BioAge Labs raises $10.9M in Series A financing to accelerate drug discovery for aging
Old age comes to us all, and with it illness and disability. If you’re lucky enough to live long enough, at some point you’ll suffer from one — and more likely several — slow killers, chronic diseases of aging like heart disease, diabetes, cancer, and Alzheimer’s. But does it have to be this way? Recent scientific advances have provided proof of principle in mice that some therapies (drugs like rapamycin  and interventions like senescent cell ablation ) can not only significantly extend lifespan, but also delay the onset of age-related diseases and thereby enhance healthspan — the period of life where we are healthy and functional. Human therapies of similar effectiveness could add 10 to 20 healthy years to the average person’s lifespan.
Treating aging as a medical problem itself represents a marked divergence from the traditional strategy of treating each age-related disease separately (e.g. with a diabetes drug or an Alzheimer’s drug). The traditional approach can only ever have a limited effect on population health, because the risk of many different chronic diseases rises precipitously with age. In contrast, the positive impact of any new therapy that addresses the root causes of aging may be enormous [3–4].
Aging will not be an easy problem to solve — much of the underlying biology is still a mystery. But there are several clues emerging from recent scientific discoveries, and with new genomic and data-driven technologies, we may soon be in a position to address some of the major bottlenecks to intervening in aging.
I founded BioAge Labs in 2015 to accelerate drug discovery for aging. The company is based on two core ideas:
1. We can massively accelerate drug testing by developing molecular signatures of aging
Currently, there are only a handful of interventions that reliably extend mouse lifespan (never mind human lifespan). One critical obstacle is that testing any candidate therapy in a traditional lifespan experiment takes several years. This time frame makes large-scale screening efforts impractical, and is one reason that only few compounds have been tested in mice or other mammals. We need to identify molecular signatures of aging that can serve as surrogate assays for lifespan to enable faster and higher-throughput drug screening.
2. The best signatures of aging will come from deeply phenotyping large human cohorts
Human aging is complex and still poorly understood, and much of our current knowledge originated in mouse or invertebrate models. Working with these more experimentally tractable animals can be powerful for studying evolutionarily conserved mechanisms of aging, but this strategy is limited. Newer high-throughput technologies such as metabolomics, transcriptomics, and methylomics have made it possible to measure aging directly in human populations. Carefully designed cohorts and unbiased, data-driven analyses will be key to identifying the most predictive molecular signatures of human aging.
At BioAge, we’re betting on the power of high-throughput human data, coupled with innovative machine learning, to substantially accelerate drug discovery for aging. We take a hybrid experimental and computational approach to identifying the molecular signatures that drive aging, working with multiple partners in academia and industry.
Today I’m excited to announce that we’ve raised approximately $10.9M in Series A financing. This round was led by the Andreessen Horowitz Bio Fund (with Dr. Vijay Pande joining our Board of Directors) with participation from Felicis Ventures, AME Cloud Ventures, PEAR Ventures, Caffeinated Capital, Elad Gil, and other angels.
This new funding will enable us to build our team, refine and test our signatures of aging, and begin in vivo evaluation of drug candidates. Our initial targets for drug development will be specific diseases where aging is causal; however, our ultimate goal is more ambitious — to combat the suffering and disability caused by all aging-related diseases, and to restore both the quality and quantity of life that is so often lacking in old age.
 Harrison, D et al. 2009. Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature 460, 392–395.
 Baker, DJ et al. 2016. Naturally occurring p16Ink4a-positive cells shorten healthy lifespan. Nature 530, 184–189.
 Martin, GM et al. 2003. Research on aging: the end of the beginning. Science 299, 1339–1341.
 Stipp D. (2012). The transformative promise of aging science. Cell Cycle, 11, 3903–3904.