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Portrait of John R. Vane
Photo: Unknown author, [1] · CC BY 4.0 via Wikimedia Commons

Nobel Prize in Physiology or Medicine · 1982

John R. Vane

He found how aspirin works and co-discovered prostacyclin, explaining aspirin's heart benefits and helping start a new class of heart drugs.

The Nobel citation: “for their discoveries concerning prostaglandins and related biologically active substances”
Born
March 29, 1927, Tardebigg, United Kingdom
Died
November 19, 2004, Farnborough, United Kingdom
Shared with
Sune K. Bergström, Bengt I. Samuelsson
Affiliation at the time
The Wellcome Research Laboratories, United Kingdom

Medicine prize

1982

Shared with 2 other laureates.

Age that year

55years

Born in 1927.

Headline credited impact

33,000–138,000lives saved

Vascular deaths prevented by long-term aspirin in people with heart disease or stroke (1980-2025). How it was built

Sources cited

24

Fact-checked September 24, 2026.

  • The idea for how aspirin works came to him over a weekend. On Monday he told two colleagues he thought he knew, and by that evening one lab test had convinced him.
  • His first real lab was a garden shed his father built after a chemistry-set explosion at the kitchen stove turned the fresh blue paint a dirty green.
  • Asked his plans after a chemistry degree, he said he wanted to do anything else, then went to the library to find out what pharmacology was.
  • A snake-venom extract brought to his lab by Brazilian colleague Sérgio Ferreira helped persuade Squibb to seek a synthetic ACE inhibitor: captopril, approved in 1981.
  • In 1973 he left academia to run research at Wellcome, though a few friends felt good science belonged only in universities. His team there discovered prostacyclin.

The breakthrough

How aspirin works, and the discovery of prostacyclin (1971-1976)

Aspirin was among the most used drugs in the world, yet for decades nobody could explain how it eased pain, fever and swelling. Vane's clue came from prostaglandins, tiny local messengers that body tissues make from a fatty acid when they are injured or stressed. Around 1970 he noticed that aspirin given to a dog cut the release of prostaglandins. Over a weekend he formed a hunch, and on the Monday he tested it. He ground up guinea-pig lungs, added the fatty acid the lungs use to make prostaglandins, and dosed some tubes with aspirin, indomethacin or morphine. Aspirin and indomethacin strongly cut the making of prostaglandins; morphine did not. He published the finding in 1971. Think of prostaglandins as alarm bells. Aspirin does not muffle the bells; it shuts the workshop that makes them. That idea explained aspirin's benefits and also its side effects, because the stomach relies on prostaglandins to protect its lining. In 1976 Vane's team at the Wellcome laboratories, led by Salvador Moncada, found a new member of the family in blood-vessel walls. They called it prostacyclin. It relaxes vessels and stops blood platelets from clumping, the opposite of thromboxane, a clotting signal that platelets make. Much of this work relied on a method Vane built, called cascade bioassay, in which strips of animal tissue bathed in a flowing stream reacted almost instantly to short-lived substances.[2],[3],[4],[9]

“I think I know how aspirin works”
John R. Vane, What he told colleagues Sergio Ferreira and Priscilla Piper one Monday morning around 1970, as he recalled in his Nobel lecture; the finding was published in 1971.[3]

What it meant for humanity

Vane's finding explained why an old painkiller could also prevent clots, a use doctors were already testing in trials, the first reported in 1974. Aspirin stops platelets from making thromboxane, their clotting signal, so a small daily dose can lower the risk of clots in the arteries of the heart and brain. In trials of people with existing heart or artery disease, such as a past heart attack or stroke, long-term aspirin cut serious vascular events, meaning heart attacks, strokes and vascular deaths, from 8.2% to 6.7% a year. The benefit far outweighs the added risk of bleeding for these patients. Yet a 2023 study of national surveys from 51 countries found that only about 40% of people with a history of heart disease or stroke took aspirin, and fewer than a quarter in low- and lower-middle-income countries. Prostacyclin became a medicine too. Given as epoprostenol, it was the first treatment shown in a randomised trial to improve survival in severe primary pulmonary hypertension, a deadly disease of the lung's blood vessels. In that 12-week trial, published in 1996, all eight deaths were among patients who did not receive it. Vane's earlier work led to another drug family. His lab showed that the lungs convert the hormone angiotensin I into angiotensin II, and that peptides from a snake venom brought by his Brazilian colleague Sérgio Ferreira block this step. He and Ferreira took the idea to Squibb, whose chemists developed captopril, the first ACE inhibitor taken as a pill, approved in 1981. ACE inhibitors are now routine treatment for high blood pressure and some heart disease. His Guardian obituarist judged that daily aspirin and ACE inhibitors would be his lasting legacy.

