Daniel Ives, PhD
CEO of Shift Bioscience, UK
At Shift Bioscience, Dr. Ives is making drugs for safe cellular rejuvenation and avoidance of age-linked diseases through the application of machine-learning to cellular reprogramming. He is also a founding fellow of the OnDeck Longevity Biotech fellowship, a continuous community for people to come together to build, join, or invest in revolutionary longevity biotechnology startups.
Dr. Ives was inspired to pursue a Longevity mission in 2009 after reading Aubrey de Grey’s 2007 book ‘Ending Aging’. As a University of Cambridge PhD student, he joined Ian Holts group at the Mitochondrial Biology Unit to pursue damage-removal strategies for mitochondrial DNA mutations, which cause rare mitochondrial disease and are sufficient to accelerate ageing phenotypes in mouse models. Harnessing publicly available transcriptome data from the NCBI GEO database, he used a computationally guided screen to identify small-molecule tools that eliminate mitochondrial DNA mutations. Dr. Ives followed Ian to the Crick Institute to further validate these small molecule-tools (publication-pending).
In 2016, he left the Crick Institute and personally funded ageing-focused experiments using local contract research organisations (Total Scientific, now RxCelerate). Once friend and family financing was exhausted, Dr. Ives approached Cambridge angel Jonathan Milner and with his support, Shift Bioscience was founded to commercialise mitochondrial drugs for age linked diseases, quickly embracing a breakthrough ageing biomarker - DNA methylation or epigenetic ageing clocks. These clocks clarified the role of mitochondrial DNA mutations in physiological ageing and pivoted Shift to a first-principles approach to drug-target discovery for ageing and rejuvenation.
Dr. Ives helped guide Shift intern Brendan Swain (U. Cambridge PhD student) to develop a single cell ageing clock based on transcriptome data. This enabled a CRISPR screen for ageing on the 10X Genomics Chromium machine, but more excitingly, the constituent genes making up the clock were enriched for functional 'drivers' of ageing phenotypes. This suggested they had arrived at a causal or 'driver' clock for ageing. The same clock methodology was then used to extract non-pluripotent candidate drivers of rejuvenation from a cellular rejuvenation time-course (cellular reprogramming with OSKM) and they are now gearing up to validate these candidates.