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Gerhard Johannes Paul Domagk (German pronunciation: [ˈɡeːɐ̯haʁt ˈdoːmak] ⓘ; 30 October 1895 – 24 April 1964) was a German pathologist and bacteriologist. He is credited with the discovery of sulfonamidochrysoidine (KL730) as an antibiotic for which he received the 1939 Nobel Prize in Physiology or Medicine .
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Apr 20, 2024 · Gerhard Domagk was a German bacteriologist and pathologist who was awarded the 1939 Nobel Prize for Physiology or Medicine for his discovery (announced in 1932) of the antibacterial effects of Prontosil, the first of the sulfonamide drugs. Domagk earned a medical degree from the University of Kiel.
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German pathologist Gerhard Domagk was forced to reject the Nobel Prize he won for his discovery of the first sulfa drug. Print Republish Google Classroom. about SCIENTIFIC BIOGRAPHIES. Prontosil was the first drug to successfully treat bacterial infections and the first of many sulfa drugs—forerunners of antibiotics.
Biographical. Gerhard Johannes Paul Domagk was born on October 30, 1895, at Lagow, a beautiful, small town in the Brandenburg Marches. Until he was fourteen he went to school in Sommerfeld, where his father was assistant headmaster.
Gerhard Domagk. The Nobel Prize in Physiology or Medicine 1939. Born: 30 October 1895, Lagow, Germany (now Poland) Died: 24 April 1964, Burgberg, West Germany (now Germany) Affiliation at the time of the award: Munster University, Munster, Germany. Prize motivation: “for the discovery of the antibacterial effects of prontosil”.
1 day ago · Gerhard Domagk. (1895—1964) Quick Reference. (1895–1964) German bacteriologist and pathologist awarded the Nobel Prize for Physiology or Medicine in 1939 for his discovery of the antibacterial effects of Prontosil, the first sulphonamide drug. Domagk was born in Brandenburg (now in Poland) and trained in medicine at the University of Kiel.
May 21, 2018 · Domagk became extraordinary professor of general pathology and pathological anatomy at Münster in 1928 and ordinary professor in 1958. In 1924 Domagk published a paper on the defensive function of the reticuloendothelial system against infections.
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