Who discovered glutathione? Joseph de Rey-Pailhade reported its early chemistry in 1888. Frederick Gowland Hopkins isolated the material and named it in 1921. In 1929, a purer preparation showed that its makeup needed correcting.
Those dates describe different steps: noticing a reaction, separating the substance responsible, and working out what it contained. Giving one person one discovery date loses part of the story.
Who discovered glutathione before Hopkins?
In 1888, de Rey-Pailhade found that yeast and watery yeast extracts could turn sulfur into hydrogen sulfide, a gas. He called the substance behind the reaction philothion.
Hopkins acknowledged this earlier work at the start of his 1921 Biochemical Journal paper. He connected his own material with de Rey-Pailhade's philothion. The priority wasn't something later historians had to invent.
De Rey-Pailhade had detected a chemical activity. That didn't yet provide a pure sample with a settled chemical identity.
Hopkins's glutathione discovery in 1921
Hopkins worked at the Biochemical Laboratory in Cambridge. His paper describes two starting questions: whether sulfur-containing compounds included vitamins, and how muscle chemistry worked.
Separating material from yeast and animal tissue led him toward a small substance that could change chemical form and change back. He interpreted it as a dipeptide: two linked amino acids, the building blocks used to make proteins. He identified glutamic acid and cysteine.
That was the working explanation in 1921. Glycine, the third building block, was still missing from the account.
Why is glutathione called glutathione?
Hopkins explained the name himself. It recalled glutamic acid and a sulfur-containing compound, kept a connection with philothion, and echoed the ending of peptone, an older term for protein fragments.
He proposed the name provisionally, while the structure was still unsettled. The name lasted longer than the original two-part explanation.
Glutathione is coming soon to Promise. Its history explains the molecule's identity; a treatment decision needs evidence about the preparation and the person.
The glutathione tripeptide structure: the 1929 correction
In a September 21, 1929 Nature letter, Hopkins reported crystals containing three building blocks: glutamic acid, cysteine and glycine. A tripeptide is a chain of three amino acids.
The cleaner material exposed the problem with earlier preparations. Those samples had contained a mixture, rather than one pure substance. Hopkins publicly corrected the account before his longer investigation appeared. He wasn't the only chemist on the problem: Hunter and Eagles had published a critical study of glutathione preparations in 1927, and Edward Kendall's group at the Mayo Clinic reported crystalline glutathione and its identification in September 1929, the same month as Hopkins's letter.
More work followed to establish how the pieces joined. Charles Robert Harington and Thomas Hobson Mead, at University College Hospital Medical School in London, published a laboratory synthesis in 1935. Synthesis means building a molecule through chemical reactions.
When did glutathione reach human studies?
Glutathione's move from cell chemistry into human experiments was underway by 1955. A Metabolism paper by Henneman and colleagues that year studied glutathione given into a vein. It examined blood sugar and related blood measurements, a narrower question than whether glutathione improves general well-being.
In 1965, G. C. Cook and Sheila Sherlock at London's Royal Free Hospital published a controlled trial of glutathione. A controlled trial uses a comparison group. They studied people with liver cirrhosis, meaning lasting liver scarring. Their report found no demonstrable benefit from glutathione taken by mouth in that study.
The distinction matters. A molecule can have an important job inside cells while an administered preparation fails to improve a particular illness. Each treatment question needs its own comparison.
Glutathione and NAD+: two different cell systems
NAD+ belongs in this history because it also emerged from early work on cell chemistry. Our history of NAD+ follows that separate discovery and the researchers behind it.
NAD+ is a coenzyme, a small molecule that helps enzymes carry out reactions. Enzymes are proteins that make chemical reactions happen. NAD+ carries electrons, tiny charged particles, as cells process nutrients. Glutathione's sulfur-containing part participates in a different chemical cycle.
Both appear in redox chemistry, meaning reactions that transfer electrons. Sharing that broad description doesn't make them interchangeable treatments. A study of glutathione cannot establish a benefit from NAD+, or the other way around.
From cell chemistry to clinical preparations
Glutathione became familiar as an antioxidant, a substance involved in limiting damage from reactive chemicals. That description concerns what it does within a biological system. It doesn't establish what extra glutathione will do for someone receiving it.
Modern preparations also raise questions the original discovery experiments never asked: how the ingredient was made, how it reaches the body, and what outcome treatment is meant to change.
The move from a named cell constituent to a clinical preparation therefore wasn't one final discovery. It opened a different set of experiments and quality responsibilities.
Where glutathione stands today
As of November 5, 2026, the day this article was written, a recent FDA notice underlines the difference between a molecule and a finished preparation. FDA's August 27, 2026 notice reported at least 30 patients with adverse events, including fever, chills, signs of shock and some hospitalizations, after IV glutathione compounded from an ingredient lot labeled as dietary supplement grade, which FDA says is not an appropriate ingredient for injectable drugs. The glutathione injection illnesses explainer covers that investigation and the recalls that followed.
Glutathione is coming soon to Promise as a compounded medication, which is different from an FDA-approved product: the formulation Promise will offer is not FDA-approved. Compounded means prepared by a pharmacy for a prescription. FDA explains that compounded drugs do not receive its review for safety, effectiveness or quality before marketing. A licensed provider may still prescribe — that decision is between you and your doctor.
NAD+ needs its own treatment evidence
The same separation between chemistry and treatment applies to NAD+. A 2019 Frontiers in Aging Neuroscience pilot tracked blood and urine chemicals during and after NAD+ given into a vein. It wasn't a trial of longer life or improved day-to-day energy.
Those measurements help explain what happens to an administered molecule. They don't establish that someone seeking help with fatigue will feel better. Promise's compounded NAD+ is not FDA-approved, and its cellular role doesn't settle whether it fits an individual.
What a prescription visit adds
A visit brings the question back to the person: the reason for seeking treatment, medical history, medicines, allergies and expectations. The discussion also includes the evidence for the proposed preparation and how unwanted effects would be handled.
At Promise, a licensed provider reviews every request, and not everyone qualifies. If medication is prescribed, a licensed U.S. compounding pharmacy prepares and dispenses it. Discovery history provides context. The visit addresses whether a treatment makes sense for that person now.
