difficult for any single company to build alone, Fiske said, pointing to the Parkinson's Precision Medicine Initiative (PPMI), the Foundation's longitudinal study collecting clinical data and biological samples from people with and at risk for Parkinson's. Its data, biosamples and biomarkers are available to researchers and industry alike to better understand Parkinson's biology, identify trial participants and design more precise studies.
One of the clearest products of that investment is the alpha-synuclein seed amplification assay, or SAA, a biomarker test the Foundation supported from an early pilot through years of optimization before PPMI provided the scale needed to validate it.
"If we want to treat disease, we first have to be able to measure it," said Mark Frasier, chief scientist at MJFF. "Today, SAA can detect alpha-synuclein pathology in living people and is already being used to help include or exclude participants in clinical trials, particularly those testing therapies targeting alpha-synuclein."
Frasier said the Foundation is now working to measure alpha-synuclein through more accessible samples, including blood and skin, and to move the assay from a positive-or-negative readout toward a quantitative one. That precision has already begun reshaping how biopharma companies design and enroll Parkinson's trials, he said, moving beyond enrollment based on symptoms or time since diagnosis toward biomarker testing as inclusion or exclusion criteria. Companies are also revisiting biomarker samples from completed trials to better interpret past results.
"The biology of Parkinson's can begin years before diagnosis," Frasier said. He added that PPMI is helping researchers move even earlier by combining risk factors such as smell loss and REM sleep behavior disorder with tools like SAA and dopamine imaging to identify and study people before a traditional diagnosis is possible, laying groundwork for prevention trials. Biomarkers aren't only useful for enrollment, he noted; the field also needs sensitive tools that can track disease biology over time and confirm whether a treatment is actually changing it.
Looking ahead, Frasier said the next major bottleneck in translating basic science into approved therapies will be identifying and enrolling the right participants in disease-modifying trials at scale. Greater biological precision, he said, creates its own practical challenge: efficiently finding and screening the specific populations most likely to benefit.
"That's an area where MJFF is investing through PPMI," Frasier said. "We're testing scalable approaches that can help narrow the population before more intensive biomarker testing." Smell testing is one such approach, he said, since significant smell loss can help identify a group more likely to show Parkinson's-related biology before they undergo additional testing such as SAA. "As the field becomes more precise about who may benefit from a therapy, we also need more sophisticated, efficient and scalable ways to find and enroll those people in research."
