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Portrait of Fritz Lipmann
Photo: Smithsonian Institution from United States, Portrait of Fritz Albert Lipmann (1899-1986), Biochemist · No restrictions via Wikimedia Commons

Nobel Prize in Physiology or Medicine · 1953

Fritz Lipmann

Pushed out of Europe by Nazism, he found coenzyme A, the molecular forklift cells use to turn food into energy and new parts.

The Nobel citation: “for his discovery of co-enzyme A and its importance for intermediary metabolism”
Born
June 12, 1899, Koenigsberg, Germany (now Kaliningrad, Russia)
Died
July 24, 1986, Poughkeepsie, NY, USA
Shared with
Hans Krebs
Affiliation at the time
Harvard Medical School, USA; Massachusetts General Hospital, USA

Medicine prize

1953

Shared with 1 other laureate.

Age that year

54years

Born in 1899.

Headline credited impact

8,500–24,000lives saved

Deaths prevented or postponed by statin therapy worldwide (1987-2025). How it was built

Sources cited

21

Fact-checked September 24, 2026.

  • The “A” in coenzyme A stands for “activation of acetate”, the chemical step Lipmann was chasing when his team found the molecule in pigeon liver extracts.
  • His 1941 paper introduced the squiggle (~P) that biochemistry textbooks have long used to mark “energy-rich” phosphate bonds, such as those in ATP.
  • In Berlin around 1930, as uniformed Nazis began appearing on the streets, Lipmann was once beaten up. He and his future wife saw that they would have to leave Germany.
  • He often said his 1941 theory of how cells pass energy around deserved the Nobel more than coenzyme A, the discovery it actually honoured.
  • Peter Rona, whose three-month Berlin biochemistry course helped turn Lipmann toward research, taught three future Nobel laureates: Ernst Chain, Hans Krebs and Lipmann.

The breakthrough

Coenzyme A, the cell's carrier for “active acetate” (found 1945)

Cells run on chemical energy, but in the 1930s nobody knew how the energy released by burning food was passed on to the jobs that need it. In a 1941 paper Lipmann proposed an answer. Cells capture energy in phosphate groups that can be handed on to other molecules, above all in ATP, and he marked these “energy-rich” links with a squiggle (~P). They spend it by attaching an activated chemical group to a carrier and handing that group on to where it is needed. One big puzzle was “active acetate”, a two-carbon piece of food that seemed to feed the citric acid cycle and to build fats. At Massachusetts General Hospital in Boston, Lipmann's team studied how pigeon liver extracts attach acetate to a sulfa drug. The reaction needed ATP plus a heat-stable helper molecule that no known cofactor could replace. They purified it, showed that it contains vitamin B5 (pantothenic acid) and named it coenzyme A, the A standing for activation of acetate. It turned up in every animal, plant and microbe they tested. Feodor Lynen then showed that the acetate clips onto a sulfur atom at the tip of the coenzyme. Think of coenzyme A as a forklift. It picks up two-carbon pallets, holds them in a high-energy grip and delivers them to the citric acid cycle or to the assembly lines for fats, cholesterol and nerve signals. The Nobel presenter likened the find to the final tumbler of a combination lock clicking into place.[3],[4],[5],[6],[8]

“biochemistry was now developing into an adult science, best characterized, may be, as organismic technology.”
Fritz Lipmann, Nobel Lecture, 11 December 1953, looking back on how biochemistry had changed since he began research in the mid-1920s, from studying how cells break things down to understanding how they build.[3]

