Insulin: The Patent Sold for a Dollar
Before 1922, a child with type-1 diabetes had a life expectancy measured in months. After 1922, that life became 60 years longer. The molecule responsible was discovered by a surgeon who'd never run a lab — and its patent was sold for a single dollar.
A diagnosis that was a death sentence
In 1920, if your six-year-old came home unusually thirsty, urinated through the bed nightly, lost weight no matter how much they ate, and slipped into confused exhaustion, you took them to a hospital where the doctor sniffed their breath and gave the diagnosis without a blood test: diabetes mellitus type 1. Their breath smelled of acetone because their cells, unable to use sugar, were burning fat at a runaway rate that flooded their blood with ketones.
The standard treatment was the Allen starvation diet. The doctor would put the child on roughly 450 calories a day for the rest of their short life. With perfect compliance, this could extend life by 12 to 36 months. The child would be skeletal and weak. They would die slowly, of starvation or of diabetic ketoacidosis, whichever came first.
There was no other option. Doctors knew, since 1889, that something in the pancreas — when removed from a dog, the dog became diabetic — controlled blood sugar. They could not isolate it.
Many had tried. Pancreatic extracts injected into diabetic patients sometimes worked briefly, then produced violent reactions. The active substance was apparently destroyed by the digestive enzymes the pancreas itself secreted. Extraction kept failing.
A surgeon with no lab experience
Frederick Banting was a 29-year-old surgeon in London, Ontario, in October 1920. His Toronto-trained medical practice was struggling. He’d taken a part-time lectureship at the University of Western Ontario to make rent.
While preparing a lecture on the pancreas, Banting read a journal article about a man who’d died of pancreatic duct stones; the duct had been blocked for years, the digestion-enzyme-producing tissue had wasted away, but the small clusters of cells called islets of Langerhans were intact. Banting wrote down an idea in his notebook that night:
Tie off the pancreatic ducts of dogs. Wait six to eight weeks for the digestive tissue to degenerate. Then extract the islet residue. Test for relief of glycosuria in diabetic dogs.
He had never done a research experiment. He had no laboratory. He went to John Macleod, professor of physiology at the University of Toronto, who was skeptical but agreed to give him eight weeks of lab time, ten dogs, and one graduate student, Charles Best, before leaving on a summer vacation in Scotland.
That summer of 1921 in Macleod’s basement lab, Banting and Best produced a pancreatic extract that, when injected into diabetic dogs, dropped their blood sugar. They had it within weeks. The dogs, dying of diabetes induced by pancreatectomy, walked out of their cages.
Macleod, on returning from Scotland, dismissed it as a fluke. Banting, by all accounts, almost punched him. Macleod then ran the experiments himself, became convinced, and reorganized the entire lab around insulin extraction.
A boy named Leonard Thompson
The first human trial was conducted on Leonard Thompson, 13 years old, weighing 65 pounds, comatose with ketoacidosis at Toronto General Hospital. He was expected to die within days.
On 11 January 1922, he received a 7.5 mL injection of pancreatic extract. He had a mild allergic reaction. His blood sugar dropped only slightly.
The team — now including biochemist James Collip, who had joined to help purify the extract — went back to the lab. Collip worked through the night, weekend after weekend, refining the extraction procedure. On 23 January 1922, Thompson received a second, purer extract.
His blood sugar normalized within hours. His glycosuria cleared. He regained consciousness. He ate. He got up. He went home. He lived another 13 years (he died of pneumonia in 1935; his diabetes was, throughout, controlled).
Word spread. Children dying in pediatric wards across North America began receiving the new substance. Parents wrote in the medical literature about watching their comatose, dying children sit up and ask for food. One nurse described an entire ward of children all simultaneously waking from diabetic coma as the doses took effect, an event that has no parallel in medical history.
The patent
The University of Toronto applied for a patent on insulin in 1923. Macleod and Banting were named as co-inventors; Best and Collip joined later.
Banting refused to put his name on the application at first. He felt strongly that a doctor profiting from a discovery that would save lives was ethically wrong. The university convinced him that holding the patent themselves would prevent private exploitation — anyone could license it under controlled terms. Banting agreed only when he could sell his share to the university for a single Canadian dollar.
