The scientists who discovered telomerase were Carol Greider and Elizabeth Blackburn at the University of California, Berkeley. Telomerase is an enzyme, a biological tool that builds telomeres, the protective caps on chromosome ends. Chromosomes hold DNA, the material carrying our genetic instructions.
Greider saw the first signal on December 25, 1984. Their paper appeared in 1985. Jack Szostak's earlier work helped explain what the caps did. All three shared the 2009 Nobel Prize in Physiology or Medicine. The discovery explained how cells maintain their chromosome ends; it didn't establish a treatment for human aging.
The Hayflick limit: why did cells stop dividing?
The puzzle started before anyone found the enzyme. In 1961, Leonard Hayflick and Paul Moorhead at Philadelphia's Wistar Institute reported that normal human cells couldn't keep dividing indefinitely.
Their Experimental Cell Research paper described cells grown outside the body. The eventual stopping point became known as the Hayflick limit. It described a limit on cell growth, rather than a fixed number of years a person could live.
Alexey Olovnikov, at Moscow's Gamaleya Institute, proposed a possible explanation. His 1973 Journal of Theoretical Biology paper connected incomplete copying of DNA ends with limited cell division. The end-replication problem means the usual copying machinery leaves part of an end uncopied.
Olovnikov supplied a theory. Finding the machinery that could maintain those ends required experiments.
Who discovered telomerase, and where does Szostak fit?
Blackburn had studied repeated DNA sequences at chromosome ends in Tetrahymena, a single-celled freshwater organism. Szostak, working at Harvard Medical School, was studying why small linear DNA molecules were unstable in yeast.
Their collaboration joined those questions. In a 1982 Cell paper, Szostak and Blackburn showed that DNA ends from Tetrahymena could stabilize a linear DNA molecule in yeast. Protection worked across two very different organisms.
Greider, then Blackburn's graduate student, tackled the next question: what added those repeated sequences? Their 1985 Cell paper identified an activity in Tetrahymena cell extracts that added the repeats. An extract is material taken from cells for testing.
The Nobel Assembly's account dates Greider's first signal to Christmas Day, 1984. That's why both 1984 and 1985 appear in discovery histories: one marks the experiment, the other the publication.
Today's interest in epitalon, also spelled Epithalon, borrows from this biology. It is a synthetic peptide, a short chain of protein building blocks. Finding telomerase didn't establish what taking that peptide would do.
The 2009 Nobel Prize recognized a mechanism
The Nobel Assembly announced the prize on October 5, 2009. Its citation recognized the discovery of “how chromosomes are protected by telomeres and the enzyme telomerase.”
The credit covered related contributions. Blackburn and Szostak explained the protective function of the chromosome ends. Greider and Blackburn identified the enzyme that builds them. The Assembly's detailed scientific account separates those steps.
Later work showed that the enzyme uses RNA, a molecule that provides a pattern for building the repeated DNA sequence. This explained how the cell could add material without simply copying an existing chromosome end.
The prize honored fundamental cell biology. It wasn't an endorsement of a longevity treatment, and the researchers' names don't supply evidence for a product sold today.
What came of it: inherited disorders and cancer
The discovery helped explain diseases involving poor maintenance of chromosome ends. One is dyskeratosis congenita, an inherited disorder that can affect the skin, nails, blood-making tissue and lungs.
The clinical reference GeneReviews describes very short telomeres and risks including bone marrow failure, when the body cannot make enough blood cells. Here, telomere testing can contribute to a specific diagnosis.
Cancer revealed another side of the same machinery. A 2016 review in Cellular and Molecular Life Sciences describes telomerase activation in about 85% of human cancers. Maintaining the caps can help cancer cells keep dividing. More activity isn't automatically healthier.
As of October 1, 2026, the day this article was written, FDA's Rytelo record lists its June 6, 2024 approval. Rytelo contains imetelstat, a telomerase inhibitor, meaning it blocks the enzyme. Its prescribing information, marked “Revised: 4/2026,” covers certain adults with myelodysplastic syndromes, disorders of blood-cell production, who depend on transfusions. It is a disease-specific treatment, without a longevity indication.
Telomere length isn't a personal clock
Telomere length can help researchers study differences across populations. It cannot reliably tell one person how many years remain. A 2021 Frontiers in Genetics review describes substantial limits in using it alone to estimate biological age or predict mortality.
A longer measurement also doesn't prove better health. No therapy that lengthens telomeres has been shown to extend human life. A Physiological Reviews assessment describes the missing human evidence for telomerase-based aging treatments.
Epitalon's influential 2003 study came from Khavinson's group and used cultured human fetal cells. Independent cell research also exists, including a Brunel team's paper with a published figure correction. These weren't lifespan trials in people. The epitalon and telomeres guide explains the experiments separately.
NAD+ raises a similar evidence question
NAD+, a molecule cells use in energy-related chemical reactions, also appears in longevity discussions. It isn't telomerase, and evidence about one doesn't establish a benefit from the other. The history of NAD+ explains its separate discovery.
As of October 1, 2026, the day this article was written, a trial published September 25 in npj Aging offers a useful example. Older adults received oral NMN, an ingredient the body uses to make NAD+, or placebo, a comparison preparation without NMN. Over 24 weeks, blood NAD+ rose, without significant improvement in hearing or physical performance. The study tested NMN, rather than NAD+ treatment or telomere lengthening.
A change in a laboratory marker and a meaningful change in someone's health are separate findings.
What a prescription visit adds
Promise's NAD+ preparation is a compounded medication, prepared by a pharmacy for a prescription; the Epithalon preparation Promise will offer will also be compounded. They are different from an FDA-approved product: the NAD+ formulation offered here and the Epithalon formulation Promise will offer are not FDA-approved. Epithalon is coming soon to Promise — add me to the list. FDA explains that it doesn't review compounded drugs for safety, effectiveness or quality before marketing. A licensed provider may still prescribe — that decision is between you and your doctor.
At Promise, a licensed provider reviews every request, and not everyone qualifies.
The visit connects the evidence to a person's health history, current medicines and goals. It also establishes a plan for follow-up. The discovery explains why telomerase matters to cells. A prescribing discussion addresses the separate question of whether a particular treatment fits a particular person.
