Skip to content
Nobel Jews
Portrait of Edmond H. Fischer
Photo: Betsythedevine, Own work · CC BY-SA 4.0 via Wikimedia Commons

Nobel Prize in Physiology or Medicine · 1992

Edmond H. Fischer

He helped find the chemical on-off switch that controls proteins in our cells, now the target of dozens of cancer drugs.

The Nobel citation: “for their discoveries concerning reversible protein phosphorylation as a biological regulatory mechanism”
Born
April 6, 1920, Shanghai, China
Died
August 27, 2021, Seattle, WA, USA
Shared with
Edwin G. Krebs
Affiliation at the time
University of Washington, USA

Medicine prize

1992

Shared with 1 other laureate.

Age that year

72years

Born in 1920.

Headline credited impact

525–1,950lives saved

Chronic myeloid leukemia deaths averted by imatinib and later BCR-ABL kinase inhibitors, 2001-2025. How it was built

Sources cited

26

Fact-checked September 24, 2026.

  • In 1939, after Mussolini allied with Hitler, he burned his Italian passport on the steps of the Italian consulate in Geneva and took Swiss nationality.
  • He studied piano at the Geneva Conservatory for seven years and weighed a music career. He played at his grandson's wedding less than a month before he died.
  • He and Edwin Krebs solved a muscle-enzyme puzzle that Nobel laureates Carl and Gerty Cori had given up on, and did it in about 18 months.
  • He learned to fly at 60, bought a four-seat Cessna, and kept flying until he was 80.
  • The Nobel Prize came in 1992, 37 years after the 1955 experiments with Edwin Krebs that it honored.

The breakthrough

Reversible protein phosphorylation: the cell's on-off switch

Your muscles run on sugar stored as glycogen. An enzyme called glycogen phosphorylase breaks that store down, but it must be switched on at the right moment, for example when you start to run. In the 1940s Carl and Gerty Cori found that the enzyme comes in an inactive and an active form, but they could not explain what turned one into the other. Fischer, who had studied the same enzyme in potatoes, and his Seattle colleague Edwin Krebs solved the puzzle in about 18 months. The switch needs ATP, the cell's energy molecule, plus calcium. A second enzyme, which they called phosphorylase kinase, takes a small phosphate group from ATP and attaches it to one particular spot on the phosphorylase. With the phosphate on, the enzyme works. Another enzyme, a phosphatase, snips the phosphate off and turns it back off. Think of a light switch that one hand flips on and another flips off, while hormones such as adrenaline, and the calcium released when a muscle contracts, decide which hand is busier. At first this looked like a quirk of muscle sugar. It turned out to be one of life's master controls. Humans carry 518 kinase genes, and adding and removing phosphates steers how cells grow, divide, answer hormones and fight infection. Later Fischer turned to the 'off' side and, with Nicholas Tonks, purified the first enzymes that strip phosphates from the amino acid tyrosine.[3],[4],[5],[12],[13],[14],[16]

“perhaps with a little luck, a deeper understanding of these signaling pathways may suggest new avenues by which oncogenicity can be brought under control”
Edmond H. Fischer, Closing words of his Nobel lecture, 8 December 1992, on how cancer-causing genes hijack phosphorylation. The first kinase-blocking cancer drug was approved nine years later.[4]

What it meant for humanity

For years after 1955, protein phosphorylation looked like a special trick for releasing muscle sugar. By the 1980s researchers had found that many cancer-causing genes, such as src and abl, and the receptors for insulin and growth factors, are themselves protein kinases. A kinase stuck in the 'on' position can drive a cell to keep dividing. That insight made kinases drug targets. Imatinib, the first kinase-blocking drug approved for clinical use, arrived in 2001. Before it, half of people with chronic myeloid leukemia died within about five or six years of diagnosis. A 2013 editorial by more than 100 leukemia specialists estimated 10-year survival with imatinib and similar drugs at above 80 percent, up from under 20 percent before them, and said patients who stay on treatment now live close to normal lifespans. By early 2026 the US Food and Drug Administration had approved 94 small-molecule kinase inhibitors. About 80 treat cancers, including lung and ovarian cancers and leukemias, and others treat inflammatory diseases such as rheumatoid arthritis, psoriasis and ulcerative colitis. The 'off' switch matters too. Around 1990 researchers found that cyclosporin, the anti-rejection drug behind the spread of organ transplants, works by blocking a phosphatase called calcineurin. Fischer's own later work showed that CD45, a protein on white blood cells, is a tyrosine phosphatase, laying groundwork for understanding how immune T cells are switched on. His lab also found early evidence that another phosphatase, PTP-1B, plays a part in the body's response to insulin. Fischer invented none of these medicines, and many other scientists built them. But each rests on the mechanism he and Krebs uncovered: cells control their proteins by adding and removing phosphates.

