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Unity Biotechnology
http://unitybiotechnology.com/

Imagine a future in which you age, but without the diseases your parents got. Imagine a future in which it doesn’t hurt to grow old.

At UNITY, we design therapeutics that prevent, halt, or reverse numerous diseases of aging. Our medicines are designed to lengthen healthspan, the amount of time you live in good health.

The Company is targeting biological mechanisms that unify many afflictions, including arthritis, heart disease, kidney failure, loss of eyesight and loss of hearing. Many of these diseases share a common root cause in senescence biology.

With an initial focus on senescence biology, Unity is designing medicines that lengthen healthspan, the amount of time an individual lives in good health. The Company is committed to advancing the field of aging biology through an open and robust engagement of the scientific community and by facilitating dialogue around the development of drugs that change how humans age.


Destroying worn-out cells makes mice live longer
Elegant experiment confirms that targeting senescent cells could treat age-related diseases.
http://www.nature.com/news/destroying-worn-out-cells-makes-mice-live-longer-1.19287


Baker DJ, Childs BG, Durik M, Wijers ME, Sieben CJ, et al. Naturally occurring p16Ink4a-positive cells shorten healthy lifespan. Nature. 2016. http://www.nature.com/nature/journal/vaop/ncurrent/full/nature16932.html

Cellular senescence, a stress-induced irreversible growth arrest often characterized by expression of p16Ink4a (encoded by the Ink4a/Arf locus, also known as Cdkn2a) and a distinctive secretory phenotype, prevents the proliferation of preneoplastic cells and has beneficial roles in tissue remodelling during embryogenesis and wound healing. Senescent cells accumulate in various tissues and organs over time, and have been speculated to have a role in ageing. To explore the physiological relevance and consequences of naturally occurring senescent cells, here we use a previously established transgene, INK-ATTAC, to induce apoptosis in p16Ink4a-expressing cells of wild-type mice by injection of AP20187 twice a week starting at one year of age. We show that compared to vehicle alone, AP20187 treatment extended median lifespan in both male and female mice of two distinct genetic backgrounds. The clearance of p16Ink4a-positive cells delayed tumorigenesis and attenuated age-related deterioration of several organs without apparent side effects, including kidney, heart and fat, where clearance preserved the functionality of glomeruli, cardio-protective KATP channels and adipocytes, respectively. Thus, p16Ink4a-positive cells that accumulate during adulthood negatively influence lifespan and promote age-dependent changes in several organs, and their therapeutic removal may be an attractive approach to extend healthy lifespan.