Jeff Bezos, Mayo Clinic back anti-aging startup Unity Biotechnology for $116 million

March 30, 2017

Every once in a while someone in Silicon Valley brings up the possibility of living forever, or at least a really long time, but first we’re going to need to figure out a way to enjoy all those extra years. Unity Biotechnology is a startup focusing on medicines to help us do that by slowing the effects of age-related diseases. And the company announced it has pulled in a whopping $116 million in Series B financing today — some of which came from Amazon’s Jeff Bezos.

Sometimes your body keeps aging cells around longer. These cells stop dividing after some form of stress,which is an anti-cancer mechanism that keeps damaged cells from dividing and growing out of control. But too much build-up of those types of cells leads to other problems as we age. Unity looks for ways to help your body shed older cells causing inflammation and other diseases linked to aging.

Unity holds a great amount of potential in preventing our bodies from aging as fast and that has perked some of the top investors in science and medicine and is one of the larger private financings in biotech history.

But it’s not the first time Bezos has invested in biotech. The Amazon CEO placed his bets on Juno Therapeutics back in 2014, through his venture capital arm Bezos Expeditions. Juno is one of the IPO success stories in the biotech world for its breakthrough discoveries in cancer medicine.

The Scottish-based mutual fund Baillie Gifford, which has also invested in several biotech companies, also invested in this round — as did Venrock, ARCH Venture Capital, Mayo Clinic and WuXi Pharmaceuticals.

The company also announced it would be placing Keith Leonard — the former CEO of KYTHERA Biopharmaceuticals — in the role of CEO and that previous CEO and co-founder Nathaniel “Ned” David will now be Unity’s president.

Jeff Bezos, Mayo Clinic back anti-aging startup Unity Biotechnology for $116 million

Mayo Clinic Taps Silicon Valley to Help People Age Gracefully

April 23, 2016

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Could there be a recipe for a longer, healthier life?

Pop a pill and live a long, healthy life. It might not be quite that easy yet, but researchers at Mayo Clinic believe they have found a cell that could hold the secret to aging extra gracefully.

Their research, published in the journal Nature Wednesday, helped patients live longer, healthier lives. The only catch is their patients are mice. But the researchers believe they could someday translate it into a recipe for human longevity, too.

In fact, the research has been so convincing that Mayo Clinic invested in Unity Biotechnology, a San Francisco-based startup built around the researchers’ approach. Other investors in the company include ARCH Venture Partners, Venrock, and Chinese WuXi, and the study’s lead author Jan van Deursen is listed as a Unity co-founder.

The anti-aging method works like this: scientists inject the mice with a drug that pushes out toxic, worn-out cells called “senescent cells.” The senescent cells are old and stressed and don’t behave properly anymore. Instead, they “litter the body with aging” as van Deursen puts it.

Discovery of new code makes reprogramming of cancer cells possible

August 27, 2015

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Cancer researchers dream of the day they can force tumor cells to morph back to the normal cells they once were. Now, researchers on Mayo Clinic’s Florida campus have discovered a way to potentially reprogram cancer cells back to normalcy.

The finding, published in Nature Cell Biology, represents “an unexpected new biology that provides the code, the software for turning off cancer,” says the study’s senior investigator, Panos Anastasiadis, Ph.D., chair of the Department of Cancer Biology on Mayo Clinic’s Florida campus.

That code was unraveled by the discovery that adhesion proteins — the glue that keeps cells together — interact with the microprocessor, a key player in the production of molecules called microRNAs (miRNAs). The miRNAs orchestrate whole cellular programs by simultaneously regulating expression of a group of genes. The investigators found that when normal cells come in contact with each other, a specific subset of miRNAs suppresses genes that promote cell growth. However, when adhesion is disrupted in cancer cells, these miRNAs are misregulated and cells grow out of control. The investigators showed, in laboratory experiments, that restoring the normal miRNA levels in cancer cells can reverse that aberrant cell growth.

“The study brings together two so-far unrelated research fields — cell-to-cell adhesion and miRNA biology — to resolve a long-standing problem about the role of adhesion proteins in cell behavior that was baffling scientists,” says the study’s lead author Antonis Kourtidis, Ph.D., a research associate in Dr. Anastasiadis’ lab. “Most significantly, it uncovers a new strategy for cancer therapy,” he adds.

That problem arose from conflicting reports about E-cadherin and p120 catenin — adhesion proteins that are essential for normal epithelial tissues to form, and which have long been considered to be tumor suppressors. “However, we and other researchers had found that this hypothesis didn’t seem to be true, since both E-cadherin and p120 are still present in tumor cells and required for their progression,” Dr. Anastasiadis says. “That led us to be believe that these molecules have two faces — a good one, maintaining the normal behavior of the cells, and a bad one that drives tumorigenesis.”

Their theory turned out to be true, but what was regulating this behavior was still unknown. To answer this, the researchers studied a new protein called PLEKHA7, which associates with E-cadherin and p120 only at the top, or the “apical” part of normal polarized epithelial cells. The investigators discovered that PLEKHA7 maintains the normal state of the cells, via a set of miRNAs, by tethering the microprocessor to E-cadherin and p120. In this state, E-cadherin and p120 exert their good tumor suppressor sides.

However, “when this apical adhesion complex was disrupted after loss of PLEKHA7, this set of miRNAs was misregulated, and the E-cadherin and p120 switched sides to become oncogenic,” Dr. Anastasiadis says.

“We believe that loss of the apical PLEKHA7-microprocessor complex is an early and somewhat universal event in cancer,” he adds. “In the vast majority of human tumor samples we examined, this apical structure is absent, although E-cadherin and p120 are still present. This produces the equivalent of a speeding car that has a lot of gas (the bad p120) and no brakes (the PLEKHA7-microprocessor complex).

“By administering the affected miRNAs in cancer cells to restore their normal levels, we should be able to re-establish the brakes and restore normal cell function,” Dr. Anastasiadis says. “Initial experiments in some aggressive types of cancer are indeed very promising.”

The study was supported by the National Institutes of Health grants R01 CA100467, R01 NS069753, P50 CA116201, R01 GM086435, R01CA104505, R01CA136665; the Florida Department of Health, Bankhead-Coley grants 10BG11; the Breast Cancer Research Foundation; the Swiss Cancer League; and the Jay and Deanie Stein Career Development Award for Cancer Research at Mayo Clinic.


Story Source:

The above post is reprinted from materials provided by Mayo Clinic. Note: Materials may be edited for content and length.


Journal Reference:

  1. Siu Ngok, Ryan Feathers; Lomeli Carpio; Tiffany Baker; Jennifer Carr; Irene Yan; Sahra Borges, Edith Perez, Peter Storz, John Copland, Tushar Patel, E. Aubrey Thompson, Pamela Pulimeno, Sandra Citi. Distinct E-cadherin-based complexes regulate cell behaviour through miRNA processing or Src and p120-catenin activity. Nature Cell Biology, 2015 DOI: 10.1038/ncb3227

http://www.sciencedaily.com/releases/2015/08/150824064916.htm