What it meant for humanity

Coenzyme A turned out to be one of life's universal parts. Every living thing uses it, and human cells need it to get energy from fats, carbohydrates and proteins and to build fatty acids, cholesterol, the nerve messenger acetylcholine, heme for blood and much more. Lipmann's own measurements showed that the vitamin B5 in cells is held in coenzyme A, which revealed what that vitamin does. His 1941 idea of energy-rich bonds and group transfer gave biochemists one framework for how cells pay for muscle contraction, for moving molecules across membranes and for making proteins. The map he helped complete also led toward medicine. Feodor Lynen, Konrad Bloch and others showed how cells assemble cholesterol from acetyl-CoA, with an enzyme called HMG-CoA reductase setting the pace. In the 1970s Akira Endo screened thousands of fungi for chemicals that would block that enzyme and found compactin, the first statin. By 2018 an estimated 173 million people in 83 countries were taking cholesterol-lowering drugs, most often statins. At the Rockefeller Institute in the 1960s, Lipmann's group identified the elongation factors EF-Tu and EF-Ts, proteins needed to translate genetic messages into proteins, and showed that antibiotics such as gramicidin and tyrocidine are built by enzyme assembly lines rather than by ribosomes. A rare inherited brain disease, PKAN, has since been traced to a faulty gene for one form of the enzyme that starts the cell's coenzyme A production line. None of these advances belongs to Lipmann alone, but much of modern metabolism is described in terms of coenzyme A and acetyl-CoA, a language his work helped create.

  • Every living organism depends on coenzyme A. Human cells use it to get energy from fats, carbohydrates and proteins and to make fatty acids, cholesterol, acetylcholine and heme.[11]
  • In his Nobel lecture Lipmann reported that all the pantothenic acid (vitamin B5) in cells could be accounted for as coenzyme A, which showed what the vitamin does in the body.[3]
  • Cholesterol is built from acetyl-CoA, and the enzyme HMG-CoA reductase controls the slowest, pace-setting step. Akira Endo's compactin, the first statin, published in 1976, works by blocking that enzyme.[9],[10]
  • At the Rockefeller Institute, Lipmann's group identified two of the helper proteins, EF-Tu and EF-Ts, that cells need to turn the genetic messages carried by RNA into proteins.[8]
  • His group found that bacteria build some ring-shaped antibiotics, such as gramicidin S and tyrocidine, on large enzyme assembly lines that add one amino acid at a time, with no ribosome involved.[5],[6]

Impact in numbers

Lipmann's impact is mostly foundational. Coenzyme A and his idea of energy-rich group transfer sit at the centre of how biochemistry explains metabolism, and they shaped later work on fats, cholesterol, nerve signalling and protein synthesis. Most of that value cannot honestly be counted. The one countable path we found runs through cholesterol: Lynen and others built on coenzyme A to map how cells make cholesterol from acetyl-CoA, and statins work by blocking a step in that pathway. We therefore credit Lipmann with a very small share, 0.5%, of the deaths our model estimates statins have prevented or postponed since 1987 (1.7 to 4.8 million), and the same share of the extra diabetes diagnoses they have caused (1.4 to 4.1 million). That works out to roughly 8,500 to 24,000 lives, against 7,000 to 20,500 diabetes diagnoses. Both figures are low-confidence, because the chain is long and other scientists found the same cofactor independently. We make no claims for his work on protein synthesis or peptide antibiotics.

Fundamental scienceHealth

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

    Deaths prevented or postponed by statin therapy worldwide (1987-2025)

    8,500–24,000

    lives saved, credited share

    That is 0.5% of 1.7–4.8 million lives saved since 1987.

    How this number was built

    Whole-outcome range reused from our Goldstein and Brown profiles so totals line up: about 2.9-3.4B statin person-years in 1987-2025 (scaled from Blais et al.'s 173M lipid-drug users in 2018) x 0.6-1.4 deaths averted per 1,000 person-years (CTT: 10% fewer deaths per 1 mmol/L LDL cut, discounted for real-world use) = 1.74M-4.76M, rounded to 1.7M-4.8M. Link: cholesterol is built from acetyl-CoA, and statins block HMG-CoA reductase, the rate-limiting step (Endo; Lynen's Nobel lecture, which builds on Lipmann's coenzyme A). Share 0.005, below our usual range for foundational work: the chain also needed Lynen, Bloch, Cornforth, Popják, Bucher, Endo, drug makers and trialists, and Nachmansohn and Feldberg found the same cofactor independently.[6],[9],[10],[15],[16]

    Sources: NobelPrize.org; Proceedings of the Japan Academy, Series B (via PubMed Central); Atherosclerosis (PubMed record); The Lancet (via PubMed Central); Encyclopedia.com (Gale)

  • HarmLow confidenceRippleModeledHealth

    Extra diabetes diagnoses caused by statin therapy worldwide (1987-2025)

    10,500–25,500

    people harmed, credited share

    That is 0.5% of 2.1–5.1 million people harmed since 1987.