  • Imatinib, the first protein kinase inhibitor approved for clinical use (2001), changed chronic myeloid leukemia from a disease that killed half of patients within about six years into one most people can live with long-term.[5],[19],[20],[24]
  • By early 2026 the FDA had approved 94 small-molecule protein kinase inhibitors; about 80 are used against cancers and the rest mainly against inflammatory and other diseases.[17],[18]
  • Around 1990, cyclosporin, the anti-rejection drug that helped make organ transplants routine, was found to work by blocking calcineurin, a calcium-regulated protein phosphatase.[3],[5]
  • In 1988 Fischer and Nicholas Tonks purified the first protein tyrosine phosphatases and showed that CD45, a white-blood-cell protein, is one. The family now counts about 100 enzymes.[5],[14],[15]
  • The human genome holds 518 protein kinase genes, and 244 of them map to disease-linked regions or regions amplified in cancer.[16]

Impact in numbers

Fischer and Krebs revealed a language cells use to pass messages: attaching and removing phosphate groups on proteins. Because this switch runs through almost every process of life, from burning sugar to cell division, hormone signalling and immunity, its full impact cannot be captured in one number. Its clearest medical payoff is the family of kinase-blocking drugs, 94 approved in the US by early 2026, which changed the outlook for several cancers and some inflammatory diseases. Drugs aimed at the phosphatases, the 'off' switches Fischer studied for much of his later career, were only beginning to enter clinical trials in 2023. We count one narrow outcome, deaths from chronic myeloid leukemia averted by BCR-ABL kinase inhibitors, and credit Fischer with a small share, because many later discoveries stood between his work and those medicines. The real benefit of his discovery is almost certainly larger than this count.

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.

  • Low confidenceRippleModeledHealth

    Chronic myeloid leukemia deaths averted by imatinib and later BCR-ABL kinase inhibitors, 2001-2025

    525–1,950

    lives saved, credited share

    That is 1.5% of 35,000–130,000 lives saved since 2001.

    How this number was built

    Range reused from our Varmus profile. Counts only CML deaths averted by BCR-ABL inhibitors (imatinib approved 2001), a floor for kinase drugs. SEER US CML death rate: 0.87 per 100,000 in 1996-98, 0.65 in 1999-2000, 0.3 in 2020-24. Low: counterfactual 0.65 falling 2%/yr x US population (World Bank) = 13,300 US; other high-income countries at half the US per-capita gain = 35,000. High: 0.65 held flat (the last pre-imatinib level) = 25,000 US; x4.28 with full gain abroad = 107,000; plus 25,000 in poorer countries (Max Foundation) = 130,000. Cross-check: Blood 2013 put 235,000-250,000 patients on imatinib and yearly CML mortality at 2% vs 10-20% before. Share 0.015: Fischer and Krebs found protein kinases and reversible phosphorylation, the switch imatinib blocks (0.03 for the pair, split evenly); oncogene, BCR-ABL and drug work by others was essential.[5],[19],[20],[21],[22],[23],[24]

    Sources: National Cancer Institute, SEER Program; World Bank, World Development Indicators API; The Max Foundation; Blood (American Society of Hematology), via PubMed Central; National Cancer Institute; Lasker Foundation; National Academy of Sciences

The double edge

We found no harms or controversies tied to Fischer's own conduct or research. The costs lie downstream, in the drugs his discovery helped make possible. Kinase inhibitors can be very expensive, and many patients must take them every day for life. In 2013 more than 100 leukemia specialists warned in the journal Blood that US prices for chronic myeloid leukemia kinase inhibitors, $92,000 to $138,000 a year, were unsustainable and might be keeping many patients from treatment. Imatinib itself rose from about $30,000 a year at its 2001 launch to $92,000 in 2012. The same experts estimated that only about 25 to 30 percent of the world's patients with this leukemia were receiving the drugs.

