We are leveraging our deep understanding of the biology of hepatocyte growth factor (HGF) in organ regeneration to develop therapies that trigger self-repair after acute organ injury. Our founder and chief scientific officer made seminal discoveries related to HGF’s anti-apoptotic and restorative properties that we are harnessing for therapeutic development.

Hepatocyte growth factor


Hepatocyte growth factor (HGF) is a systemic organ repair protein that enables the liver’s unique ability to regenerate and that triggers extensive self-repair pathways in other organs, including the kidneys, livers, heart, brain and lungs.



Acute kidney injury (AKI) is a sudden loss of kidney function due to reduced oxygenation, toxic injury or direct obstruction that may become permanent and result in death. One well-known cause of AKI is the use of a heart-lung machine during open heart surgery. Surgery patients with certain risk factors, such as pre-existing kidney disease, previous cardiac surgery, compromised heart function, advanced age and diabetes are at higher risk of AKI during this type of surgery. Prolonged AKI leads to increased mortality, higher hospital costs and re-admission rates, and a risk of patients developing CKD. Annual cases in of AKI in the U.S. range from 1.2 to 2 million. There are 2 million deaths annually worldwide due to AKI and currently no approved treatment exists.



Chronic kidney disease (CKD) describes the gradual loss of kidney function that can progress to end-stage kidney failure, which is fatal without dialysis or a kidney transplant. Potential complications of CKD include fluid retention, dangerous increases in potassium levels, heart and blood vessel disease, weak bones, decreased immune response and irreversible damage to one’s kidneys. There are more than 200,000 cases of CKD in the U.S. annually. CKD has no cure and represents a significant unmet need in the nephrology space.



Focal segmental glomerulosclerosis (FSGS) is a serious kidney disorder characterized by progressive scarring of the glomeruli, the filtering units of the kidney. There are approximately 80,000 cases of GSFS in the U.S. and Europe, and 30-60% of patients will progress to end-stage kidney disease over 5-10 years from time of diagnosis. FSGS has no approved therapies and only limited treatment options, including corticosteroids, immunosuppressants and diuretics. If uncontrolled, FSGS can lead to kidney failure and the need for dialysis or a kidney transplant.



Kidneys for transplantation come from two sources: a living donor such as a relative or a deceased donor. A frequent complication that occurs after kidney transplantation from a deceased donor is known as delayed graft function (DGF), when the new kidney does not function adequately yet, requiring the patient to continue on dialysis until the new kidney gains function. While most DGF organs gain function, the longer the post-transplant patient requires dialysis, the poorer the survival of the graft. There is no effective treatment for DGF.

We believe that a drug that treats will not only increase the long-term success of renal transplants, but also reduce the large and widening gap between available organs and the waiting list of end stage renal disease patients on dialysis.


We believe that a drug that treats delayed graft function will not only increase the long-term success of renal transplants but also reduce the large and widening gap between available organs and the waiting list of end stage renal disease patients on dialysis.

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Chart based on data from National Kidney Foundation