Biochemist Svetlana Mojsov, PhD, has been awarded the Frontiers of Knowledge Award in Biology and Biomedicine, presented by Spain’s BBVA Foundation, for her collaborative research with Daniel Drucker, Joel Habener, and Jens Holst. Their work revealed the biological function of the hormone GLP-1, a key regulator of glucose metabolism and appetite.
These discoveries paved the way for a new generation of therapies that have transformed the management of type 2 diabetes (T2D) and obesity, offering not only improved glycemic control and weight loss but also reduced cardiovascular risk. The findings have also sparked new lines of basic and translational research in multiple disease areas.
Speaking to El Médico Interactivo, a Medscape Network platform, during the recent awards ceremony in Bilbao, Spain, Mojsov shared her perspective on the future of research. “We are witnessing a new paradigm in which clinical experience is guiding future research to help us understand very fundamental concepts,” said Mojsov, currently a research associate professor at Rockefeller University in New York.
How does it feel to see that drugs derived from your GLP-1 research are helping millions of people manage diabetes and obesity?
I’m very happy to have contributed to something that has helped so many people. These drugs improve not only health outcomes but also overall quality of life. Being a scientist is a profession with many rewards — and certainly more benefits than setbacks — when your work can make a real difference. All scientists are driven by the goal of advancing knowledge and human health. I feel privileged to have been part of the early stages of this long scientific journey.
Over the past two decades, GLP-1-based therapies have represented a major breakthrough in the treatment of T2D and obesity, improving both quality of life and clinical outcomes for millions of patients. For the first time, we’ve seen body weight reductions of up to 20% — which is particularly important because excess weight worsens the prognosis of T2D. Most earlier treatments actually caused weight gain, which limited their effectiveness. GLP-1 therapies, in contrast, help patients lose weight and improve disease outlook at the same time.
What led you to investigate gut hormones, particularly GLP-1 and glucose-dependent insulinotropic polypeptide (GIP)?
My interest in peptide-based therapies for glucose metabolism goes back to the mid-1970s, when I was a graduate student working with Dr Bruce Merrifield at Rockefeller University. We were studying the biology of glucagon — a hormone that raises blood glucose — and exploring how to synthesize glucagon analogs and inhibitors using solid-phase peptide synthesis.
At that time, however, the available synthesis techniques often produced biologically inactive glucagon due to chemical modifications in the amino acid sequence. Merrifield encouraged me to develop new strategies to overcome this limitation, which laid the foundation for my later work on GLP-1.
Were these the strategies you went on to explore in your research?
Yes. For my doctoral thesis and later during my postdoctoral work, I focused on the amino acid sequence and biology of glucagon. That experience was instrumental in my discovery of GLP-1 in the early 1980s at Massachusetts General Hospital in Boston. In 1983, I identified the biologically active form of GLP-1 as a 31-amino acid peptide, which I named GLP-1 (7-37). I also hypothesized that it functioned as an incretin, a gut-derived peptide that stimulates insulin secretion in response to food intake.
You and the other three awardees worked on the same hormone. Did you collaborate directly, or was the work conducted independently? How important is collaboration in this field?
To detect GLP-1 (7-37) in the gut, I synthesized it myself in the endocrinology unit of my lab using solid-phase peptide synthesis. I also developed highly specific antibodies, radioimmunoassays, and chromatographic techniques that allowed me to confirm the presence of GLP-1 (7-37) at the site of incretin secretion.
Although I conducted this initial work independently as a chemist, that kind of foundational research still requires close collaboration across disciplines. After identifying GLP-1 (7-37), I began working closely with Drs Joel Habener and David Nathan at Massachusetts General Hospital, and with Dr Gordon Weir at the Joslin Diabetes Center. So yes, throughout my work, I collaborated extensively with both biologists and clinical researchers.
Your first GLP-1 findings date back to 1986. The first drugs came in 2005, and those widely used today appeared in 2017. Has the translation from discovery to clinic taken too long? What could be done to accelerate this process?
