is a biotech company dedicated to transforming the cardio-renal disease treatment paradigm by focusing on the prevention and treatment of kidney disease. Each year, 9 million U.S. adults suffer from acute kidney injury (AKI), and today, 37 million U.S. adults are living with chronic kidney disease (CKD). As the most common complication of a number of surgical procedures, AKI occurs in approximately 30% of patients undergoing cardiac surgery. It is associated with a higher risk of mortality in both inpatient and outpatient settings, and progression to CKD within 24 months occurs in approximately 15-20% of patients who survive AKI. The quality of life and financial burdens of AKI and CKD have reached insurmountable proportions for patients and their families. Unfortunately, there are currently no approved therapies for prevention or treatment of AKI or to stop the progression of CKD leading to dialysis.  

Rénibus’ lead product, RBT-1, is a novel pharmacologic intervention combining stannous protoporphyrin and iron sucrose, that induces a preconditioning protective effect on the kidney, upregulating production of protective proteins to prevent AKI during cardiac surgery. Phase I development is completed, and a RBT-1’s first Phase II trial initiated in April 2021 and is expected to be completed in Q3 2022; a Phase 2, Double-Blind, Randomized, Placebo-Controlled Study to Evaluate the Effect of RBT-1 on Preconditioning Response Biomarkers in Subjects Undergoing Coronary Artery Bypass Graft (CABG) and/or Cardiac Valve Surgery (The START Study).

RBT-2 (Tetrahydrocurcumin) is an active metabolite of an antioxidant natural product that reduces CKD progression by restoring cellular homeostasis and reducing inflammation and fibrosis development. Protective effects of RBT-2 have been observed in the heart. RBT-2: formulation and IND enabling work in progress. Phase I study expected to start in Q4 2022.

RBT-3 is a proprietary and differentiated form of iron sucrose that rapidly increases plasma ferritin and activates the body’s key cytoprotective pathway, Nrf2. It does so without inducing any signs of toxicity, as assessed both in healthy human subjects and patients with chronic kidney disease. In addition to Nrf2 activation, RBT-3 also increases plasma and tissue levels of hepcidin, a well known cytoprotectant in animals. Phase III development with RBT-3 is expected to be in 2H, 2022, using the 505b2 pathway.