    How this number was built

    Same 2.9-3.4B statin person-years (1987-2025) as the benefit claim (Blais). CTT 2024 individual-patient meta-analysis (19 placebo trials, 123,940 people): in people without diabetes, low/moderate-intensity statins added 1.2 new diagnoses per 1,000 person-years (RR 1.10, placebo 1.2%/yr); high-intensity raised diagnoses 36%, or 4.3 per 1,000 at that 1.2%/yr baseline. MEPS 2008-19: 20% of US statin use was high-intensity (less abroad and earlier, so 5-20%) and 18% of users already had diabetes, so 82% of person-years are at risk. Low: rates cut by a third for real-world dose and adherence, 5% high-intensity: (0.95 x 0.8 + 0.05 x 2.9) x 2.9B x 0.82 = 2.1M. High: (0.8 x 1.2 + 0.2 x 4.3) x 3.4B x 0.82 = 5.1M. CTT: about 62% of new diagnoses were in people already in the top quarter of baseline blood sugar. Share 0.005, matching the benefit claim's long causal chain.[15],[20],[21]

    Sources: The Lancet Diabetes & Endocrinology (PMC full text); Saudi Pharmaceutical Journal (PMC full text); Atherosclerosis (PubMed record)

The double edge

No harm has been traced to Lipmann's own discoveries, and we found no personal controversy. Two indirect issues are worth noting. First, statins, which block an enzyme in the cholesterol pathway built on coenzyme A, have real if uncommon side effects. A 2016 Lancet review estimated that treating 10,000 people for five years with an effective dose, such as 40 mg of atorvastatin a day, causes about 5 cases of muscle damage, 50 to 100 new cases of diabetes and probably 5 to 10 bleeding strokes, while sparing 500 to 1,000 of them a heart attack, stroke or other major vascular event. We credit Lipmann with only a tiny share of statins, good and bad. Second, his squiggle for “energy-rich” bonds became a classroom shorthand that education researchers say helps mislead students into thinking that breaking a chemical bond releases energy, when it actually takes energy. Lipmann himself argued that “bond energy” was being misused and preferred the term “group potential”, but the shorthand spread anyway.

  • Minor

    Statin side effects, far downstream

    Per 10,000 people treated for five years with an effective statin dose, a 2016 Lancet review estimated about 5 cases of myopathy, 50 to 100 new cases of diabetes and probably 5 to 10 bleeding strokes. A 2010 meta-analysis found one extra diabetes diagnosis for every 255 people treated for four years. Lipmann's link to statins is distant.[17],[18]

  • Minor

    The “high-energy bond” shorthand misleads students

    Biology textbooks long described ATP as holding “high-energy bonds”, a phrase that grew out of Lipmann's “energy-rich phosphate bond” and its squiggle. A 2025 study found 13% of biology textbook figures of ATP hydrolysis singled out such a bond, while no chemistry figures did, and linked the phrasing to the false idea that breaking bonds releases energy.[5],[7],[19]

Against the odds

Lipmann grew up in a liberal German-Jewish family in Königsberg, and his early research career in Berlin was poorly paid. Around 1930, as uniformed Nazis began appearing on the city's streets, he and Freda Hall, his future wife, both had unpleasant run-ins, and he was once beaten up. They saw that they would have to leave. After a fellowship in New York in 1931 and 1932, he moved to Copenhagen. Hitler took power in January 1933, when Germany had about 523,000 Jews, under 1% of its people. On 7 April a new law began pushing Jews out of civil service jobs, including posts at state universities. Lipmann stayed in Denmark, supported by the Rockefeller Foundation. Danish friends told him that staying was risky, and in 1939 he left for the United States to escape fascism and antisemitism. He and his wife arrived nearly penniless. His prospects at Cornell vanished when his host left for the National Institutes of Health, and a fellowship in a Boston hospital's surgery department rescued his career. In April 1940 Germany occupied Denmark; in 1943 about 7,200 Danish Jews had to flee by boat to Sweden. Lipmann escaped dismissal and deportation, but from 1930 to 1941 he moved through fellowships and research posts in Germany, the United States and Denmark before he settled in Boston.