  • Vane showed in 1971 that aspirin and related drugs work by blocking the body's production of prostaglandins, solving a long-standing puzzle about one of the most common medicines.[4],[9]
  • For people with existing heart or artery disease, daily aspirin cut serious vascular events from 8.2% to 6.7% a year across 16 trials of about 17,000 patients.[15]
  • His team discovered prostacyclin in 1976. As the drug epoprostenol, it improved survival in severe primary pulmonary hypertension: all eight deaths in a 12-week trial published in 1996 were in the group that did not get it.[3],[19]
  • Lung and snake-venom studies in his lab helped persuade Squibb to search for a synthetic ACE inhibitor. The result, captopril, was approved in 1981, and drugs of this class now routinely treat high blood pressure.[6],[10]
  • He published around 900 original articles and mentored visiting scientists from Honduras, Brazil, Poland, Australia, the US, Japan and Canada as well as Britain, many of whom became leaders in their fields.[5]

Impact in numbers

Vane's work changed medicine in three ways. First, by showing how aspirin works, he explained why low doses can prevent clots in people with heart disease or stroke, a use that clinical trials were testing on a separate track. We count about 1.1 to 4.6 million deaths prevented this way since 1980 and credit him with 3%. Second, his team's discovery of prostacyclin became a treatment for severe pulmonary hypertension and a key to understanding how blood vessels keep blood flowing. Third, his lab's lung and snake-venom studies set the stage for ACE inhibitors, among the most widely used blood-pressure drugs. We do not put a number on that last one, because the chemists at Squibb who designed captopril, and Sergio Ferreira, deserve much of the credit. We also count harms: major bleeding from low-dose aspirin, credited at the same 3%, and the heart attacks caused by the COX-2 drug Vioxx in the US, credited to him at only 1%. His cascade bioassay method and his training of scientists across five continents shaped pharmacology in ways no number captures.

HealthFundamental science

Each number is the laureate’s credited share of a real-world outcome, cumulative to 2025. The whole outcome, the share of credit, and the reasoning are shown so you can check the arithmetic. Outcomes shared with other laureates are counted once on the impact page.

  • Medium confidenceRippleModeledHealth

    Vascular deaths prevented by long-term aspirin in people with heart disease or stroke (1980-2025)

    33,000–138,000

    lives saved, credited share

    That is 3% of 1.1–4.6 million lives saved since 1980.

    How this number was built

    Users: GBD 2019 counts 197M people with IHD and 101M with stroke. Aspirin use among them was 40% in 51 countries (Yoo 2023, no China/India) and 11-64% by income group in PURE, so assume 50-90M users in 2019, rising linearly from zero (1985 low, 1980 high), flat to 2025: 50M x (17+6 yrs) = 1.15B; 90M x (19.5+6) = 2.3B person-years. Effect: ATT 2009 secondary-prevention trials cut vascular death by 0.29%/yr (2.9 per 1,000 person-years, bleeding deaths included); ATT notes other treatments roughly halve event rates, so use 1.0-2.0 per 1,000 person-years. Result: 1.15B x 1.0 = 1.15M; 2.3B x 2.0 = 4.6M. Check: 50k-180k/yr in 2019, near Elwood's 100k/yr possible. Share 0.03: clinical use grew on a separate track (earlier platelet studies, Elwood's 1974 trial); Smith and Willis, Samuelsson (thromboxane) and the trialists share credit.[9],[10],[15],[16],[17],[18]

    Sources: Journal of the American College of Cardiology (via PubMed Central); JAMA (via PubMed Central); The Lancet (via PubMed Central); Postgraduate Medical Journal (via PubMed Central); Nature Publishing Group; MDPI Toxins (via PubMed Central)

  • HarmLow confidenceRippleModeledHealth

    Major bleeds caused by long-term low-dose aspirin for heart disease or stroke (1980-2025)

    23,100–303,000

    people harmed, credited share

    That is 3% of 770,000–10.1 million people harmed since 1980.