  • Moderate

    High prices for kinase-inhibitor drugs

    In 2013 more than 100 experts on chronic myeloid leukemia called US prices for its kinase-inhibitor drugs ($92,000 to $138,000 a year) unsustainable. They noted imatinib had risen from about $30,000 a year in 2001 to $92,000 in 2012 and estimated that only about 25 to 30 percent of patients worldwide were being treated.[24]

Against the odds

Fischer faced little direct persecution, and it would be wrong to claim otherwise. He was born into a prosperous family in Shanghai, where his Austrian father, who had come from Vienna with doctorates in law and business, worked as a lawyer and in the import-export trade. From age seven he was educated at Swiss schools. His father had taken Italian citizenship for business reasons, so Fischer was born an Italian citizen. In 1938 Fascist Italy passed antisemitic laws that removed Jews from government jobs, public-school teaching, the army and the press, and banned marriages between Jews and non-Jews. In 1939, when Mussolini allied with Hitler, Fischer burned his Italian passport on the steps of the Italian consulate in Geneva and became Swiss. He spent the Second World War studying chemistry in neutral Switzerland. After Germany occupied northern Italy in 1943, it sent more than 4,700 Jews from Italian transit camps to Auschwitz; only 314 survived. Shanghai, his birthplace, became one of the few havens for Jews fleeing Nazi Germany and Austria without visas, and about 17,000 arrived. His own losses were private: his father died of tuberculosis, which drew him toward microbiology, and his first wife died in 1961. He moved to the United States in 1953 by choice, planning a postdoctoral fellowship, and stayed when offered a faculty post at a time when academic jobs in Europe were very hard to find.

  • 1939

    Other

    Born an Italian citizen through his father, he burned his Italian passport on the steps of the Italian consulate in Geneva when Mussolini allied with Hitler, and took Swiss nationality. Italy had passed antisemitic racial laws the year before.[5],[25]

  • 1939

    War

    He finished high school weeks before the Second World War began and spent the war studying in neutral Switzerland, while Germany deported Jews from occupied Italy to Auschwitz and his birthplace, Shanghai, sheltered about 17,000 German and Austrian Jewish refugees.[5],[7],[25],[26]

  • —

    Other

    His father died of tuberculosis, a loss that helped turn him toward Louis Pasteur as a hero and toward the study of microbiology.[5],[6]

Jewish background

Jewish fatherRelationship to Jewish identity not documented

Fischer's father, Oscar Fischer, came to Shanghai from Vienna; his mother, Renée Tapernoux, was French. In 1992 the Jewish Telegraphic Agency reported that a Nobel expert believed Fischer was Jewish, and Jinfo, citing a later JTA dispatch, records a Jewish father and a non-Jewish mother. The Encyclopaedia Judaica has an entry on him. Fischer did not discuss religion in his Nobel autobiography, and we found no statement of his own on Jewish identity; a tribute co-written by his granddaughter mentions him insisting on hosting family Christmas dinners. He had long ties to Israeli science, including a 1963 sabbatical at the Weizmann Institute and later service on its board.[2],[5],[6],[7],[8],[9],[10],[11]

Key dates

  1. April 6, 1920

    Born in Shanghai, China, to a French mother, Renée Tapernoux, and an Austrian father, Oscar Fischer, who had come from Vienna.[1],[2],[6]

  2. 1927

    The family leaves China on the Trans-Siberian Railway; he and his two older brothers attend La Châtaigneraie boarding school in Switzerland.[2],[5]

  3. 1935

    Enters Geneva's Collège Calvin and is accepted as a piano student at the Geneva Conservatory.[2],[5]

  4. 1939

    Burns his Italian passport after Mussolini allies with Hitler, takes Swiss nationality, and finishes high school as war begins.[5]

  5. 1947

    Earns his PhD at the University of Geneva under Kurt Meyer for work on polysaccharides and starch-digesting alpha-amylases.[5],[6]

  6. 1953

    Moves to the United States for a postdoctoral post at Caltech, then accepts an assistant professorship at the University of Washington's new medical school in Seattle.[2],[5],[10]

  7. 1955

    With Edwin Krebs, shows that muscle phosphorylase is switched on by attaching phosphate from ATP: the first known case of reversible protein phosphorylation.[5],[12]

  8. 1956

    Krebs and Fischer describe the converting enzyme, phosphorylase kinase, the first protein kinase to be discovered.[3],[5],[13]

  9. 1961

    His first wife, Nelly Gagnaux, dies; he marries Beverly Bullock in 1963.[2],[5]

  10. 1963

    Spends a sabbatical at the Weizmann Institute of Science in Israel, later serving on its board of governors.[5]

  11. 1973

    Elected to the US National Academy of Sciences.[2],[5]

  12. 1988

    With Nicholas Tonks, purifies the first protein tyrosine phosphatases and shows the immune-cell protein CD45 is one.[5],[14],[15]

  13. 1992

    Shares the Nobel Prize in Physiology or Medicine with Edwin Krebs, 37 years after their key finding.[1],[3],[5]

