23 year old Laura Deming started the Longevity Fund which just closed its second fund with $22 million. The first fund was for $4 million.
Longevity fund companies target breakthrough antiaging technology including addressing senescent cells, new genome editing, mTorc pathways and more.
They look for three things when they invest:
1. Companies testing the hypothesis that aging can be modified by single things – specific targets, small molecules or biologics. We think there’s enough cross-species evidence of oddly broad-acting genetic pathways that it is worth testing this hypothesis in humans.
2. Companies developing novel technologies for manipulating biological systems. We’re fans of the idea that living things, or things made by them, can treat life (antibodies, cellular therapy, things that manipulate the immune system or electroceuticals). We’re very open to anything in this regard.
3. Things which don’t fall into either bucket above, or combine the two. We try to be non-dogmatic, so if you can make a good case for it, we’ll take a look.
All of the companies in that portfolio have at least raised Series A rounds of $30 million or more to get to that proof of concept.
They look to invest in Eight to 10 companies in the new round.
UNITY Biotechnology, Inc. (“UNITY”), a privately held biotechnology company creating therapeutics that prevent, halt, or reverse numerous diseases of aging, today announced the closing of an additional $35 million in Series B financing. This second close of the Series B, in addition to the initial close in fall of 2016, brings the total amount of this financing to $151 million.
The initial focus at UNITY is on selectively eliminating senescent cells.
Cellular senescence is a biological “emergency brake” cells use to stop dividing. It’s an important anti-tumor mechanism, because it prevents cells from multiplying out of control. But after this “brake” has been pulled, senescent cells remain in the body, accumulating with age. And unlike normal cells, these cells secrete inflammatory molecules that harm neighboring cells and tissues.
UNITY has demonstrated in animal models that selectively eliminating senescent cells reverses or prevents a wide range of diseases, including osteoarthritis, atherosclerosis, eye diseases, and kidney diseases.
At Precision, they utilize a proprietary genome editing method they call ARCUS combined with a team made up of some of the leading minds and pioneers in genome editing in an effort to overcome cancers, cure genetic diseases, and enable the development of safer, more productive food sources.
Genome editing technologies allow us to rethink their approach to a broad array of serious challenges faced by the world today. We now have the ability to precisely edit the DNA of a living organism, opening up the possibility of correcting genetic problems at their source.
ARCUS is a next-generation genome editing platform derived from a natural genome editing enzyme called a homing endonuclease.
Multi-functional – ARCUS isn’t limited to deletions. ARCUS can be used to insert, delete or edit DNA.
Specific – ARCUS doesn’t miss its target. ARCUS doesn’t generate truly random DNA-breaks.
Small – 310 amino acids. 930 base pairs. ARCUS is compatible with essentially any delivery strategy.
One – Polypeptide. ARCUS is a single protein expressed from a single gene. There’s no need to deliver multiple parts.
Seamless – Matched 4 base pair 3′ overhangs result in perfect, predictable removal of DNA.
The backbone of the ARCUS technology is the ARC Nuclease – a fully synthetic enzyme that is very similar to a homing endonuclease but is modified to be a better starting point for the development of new gene editing reagents. ARC Nuclease shares many of the positive attributes of a homing endonuclease, such as small size and unparalleled sequence specificity, but it can more easily be evolved into a custom gene editing tool that recognizes a DNA sequence of our choosing. Each ARCUS reagent is optimized using a set of proprietary in silico and lab-based techniques to ensure maximum gene editing efficiency with minimum off-target activity.
Homing endonucleases are nature’s genome editing system. They are site-specific DNA-cutting enzymes encoded in the genomes of many eukaryotic species. Homing endonucleases have the unusual ability to precisely recognize long DNA sequences (12-40 base pairs) that are typically rare enough to occur only once in a complex genome. By targeting a double strand DNA break to a specific site in the genome of a cell, a homing endonuclease triggers the cell’s DNA repair pathways and stimulates homologous recombination. In nature, this results in gene conversion events in which the genome of the cell is modified in a very precise way, most frequently by the insertion of a foreign gene at the site of the DNA break. The ability to generate a single DNA break in a complex genome to achieve gene modification – without off-targeting – makes homing endonucleases the ideal starting material for a genome editing technology.