    How this number was built

    Same 1.15-2.3B aspirin person-years as the benefit claim. Low rate: across 13 primary-prevention trials (1.05M participant-years, median age 62), aspirin gave 23.1 vs 16.4 major bleeds per 10,000 person-years, an excess of 0.67 per 1,000 (Zheng 2019); heart and stroke patients are older and bleed more, so this is a floor. High rate: in the Oxford Vascular Study, patients on aspirin-based treatment after a heart attack, stroke or TIA had 1.46% major bleeds a year in routine care (half aged 75+, no routine stomach protection); at Zheng's hazard ratio of 1.43, 30% of these, 4.4 per 1,000, are due to aspirin. ATT 2009's secondary-prevention trials recorded bleeds too incompletely to use. Result: 1.15B x 0.67 = 770,000; 2.3B x 4.4 = 10.1M. Fatal bleeds are already netted out of the benefit claim's vascular deaths. Share 0.03, matching the benefit claim.[15],[23],[24]

    Sources: JAMA (PubMed record); The Lancet (PMC full text); The Lancet (via PubMed Central)

  • HarmLow confidenceRippleSourced totalHealth

    Excess heart attacks and sudden cardiac deaths caused by rofecoxib (Vioxx) in the US, to its 2004 withdrawal

    280–1,390

    people harmed, credited share

    That is 1% of 28,000–139,000 people harmed since 1999.

    How this number was built

    From FDA scientist David Graham's November 2004 Senate testimony: an FDA study report estimated nearly 28,000 excess heart attacks and sudden cardiac deaths caused by Vioxx in the US, which he called extremely conservative; applying risks from Merck's VIGOR and APPROVe trials gave 88,000-139,000, 30-40% probably fatal. US only, so the worldwide total is larger. Share 0.01: COX-2 was discovered by other groups and Merck made and marketed the drug. Vane's link is indirect: his 1971 finding underlies all such drugs, and his group's 1993 paper on COX-1/COX-2 selectivity predicted that selective inhibitors would have fewer side effects. The harm is thought to stem partly from suppressing prostacyclin, which his own team discovered.[11],[12],[13],[14]

    Sources: US Senate Committee on Finance; The Lancet (via PubMed); Proceedings of the National Academy of Sciences (via PubMed); Journal of Clinical Investigation (via PubMed Central)

The double edge

Vane's discovery explained aspirin's harms as well as its benefits. Prostaglandins help protect the stomach lining, so blocking them can cause ulcers and bleeding, and in the big aspirin trials long-term use raised the risk of major bleeding by about half or more. For people who already have heart disease the benefit clearly outweighs this risk; for healthy people the balance is much closer. A later chapter is more troubling. In the 1990s the drug industry built COX-2 inhibitors on the idea, which Vane's own group helped promote, that blocking only the inflammation-linked form of the enzyme would spare the stomach. One of these drugs, rofecoxib (Vioxx), raised the risk of heart attacks and was withdrawn worldwide in 2004. An FDA scientist estimated that it caused 88,000 to 139,000 excess heart attacks and sudden cardiac deaths in the US alone. Researchers later explained the harm partly through prostacyclin, Vane's own discovery: these drugs suppress the blood vessels' protective prostacyclin. Vane did not invent or market Vioxx, but the line of reasoning ran through his field.

  • Moderate

    Stomach damage and bleeding from aspirin-like drugs

    Because prostaglandins protect the stomach lining, drugs that block them can cause peptic ulcers. In the aspirin trials, long-term aspirin increased major bleeds, mostly in the gut, by about 1.5 to 2.7 times. For patients with existing vascular disease the benefit far outweighed this risk; in healthy people the balance is much closer.[4],[15]

  • Major

    The COX-2 inhibitor episode and Vioxx

    Vane's group reported in 1993 that common painkillers block the two forms of the enzyme differently and suggested that COX-2-selective drugs would have fewer side effects. Rofecoxib, one such drug, was withdrawn in 2004 after it was found to raise heart attack risk. An FDA scientist put US excess cases at 88,000 to 139,000, 30-40% probably fatal; a study report he co-wrote had estimated nearly 28,000, which he called extremely conservative.[11],[12],[13],[14]

