Sinclair claimed his experimental drug SL-100 extended maximum lifespan in progeria mice by more than 33%. A journalist in the same room heard different numbers: a 15.4% increase in median lifespan, not statistically significant
Sinclair claimed his experimental drug SL-100 extended maximum lifespan in progeria mice by more than 33%. A journalist in the same room heard different numbers: a 15.4% increase in median lifespan, not statistically significant
On October 1, at ARDD, a specialized aging conference at Harvard, Chris Petty, a graduate student in David Sinclair's lab, presented the first data on the experimental drug SL-100, which Sinclair had previously announced without a single efficacy figure and calls "v2". Sinclair himself wrote on X that the pilot experiment protected mice from frailty and increased maximum lifespan by more than 33%, with some treated mice still alive. Antonio Regalado, a science journalist at MIT Technology Review who was sitting in the same room, described the same data differently: median lifespan increased by 15.4%, but the result was not statistically significant because the sample was small, the experiment was unfinished, and the composition of SL-100 was undisclosed.
The lab used the LAKI mouse line, which carries a mutation in the lamin A gene, the same mutation that causes Hutchinson-Gilford syndrome (childhood progeria) in humans: because of the accumulation of defective protein, cells in these mice age in months rather than years. This line played a special role in the history of the method itself: it was in LAKI mice that partial cellular reprogramming, a way to temporarily return a cell to a younger state without losing its specialization, first worked in a living organism, about ten years ago.
Median and maximum lifespan follow different accounting logic. The median is the age at which half the group has died: it can be calculated now, and further deaths in the cohort do not change it. The maximum is the lifespan of the longest-lived animal in the group; as long as at least one treated mouse is still alive, this number can only grow. An early claim about an increase in maximum lifespan can therefore sound premature without being wrong: the number is already unable to decrease. In his post, Sinclair states specifically that maximum lifespan increased by more than 33% and immediately notes that some treated mice are still alive, which means the maximum itself is not yet final.
The scale of the claim can be checked against prior results in the same model. In 2016, biologist Alejandro Ocampo and colleagues extended the lifespan of a living mammal by partial reprogramming for the first time: by cyclically switching Yamanaka factors on and off in LAKI mice (these factors temporarily activate a rejuvenation program in the cell), they achieved a 33% increase in median lifespan and an 18% increase in maximum lifespan. By the same strict metric, maximum lifespan, Sinclair in 2026 claims a gain nearly twice as large as Ocampo's: over 33% versus 18%. These are, however, different interventions: Ocampo switched genes on and off inside cells, while Sinclair's SL-100 is a chemical compound whose trial, by his own account, is not yet complete.
For scientific public relations, this is a rare case of live verification: ordinarily, an independent assessment of unpublished data arrives months later, after a peer-reviewed paper. Regalado was in the room and published his version of the numbers the same evening.
Petty, according to Regalado, confirmed that the experiment is far from finished: "I have hundreds of mice on campus... breeding." The following evening, Sinclair posted a link on X to an Endpoints News article captioned "SL-100 update." The article confirmed the drug's code name and pill form but contained no lifespan percentages.
Regalado summed it up in the same thread:
"Suggestive claims, but an unknown substance. Not much to believe in yet. What is certainly true: we would all like to have a rejuvenation pill."