The exact quote, frequently cited but with disputed attribution, is some version of: “Insulin belongs to the world, not to me.”
The University of Toronto then licensed insulin production to Eli Lilly in the US and to Allen and Hanburys in the UK — both at non-exclusive, modest royalties. By 1923, insulin was in mass production. By 1924, it was in pharmacies around the world.
Banting and Macleod received the Nobel Prize in 1923, the fastest Nobel ever awarded for a discovery (the work was less than two years old). Banting was so angry about Macleod sharing the prize — he felt Best deserved it, not Macleod — that he split his half of the prize money with Best on principle. Macleod, in turn, split his half with Collip.
What the molecule actually does
Insulin is a small protein — 51 amino acids in two chains held together by disulfide bonds. By protein standards it is tiny. But the formula (C₂₅₇H₃₈₃N₆₅O₇₇S₆) is far larger than every other molecule in this library combined.
It is secreted by the beta cells of the islets of Langerhans whenever blood glucose rises after a meal. It binds to insulin receptors on the surface of muscle, fat, and liver cells. The receptor, on binding, fires a downstream signaling cascade whose end effect is the insertion of GLUT4 glucose transporters into the cell membrane. Glucose pours from blood into cell. Blood glucose drops back to baseline within a few hours.
In type-1 diabetes, the patient’s immune system has destroyed their own beta cells. They have no insulin. Without injection, glucose cannot enter cells. Cells starve in the middle of glucose-rich blood. The body responds by burning fat at runaway rates, producing the ketones that cause acidosis, coma, and death.
In type-2 diabetes, beta cells still produce insulin, but the receptors have become resistant. The same exogenous insulin can supplement, eventually replace, what the body can no longer use effectively.
Both conditions, before 1922, were death sentences within months to years. After 1922, both became manageable chronic conditions.
What price equals what life
Insulin’s history makes its modern price story especially galling. The University of Toronto sold the patent for 5–10 to produce.
By 2020, a one-month supply of analog insulin in the United States cost a typical type-1 diabetic about $300. People rationed doses. People died. There were documented cases of young Americans dying of diabetic ketoacidosis because they had skipped doses to stretch a vial across more weeks.
In 2023, after relentless public and political pressure, Eli Lilly, Novo Nordisk, and Sanofi (the three insulin makers worldwide) announced significant price caps and reductions in the US market. The Inflation Reduction Act capped Medicare insulin co-pays at 1 to prevent exactly this outcome.
A child born today with type-1 diabetes can expect to live a full normal life. They will inject or pump insulin for sixty or seventy years. They will have to count carbs at every meal, prick their finger or wear a continuous glucose monitor, navigate insurance, hold down jobs that include health coverage, never travel anywhere without backup supplies. But they will live. Most of their life will look like everyone else’s. They will fall in love, raise children, retire, die slowly of something else.
This was unimaginable in 1920. It became possible because a 29-year-old surgeon with no research experience read about a pancreatic duct blockage and wrote an idea in his notebook at 2 AM in October.
A footnote on Charles Best
Charles Best was 22, an undergraduate, when he co-discovered insulin. Macleod paid him not at all that summer; he split a single graduate-student stipend with another student. When the Nobel was awarded only to Banting and Macleod, Best was a footnote.
Banting felt about this exactly the way most people would. He refused to attend the Nobel ceremony in protest. He never personally reconciled with Macleod and never spoke of him warmly. He shared his prize money with Best for the rest of his life.
Best went on to direct the Banting & Best Department of Medical Research at the University of Toronto, the laboratory where insulin had been discovered. He spent his career trying to ensure that the discovery was credited correctly. Most of the credit for him came posthumously.
Banting died in 1941 in a plane crash en route to England during the Second World War, where he was working on aviation medicine. He was 49. He never knew that the molecule he had isolated in a borrowed basement lab over a single summer would, a century later, be keeping eight million people alive worldwide.
The insulin molecule has its own 3D page in the library — rotate it, see the disulfide-bridged two-chain protein that turned diabetes from a death sentence into a manageable chronic disease, download the structure file. It also has its own bouncing wallpaper.