We have a robust pipeline of programs to prevent disease progression, improve outcomes and protect against organ damage in cardiorenal diseases.
Reducing the risk of post op complications in cardiothoracic surgery
Slows progression of CKD
SnPP / FeS Progression of NASH
Limits damage associated with Cisplatin Induced Nephrotoxicity
Rénibus’ lead product, RBT-1, is a novel pharmacologic intervention combining stannous protoporphyrin and iron sucrose, induces a preconditioning protective effect on the kidney and other organs, upregulating production of protective proteins to prevent post operative complications following cardiothoracic surgery, including AKI, days in the ICU, time on ventilator, and hospital readmission rates. Pre-clinical and Phase I development is complete, and RBT-1’s Phase II trial 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) was initiated in April 2021 and is expected to be completed in Q4 2022. A pre-specified interim analysis was conducted following the enrollment of the first 60 patients, yielding statistically significant results in both the primary and several secondary endpoints (even though the study was not powered for this).
An End of Phase 2 Meeting with the FDA will take place in Q3 2022 and Renibus is planning to start a Phase 3 registration study in Q4 2022.
RBT-2 (Tetrahydrocurcumin) is an active metabolite of an antioxidant natural product that slows the progression of CKD 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/II studies are expected to start in Q1 2023.
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. A Phase III development program looking at how RBT-3 limits the damage associated with cisplatin-induced nephrotoxicity is expected to begin in the 2H, 2022, using the 505b2 pathway.