Retro Biosciences
Organization Description
RetroBio is a longevity biotech company founded in 2021 with the intention of building a generational pharma company on a scale proportional to their mission: to increase healthy human lifespan by 10 years. In 2022, the company stated that its strategy was to identify mechanisms of aging that, when targeted, had been shown to robustly impact aging in mammals and had “a feasible path to translation to humans,” and that its main focuses were cellular reprogramming, “plasma-inspired therapeutics,” and autophagy.
Retro was founded by technologist Joe Betts-LaCroix; Sheng Ding, a Professor of Pharmaceutical Sciences and founder or cofounder of multiple companies; and Matt Buckley, a PhD in Genetics from Stanford who was formerly in Anne Brunet’s lab and has worked on using machine learning to quantify aging. The company was established with an initial $180 million investment from Sam Altman, formerly of celebrated technology accelerator Y Combinator and more recently CEO of OpenAI.
RTR242
RTR242 is Retro’s most advanced candidate. described as a small molecule activator of autophagic flux, with the target indication neurodegenerative aging of the Alzheimer’s type (AD). In animal models, many autophagy “boosters,” such as rapamycin, have been shown to slow the accumulation of the two signature forms of molecular damage in the brains of people with AD: beta-amyloid and aberrant tau. Aberrant tau is most harmful within neurons, and beta-amyloid exerts harmful effects within neurons and likely accumulates in plaques because of the failure of microglial lysosomes to degrade it. Thus, a drug that upregulated autophagy might be expected to delay, prevent, or partially reverse AD.
RTR242 is Retro’s most advanced candidate. described as a small molecule activator of autophagic flux, with the target indication neurodegenerative aging of the Alzheimer’s type (AD). In animal models, many autophagy “boosters,” such as rapamycin, have been shown to slow the accumulation of the two signature forms of molecular damage in the brains of people with AD: beta-amyloid and aberrant tau. Aberrant tau is most harmful within neurons, and beta-amyloid exerts harmful effects within neurons and likely accumulates in plaques because of the failure of microglial lysosomes to degrade it. Thus, a drug that upregulated autophagy might be expected to delay, prevent, or partially reverse AD.
On September 14, 2025, Betts-LaCroix told Business Insider that the company anticipated dosing its first subject with RTR242 in a Phase I trial in Australia by the end of the year. The trial (ACTRN12625001274460) will enroll a total of 48 healthy subjects in the single ascending dose (SAD) phase, divided into five cohorts of eight subjects each: six receiving RTR242 solution and two receiving a placebo, with different cohorts taking different doses, either with a high-fat meal or on an empty stomach. A multiple ascending dose (MAD) study will begin after the Safety Review Committee has had the opportunity to review the data from the SAD study.
iMG
These are said to be microglial progenitors derived from cellular reprogramming (“iMG” = “induced microglia”?); the pipeline page is not clear as to whether these are “off-the-shelf” cells or cells derived from reprogrammed cells from the patient him- or herself. Both microglial transplantation and ablation have been proposed as therapies for AD; Retro says only that the indication for these cells is unspecified CNS conditions. They are in preclinical research.
Team