  14. August 27, 2021

    Dies in Seattle at age 101.[1],[5],[6]

Sources

  1. 1.Edmond H. Fischer - Facts · NobelPrize.org (Nobel Prize Outreach)
  2. 2.Edmond H. Fischer - Biographical · NobelPrize.org (Nobel Foundation, from Les Prix Nobel 1992), 1992
  3. 3.The Nobel Prize in Physiology or Medicine 1992 - Press release · The Nobel Assembly at the Karolinska Institute, 1992
  4. 4.Protein Phosphorylation and Cellular Regulation, II (Nobel Lecture, 8 December 1992) · NobelPrize.org (Nobel Foundation), 1992
  5. 5.Edmond H. Fischer, 1920-2021: A Biographical Memoir (Philip Cohen) · National Academy of Sciences, 2023
  6. 6.In Memoriam: Nobel Laureate Edmond Fischer · UW Medicine Newsroom, University of Washington, 2021
  7. 7.Edmond H. Fischer (1920-2021) (retrospective by Élyse S. Fischer and John D. Scott) · ASBMB Today (American Society for Biochemistry and Molecular Biology), 2022
  8. 8.Jews Are Among the Winners of This Year's Nobel Prizes · Jewish Telegraphic Agency, 1992
  9. 9.Jewish Nobel Prize Winners in Medicine (note 7 on Edmond Fischer) · Jinfo.org
  10. 10.Fischer, Edmond (Encyclopaedia Judaica, 2nd ed., via Encyclopedia.com) · Encyclopaedia Judaica (Macmillan Reference USA / Gale), 2007
  11. 11.Edmond H. Fischer · Wikipedia
  12. 12.Conversion of phosphorylase b to phosphorylase a in muscle extracts (Fischer EH, Krebs EG), Journal of Biological Chemistry 216:121-132 · Journal of Biological Chemistry (PubMed record), 1955
  13. 13.The phosphorylase b to a converting enzyme of rabbit skeletal muscle (Krebs EG, Fischer EH), Biochimica et Biophysica Acta 20:150-157 · Biochimica et Biophysica Acta (PubMed record), 1956
  14. 14.Purification of the major protein-tyrosine-phosphatases of human placenta (Tonks NK, Diltz CD, Fischer EH), Journal of Biological Chemistry · Journal of Biological Chemistry (PubMed record), 1988
  15. 15.Demonstration that the leukocyte common antigen CD45 is a protein tyrosine phosphatase (Tonks NK, Charbonneau H, Diltz CD, Fischer EH, Walsh KA), Biochemistry · Biochemistry (PubMed record), 1988
  16. 16.The protein kinase complement of the human genome (Manning G, Whyte DB, Martinez R, Hunter T, Sudarsanam S), Science 298:1912-1934 · Science (PubMed record), 2002
  17. 17.Properties of FDA-approved small molecule protein kinase inhibitors: A 2025 update (Roskoski R Jr), Pharmacological Research 216:107723 · Pharmacological Research (PubMed record), 2025
  18. 18.Properties of FDA-approved small molecule protein kinase inhibitors: A 2026 update (Roskoski R Jr), Pharmacological Research 224:108107 · Pharmacological Research (PubMed record), 2026
  19. 19.How Imatinib Transformed Leukemia Treatment and Cancer Research · National Cancer Institute, 2018
  20. 20.Molecularly targeted treatments for chronic myeloid leukemia (2009 Lasker~DeBakey Clinical Medical Research Award: Druker, Lydon, Sawyers) · Lasker Foundation, 2009
  21. 21.Cancer Stat Facts: Leukemia - Chronic Myeloid Leukemia (CML) · National Cancer Institute, SEER Program, 2026
  22. 22.Population, total (SP.POP.TOTL): high-income countries and United States, 2001-2024 · World Bank, World Development Indicators API, 2025
  23. 23.The Max Foundation (home page: people served and countries reached) · The Max Foundation, 2026
  24. 24.The price of drugs for chronic myeloid leukemia (CML) is a reflection of the unsustainable prices of cancer drugs: from the perspective of a large group of CML experts, Blood 121:4439-4442 · Blood (American Society of Hematology), via PubMed Central, 2013
  25. 25.Italy (Holocaust Encyclopedia) · United States Holocaust Memorial Museum
  26. 26.German and Austrian Jewish Refugees in Shanghai (Holocaust Encyclopedia) · United States Holocaust Memorial Museum

Fact-checked on September 24, 2026 by a separate AI fact-checking pass that re-opened the sources, with 8 corrections made. How we check

Suggest a correction