Mito Innovations: Mitochondrial Repair Medicine Company. Renal-First Clinical Path
Our Science
MARY1 is a small molecule and selective 5 Hydroxytryptamine 2B receptor (5HTR2B) antagonist designed to restore mitochondrial homeostasis and accelerate renal recovery after injury. MARY1 re-engages a PGC-1α linked mitochondrial repair program, with downstream effects on mitochondrial biogenesis and FAO/ETC biology.
Our research in cells and animal models confirms MARY1 relevance across species in proximal tubules, mechanistic dependence through PI3K/AKT and RAS/MEK/ERK signaling, and measurable renal pharmacodynamic readouts linked to mitochondrial biogenesis, bioenergetics and recovery. Preclinical acute kidney injury models showed directional improvement in mitochondrial function, injury/repair markers, and support translation to recovery endpoints in patients.
Applications
Current treatment for acute kidney injury is largely supportive. Mito is developing MARY1 to accelerate renal recovery, with cardiac surgery associated acute kidney injury (CSA-AKI) as the initial clinical wedge. Kidney transplant delayed graft function (DGF) is the first contingent follow-on indication, and AKI to CKD prevention a later durability opportunity, all supported by our preclinical data.
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MARY1’s first planned clinical entry is CSA-AKI within acute AKI. Acute AKI affects 20–30% of hospitalized patients, and CSA-AKI occurs in 25–40% of cardiac surgery patients, with even higher risk in patients with underlying chronic kidney diseases (CKD). We are pursuing CSA-AKI first because injury timing, sampling, and recovery kinetics are more interpretable than in heterogenous AKI settings.
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DGF occurs in 20–40% of deceased donor kidney transplant and is associated with worse early graft function and higher later graft loss risk. DGF is the first follow-on indication under consideration because it shares the same time anchored inpatient logic as CSA-AKI and offers a second interpretable renal recovery setting.
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A meaningful fraction of high-risk AKI survivors progress to CKD over time. MARY1 administration has shown early durability signals in preclinical models, supporting AKI to CKD prevention as a later, data-gated opportunity after coherence is established across exposure, pharmacodynamics, and recovery in acute renal settings.
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Broader renal and selected non-renal indication expansion informed by preclinical data may be possible over time, but the current strategy is renal first with focus to clinically derisk the core CSA-AKI program
Our Team
Dr. Schnellmann originated the MARY1 renal repair thesis and leads target/MOA confirmation and translational PD. He has published extensively in renal recovery, mitochondrial biology, and 5HTR2B pharmacology.
Prof. Rick G. Schnellmann, PhD
Founder & Scientific Lead | Endowed Chair
Dean Emeritus (UA College of Pharmacy)
Veena Krishnappa, PhD, MVSc, BVSc
Founding Advisor | Strategy & Execution
Dr. Krishnappa trained in veterinary medicine and regenerative medicine leads the build to CSA-AKI PoC. She brings experience in business development, operations, strategy, venture creation, and investment.