  • —

    Persecution

    In Berlin around 1930, as uniformed Nazis began appearing on the streets, Lipmann and Freda Hall both had unpleasant run-ins and he was once beaten up. The couple saw that they would have to leave Germany.[7]

  • 1933

    Exile

    When Hitler took power and his government passed its first anti-Jewish laws, including the April 1933 civil service law that reached state universities, Lipmann stayed in Denmark with Rockefeller Foundation support. About 523,000 Jews then lived in Germany, under 1% of the population.[6],[12],[13]

  • 1939

    Exile

    Warned by Danish friends of the danger of staying, he left Denmark for the United States in 1939 to escape fascism and antisemitism in Europe. He and his wife arrived nearly penniless. Germany occupied Denmark the following April.[5],[7],[8],[14]

  • 1941

    Other

    He was left without secure job prospects when his Cornell host, Dean Burk, left for the National Institutes of Health. A Ciba fellowship in the surgery department of Massachusetts General Hospital, which Lipmann called one of the lucky breaks of his life, kept him in research.[5],[7]

Jewish background

Both parents JewishCulturally Jewish

Lipmann was born in Königsberg, East Prussia, the second son of the lawyer Leopold Lipmann and Gertrud Lachmanski. The biochemist Lothar Jaenicke, writing in the Complete Dictionary of Scientific Biography, describes a liberal, middle-class German-Jewish home where schooling, the arts and civic involvement counted for more than religion. The Encyclopaedia Judaica includes him and says he left Germany as the Nazi regime rose. We found no record of religious practice and none of conversion. His later honours included honorary doctorates in humane letters from Brandeis University (1954) and Yeshiva University (1964).[2],[6],[7]

Key dates

  1. June 12, 1899

    Born in Königsberg, East Prussia (now Kaliningrad, Russia), to the lawyer Leopold Lipmann and Gertrud Lachmanski.[1],[2]

  2. 1918

    Called up during his medical studies, he serves in the German army's medical service near the front in the last months of World War I.[5],[6],[7]

  3. 1927

    After an MD from Berlin in 1924, earns a Berlin PhD for research in Otto Meyerhof's laboratory at the Kaiser Wilhelm Institute.[2],[5]

  4. 1931

    Marries the artist Freda Hall and spends 1931 and 1932 as a Rockefeller fellow in Phoebus Levene's laboratory in New York.[2],[6],[8]

  5. 1932

    Joins Albert Fischer at the Carlsberg Foundation's Biological Institute in Copenhagen, studying the metabolism of cultured cells.[2],[8]

  6. 1933

    Hitler takes power and Germany passes its first anti-Jewish laws. Lipmann stays in Denmark with Rockefeller Foundation support rather than return.[6],[12]

  7. 1939

    Warned by Danish friends, emigrates to the United States to escape fascism and antisemitism, and joins Cornell Medical School in New York.[2],[5],[8]

  8. 1941

    Publishes “Metabolic generation and utilization of phosphate bond energy”, introducing the ~P squiggle, and moves to Massachusetts General Hospital in Boston.[5],[8]

  9. 1945

    At Massachusetts General Hospital his team discovers coenzyme A, the helper molecule that activates acetate; it is later shown to contain vitamin B5.[3],[7],[8]

  10. 1949

    Becomes professor of biological chemistry at Harvard Medical School while heading his research group at Massachusetts General Hospital.[2],[8]