Against the odds

No source consulted describes Vane facing antisemitism, and his story is not one of persecution. His paternal grandparents came from the Russian Empire, where waves of anti-Jewish riots, called pogroms, swept the southern and western provinces in 1881-1884. Jewish immigration from the Russian Empire to Britain rose sharply from that year, and Britain's first modern immigration law, the Aliens Act of 1905, was aimed in large part at limiting Jewish arrivals from Eastern Europe. In the 1930s Oswald Mosley's British Union of Fascists turned increasingly antisemitic, and in 1936 crowds blocked its march through London's Jewish East End at the Battle of Cable Street. Vane's own hardships were those of his generation. As war began, his whole school was evacuated to the countryside. After it returned to Birmingham early in 1940, four years of air raids followed: his family spent nights in a shelter at the bottom of the garden, and at school he fire-watched and trained as a young soldier. His father ran a small business making portable buildings, and Vane's first laboratory was a shed his father built for him in the garden.

  • 1940

    War

    From 1940 Birmingham was bombed for about four years. Vane's family spent nights in an air-raid shelter in the garden, and at school he fire-watched and trained as a young soldier.[2]

  • —

    Discrimination

    Wider context: Jewish migrants of his grandparents' era left a Russian Empire marked by pogroms, and Britain's Aliens Act of 1905 aimed largely to limit their arrival. In 1936 British fascists tried to march through London's Jewish East End. No record shows Vane himself facing antisemitism.[2],[20],[21],[22]

Jewish background

Jewish fatherRelationship to Jewish identity not documented

Vane wrote that his father, Maurice Vane, was a son of immigrants from Russia, and that his mother, Frances, came from a Worcestershire farming family. A 2002 interview with him in the book Candid Science II, by István Hargittai, is cited by Jinfo and Wikipedia as the source for his paternal grandparents being Jewish immigrants, which gives him a Jewish father and a non-Jewish mother. The Encyclopaedia Judaica has an entry on him. No source consulted describes Jewish religious practice or Vane speaking publicly about a Jewish identity.[2],[6],[7],[8]

Key dates

  1. March 29, 1927

    Born in Tardebigg, Worcestershire, England, the youngest of three children; the family lived in a suburb of Birmingham.[1],[2]

  2. 1939

    Given a chemistry set for Christmas at age 12; his father later builds him a garden-shed laboratory.[2]

  3. 1944

    Begins studying chemistry at the University of Birmingham while the city is under wartime air raids.[2]

  4. 1946

    Moves to Harold Burn's pharmacology department at Oxford, with no biological training.[2],[5]

  5. 1953

    Completes his Oxford doctorate and joins Yale University's pharmacology department as an assistant professor.[2]

  6. 1955

    Returns to London to the Institute of Basic Medical Sciences at the Royal College of Surgeons, where he stays 18 years and becomes professor.[2],[5]

  7. 1971

    Publishes in Nature that aspirin-like drugs work by blocking the making of prostaglandins.[3],[9]

  8. 1973

    Becomes Group Research and Development Director of the Wellcome Foundation.[2]

  9. 1974

    Elected a Fellow of the Royal Society.[2]

  10. 1976

    His Wellcome team, with Moncada, Gryglewski and Bunting, reports a new prostaglandin in blood-vessel walls, later named prostacyclin.[3]

  11. 1977

    Receives the Albert Lasker Basic Medical Research Award.[2]

  12. 1982

    Shares the Nobel Prize in Physiology or Medicine with Sune Bergström and Bengt Samuelsson for discoveries on prostaglandins.[1],[4]

  13. 1984

    Knighted in the New Year Honours for services to pharmaceutical science.[5]

  14. 1986

    Founds a new laboratory at St Bartholomew's Hospital Medical College that grows into the William Harvey Research Institute.[5],[6]

  15. November 19, 2004

    Dies at 77 in Farnborough, of pneumonia, after breaking his hip twice earlier that year.[1],[5]