Alexo Therapeutics is a clinical-stage immuno-oncology company developing therapies that block the CD47 checkpoint mechanism exploited by cancer cells to evade the immune system. Our lead candidate, ALX148, is a fusion protein that comprises an engineered high affinity CD47 binding domain of SIRPα linked to an inactive Fc region of human immunoglobulin. ALX148 is designed to enhance the efficacy of antibody-based therapies and is in clinical development for a broad range of tumor types.
Metacrine will leverage two mechanistically distinct programs to target diabetes, steatohepatitis and other metabolic and liver disorders. The current focus of the company is to develop novel therapeutics for significant metabolic diseases such as type 2 diabetes and non-alcoholic steatohepatitis (NASH). There are over 30 million type 2 diabetics in the United States and despite numerous available drug classes, close to 50% of patients are unable to achieve target HbA1c levels and glucose control. Similarly, non-alcoholic steatohepatitis (NASH) is reaching epidemic proportions in the US and worldwide, with nearly 20% of Americans having some stage of fatty liver disease. Currently, there is no approved therapy for NASH.
An unprecedented and powerful therapeutic approach to address unmet needs in age-related diseases and certain rare disorders
With increasing life expectancy, the need to address chronic diseases that affect long-term health in aging populations is expanding. mTORC1 (mechanistic target of rapamycin complex 1) is a protein kinase complex that has been shown to be a central regulator of cellular aging processes and has been directly implicated in multiple diseases associated with its dysregulation. Our proprietary drug development approach selectively targets the activation of mTORC1 and offers an entirely new treatment approach for a broad range of chronic age-related diseases as well as several rare diseases that are linked to the genetic dysregulation of mTORC1 activation. Our aim is to discover and develop new medicines that restore normal activity to mTORC1 and improve human health.
Navitor’s proprietary drug discovery platform is built on new insights into the activation of mTORC1
Navitor’s drug discovery platform leverages proprietary intellectual property and know-how related to key targets within the cellular pathways required for the activation of mTORC1 as well as their fundamental role in age-related disease processes. Navitor was founded based on groundbreaking discoveries related to the mTORC1 pathway and the role of nutrient signaling, as well as other cellular mechanisms in the regulation of its activation, by the company’s scientific founder, Dr. David Sabatini, MD, PhD, at the Whitehead Institute for Biomedical Research. Dr. Sabatini’s work was instrumental in the discovery of the mTOR kinase and its two multi-protein complexes, mTORC1 and mTORC2, each of which mediates distinct aspects of the mTOR signaling network.
Navitor’s technology is applicable to developing novel product candidates addressing a wide range of diseases in which mTORC1 activation is dysregulated, including:
• Obesity, type 2 diabetes, and other metabolic diseases in which hyperactive mTORC1 activity is driven through the excess availability of nutrients and is thought to cause dysregulated cellular function and drive the disease process.
• Alzheimer’s, Parkinson’s, and Huntington’s diseases; and other neurodegenerative diseases that involve abnormal protein folding, possibly due to excessive and unrestrained protein synthesis and reduced autophagy.
• Psoriasis, rheumatoid arthritis, lupus, multiple sclerosis,and other inflammatory and autoimmune diseases in which increased mTORC1 activity is thought to contribute to the activation of a specific subpopulation of T-cells that may create inflammation and tissue injury.
• Immunosenescence, where mTORC1 selective modulation of certain T-cell populations may improve vaccine efficacy in the aging population and enhance effectiveness of cancer immunotherapy.
• Lymphangioleiomyomatosis (LAM), tuberous sclerosis,and other rare diseases caused by a genetic defect in the mTORC1 signaling network, resulting in an uncontrolled hyperactivity of this complex.
• Musculoskeletal diseases including conditions that involve muscle loss, such as following immobilization and sarcopenia, in which protein synthesis and/or cell growth is deficient.