  11. 1953

    Shares the Nobel Prize in Physiology or Medicine with Hans Krebs, for the discovery of coenzyme A and its importance for metabolism.[1],[4]

  12. 1957

    Joins the Rockefeller Institute in New York, where his group later discovers the protein-synthesis elongation factors EF-Tu and EF-Ts.[2],[8]

  13. 1966

    Receives the US National Medal of Science.[6],[8]

  14. July 24, 1986

    Dies in Poughkeepsie, New York, aged 87, a week after a stroke; he had kept working until then.[1],[5],[7]

Sources

  1. 1.Fritz Lipmann - Facts · NobelPrize.org (Nobel Prize Outreach)
  2. 2.Fritz Lipmann - Biographical · NobelPrize.org (from Nobel Lectures, Physiology or Medicine 1942-1962, Elsevier, 1964), 1964
  3. 3.Development of the acetylation problem: a personal account (Nobel Lecture, 11 December 1953) · NobelPrize.org, 1953
  4. 4.Award ceremony speech, Nobel Prize in Physiology or Medicine 1953 (Professor E. Hammarsten) · NobelPrize.org, 1953
  5. 5.Fritz Albert Lipmann, 1899-1986 (William P. Jencks and Richard V. Wolfenden), Biographical Memoirs Volume 88 · National Academy of Sciences (National Academies Press), 2006
  6. 6.Lipmann, Fritz Albert (Complete Dictionary of Scientific Biography entry by Lothar Jaenicke; Encyclopaedia Judaica entry by Samuel Miller) · Encyclopedia.com (Gale)
  7. 7.Fritz Lipmann (Encyclopedia of World Biography) · Encyclopedia.com (Gale)
  8. 8.Fritz Lipmann and Coenzyme A · The Rockefeller University Hospital Centennial
  9. 9.The pathway from “activated acetic acid” to the terpenes and fatty acids (Feodor Lynen, Nobel Lecture, 11 December 1964) · NobelPrize.org, 1964
  10. 10.A historical perspective on the discovery of statins (Endo A) · Proceedings of the Japan Academy, Series B (via PubMed Central), 2010
  11. 11.The Pathophysiological Role of CoA (Czumaj A et al.), International Journal of Molecular Sciences 21(23):9057 · MDPI (via PubMed Central), 2020
  12. 12.Law for the Restoration of the Professional Civil Service · United States Holocaust Memorial Museum, Holocaust Encyclopedia
  13. 13.Germany: Jewish Population in 1933 · United States Holocaust Memorial Museum, Holocaust Encyclopedia
  14. 14.Denmark · United States Holocaust Memorial Museum, Holocaust Encyclopedia
  15. 15.Trends in lipid-modifying agent use in 83 countries (Blais JE et al.) · Atherosclerosis (PubMed record), 2021
  16. 16.Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials (Cholesterol Treatment Trialists' Collaboration) · The Lancet (via PubMed Central), 2010
  17. 17.Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials (Sattar N et al.) · The Lancet (PubMed record), 2010
  18. 18.Interpretation of the evidence for the efficacy and safety of statin therapy (Collins R et al.) · The Lancet (PubMed record), 2016
  19. 19.Visual representations of energy and chemical bonding in biology and chemistry textbooks: A case study of ATP hydrolysis (Yang M et al.), Biochemistry and Molecular Biology Education 53(3):274-285 · Wiley, for the International Union of Biochemistry and Molecular Biology (via PubMed Central), 2025
  20. 20.Effects of statin therapy on diagnoses of new-onset diabetes and worsening glycaemia in large-scale randomised blinded statin trials: an individual participant data meta-analysis (Cholesterol Treatment Trialists' Collaboration) · The Lancet Diabetes & Endocrinology (PMC full text), 2024
  21. 21.Statins utilization trends and expenditures in the U.S. before and after the implementation of the 2013 ACC/AHA guidelines (MEPS 2008-2019) · Saudi Pharmaceutical Journal (PMC full text), 2023

Fact-checked on September 24, 2026 by a separate AI fact-checking pass that re-opened the sources, with 11 corrections made. How we check

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