Sources

  1. 1.John R. Vane - Facts · NobelPrize.org (Nobel Prize Outreach)
  2. 2.John R. Vane - Biographical (from Les Prix Nobel 1982) · NobelPrize.org (Nobel Foundation), 1982
  3. 3.Adventures and Excursions in Bioassay: The Stepping Stones to Prostacyclin (Nobel Lecture, 8 December 1982) · NobelPrize.org (Nobel Foundation), 1982
  4. 4.The Nobel Prize in Physiology or Medicine 1982 - Press release · NobelPrize.org (Nobel Assembly at Karolinska Institutet), 1982
  5. 5.Obituary: Sir John Vane (by Joe Collier) · The Guardian, 2004
  6. 6.Vane, Sir John R. (Encyclopaedia Judaica, 2nd ed., by Michael Denman) · Encyclopaedia Judaica via Encyclopedia.com, 2007
  7. 7.Jewish Nobel Prize Winners in Medicine (note 6 on John Vane) · JINFO.ORG
  8. 8.John Vane (citing István Hargittai, Candid Science II, Imperial College Press, 2002, p. 562) · Wikipedia
  9. 9.Inhibition of Prostaglandin Synthesis as a Mechanism of Action for Aspirin-like Drugs (Vane JR, Nature New Biology 231:232-235) · Nature Publishing Group, 1971
  10. 10.Sérgio Ferreira and Bothrops jararaca at the Royal College of Surgeons, London (Bakhle YS, Toxins 15:522) · MDPI Toxins (via PubMed Central), 2023
  11. 11.Selectivity of nonsteroidal antiinflammatory drugs as inhibitors of constitutive and inducible cyclooxygenase (Mitchell JA, ... Vane JR, PNAS 90:11693-7) · Proceedings of the National Academy of Sciences (via PubMed), 1993
  12. 12.Biological basis for the cardiovascular consequences of COX-2 inhibition (Grosser T, Fries S, FitzGerald GA, J Clin Invest 116:4-15) · Journal of Clinical Investigation (via PubMed Central), 2006
  13. 13.Testimony of David J. Graham, MD, MPH, on Vioxx, heart attacks and the FDA (18 November 2004) · US Senate Committee on Finance, 2004
  14. 14.Risk of acute myocardial infarction and sudden cardiac death in patients treated with COX-2 selective and non-selective NSAIDs (Graham DJ et al., Lancet 365:475-81) · The Lancet (via PubMed), 2005
  15. 15.Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials (Antithrombotic Trialists' Collaboration, Lancet 373:1849-60) · The Lancet (via PubMed Central), 2009
  16. 16.Aspirin for Secondary Prevention of Cardiovascular Disease in 51 Low-, Middle-, and High-Income Countries (Yoo SGK et al., JAMA 330:715-724) · JAMA (via PubMed Central), 2023
  17. 17.Global Burden of Cardiovascular Diseases and Risk Factors, 1990-2019 (Roth GA et al., J Am Coll Cardiol 76:2982-3021) · Journal of the American College of Cardiology (via PubMed Central), 2020
  18. 18.Platelets, aspirin, and cardiovascular disease (Elwood PC, Postgrad Med J 74:587-591) · Postgraduate Medical Journal (via PubMed Central), 1998
  19. 19.A comparison of continuous intravenous epoprostenol (prostacyclin) with conventional therapy for primary pulmonary hypertension (Barst RJ et al., N Engl J Med 334:296-301) · New England Journal of Medicine (via PubMed), 1996
  20. 20.Pogroms · United States Holocaust Memorial Museum, Holocaust Encyclopedia
  21. 21.Aliens Act 1905 · Wikipedia
  22. 22.Battle of Cable Street · Wikipedia
  23. 23.Association of aspirin use for primary prevention with cardiovascular events and bleeding events: a systematic review and meta-analysis (Zheng SL, Roddick AJ) · JAMA (PubMed record), 2019
  24. 24.Age-specific risks, severity, time course, and outcome of bleeding on long-term antiplatelet treatment after vascular events: a population-based cohort study (Li L et al., Oxford Vascular Study) · The Lancet (PMC full text), 2017

Fact-checked on September 24, 2026 by a separate AI fact-checking pass that re-opened the sources, with 13 corrections made. How we check

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