You’re right. Our early clinical studies with Nathan were the first to demonstrate that GLP-1 (7-37) stimulates insulin secretion and lowers blood glucose in people with T2D, establishing its therapeutic potential. Back at Rockefeller, my colleague Yang Wei and I showed that GLP-1 receptors are expressed not only in the pancreas but also in the brain, heart, and kidneys. This indicated that GLP-1’s effects across these organs are mediated by a common receptor.
In the 1980s and 1990s, the pharmaceutical industry was skeptical that peptides could become viable drugs because they required injection, and oral medications were strongly preferred by patients. Still, GLP-1 (7-37) held promise. In 2005, researchers discovered a longer-acting GLP-1-like peptide in lizard venom, which allowed Amylin Pharmaceuticals to act quickly since they didn’t have to develop a new compound from scratch. That said, many companies were hesitant to invest in a peptide derived from a lizard.
Twenty-five years after my original publications, Novo Nordisk and Lilly launched long-acting GLP-1 analogs. These drugs are now used to treat a wide range of conditions beyond T2D and obesity, including cardiovascular and renal disease and potentially even neurodegenerative disorders. It’s the first time a single drug class has shown such broad therapeutic utility.
Your discoveries are already benefiting millions of patients with obesity and diabetes, but cost remains a significant barrier. Do you think these drugs will become more accessible in low- and middle-income countries?
They must become more affordable — otherwise, their usefulness is fundamentally limited. The broader the access, the greater the public health impact.
I’m optimistic that continued innovation will help lower costs and improve global accessibility. These therapies shouldn’t be reserved only for patients in wealthy nations. The health benefits must be shared more equitably.
We also need to prioritize and protect scientific research. Especially given the current climate in the US, it’s worth remembering that our longer, healthier lives are built on scientific progress. While the pharmaceutical industry plays a vital role, it all starts with discovery — and discovery starts in academic and research institutions. That’s where we need to focus our support. Novo Nordisk did outstanding work, but they built on foundational research that came from the lab. Ultimately, we all have to work together. Every breakthrough starts with knowledge— knowledge, knowledge, and more knowledge.
With T2D and obesity rising globally, and GLP-1 therapies now widely available, do you worry that they might shift attention away from prevention?
No, quite the opposite. These therapies are most effective when combined with a commitment to overall health. Although some health conditions are unavoidable, I believe these drugs serve as a reminder of the importance of personal well-being. They help people take concrete steps toward better health.
GLP-1 receptor agonists are now a key part of the pharmacologic toolkit for managing obesity and diabetes. Do you think they’ll prove effective in other conditions, such as cardiovascular disease, neurodegeneration, or addiction?
We already know they offer cardiovascular benefits, and physicians are prescribing them for people with diabetes — including those on insulin — because they also support kidney function. So these therapies are already broadly accepted and widely used.
When it comes to neurodegenerative diseases, however, it’s still too early to draw conclusions. Current findings are anecdotal and based on small patient cohorts. We need a much better understanding of the mechanisms involved. The same applies to addiction. There’s speculation that GLP-1 analogs might help prevent addictive behaviors, but we need robust evidence before reaching that conclusion.
This is the exciting part of science: knowledge opens the door to new discoveries. We need to return to the lab, use animal models, and uncover the mechanisms at work. Once we do, we’ll be in a better position to confirm the full range of effects and explore new indications.
You’ve had to fight for recognition on five patents. Do you believe being a woman made that more difficult? And do young women entering science today have equal opportunities?
I grew up in Yugoslavia, where we weren’t really taught to think in terms of gender differences. I never believed someone would take advantage of me for being a woman. Whether it happened or not, I can’t say, but I never attributed any setbacks to my gender. I knew what I wanted and I fought for it. I pursued the patent issue because the original filing didn’t properly reflect my contribution.
My work resulted in five patents—four of which I secured after correcting Massachusetts General Hospital’s initial application.
Today, women are firmly part of the scientific community. Half of all researchers are women, so there should be no room for discrimination. That said, when something isn’t right, we must speak up—clearly and confidently—and have the courage to stand our ground.
Your perseverance and discipline are admirable. How important are those traits for aspiring researchers?
They’re both essential. This path is never easy.
This article was translated from El Médico Interactivo.