RENAL MITOCHONDRIAL MEDICINE
The Kidney Can Repair Itself. We Give It the Signal
MARY1 is a small molecule that targets a receptor not previously linked to renal mitochondrial repair — re-engaging the kidney's own repair program to both prevent acute injury and accelerate recovery once it occurs, while interrupting progression to chronic disease.
The first selective 5-hydroxytryptamine receptor 2B (5HTR2B) antagonist designed for renal mitochondrial repair — with a confirmed causal mechanism, a prespecified pharmacodynamic (PD) bridge designed to translate from preclinical science to human proof, and a clinical strategy built for the setting most likely to produce a clean, attributable functional signal.
THE PROBLEM
Acute Kidney Injury Has No Medicine. Only Supportive Care.
Ischemia-reperfusion injury cuts off the kidney’s energy supply within minutes — proximal tubule ATP falls to its lower point almost immediately,
leading to acute kidney injury (AKI).
Current care is supportive only: fluids, monitoring, dialysis. Nothing available today repairs the underlying mitochondrial damage.
Injury that doesn’t fully resolve becomes chronic kidney disease (CKD) progressing to end stage kidney disease — a one-way trajectory with no
approved therapy to reverse it.
“The kidney’s repair machinery doesn’t need replacing. It needs a signal to turn function back on.”
MARY1 was designed to give it that signal.
20-30% of hospitalized patients develop acute kidney injury (AKI) and 20-30% of cardiac surgery patients develop AKI — our first proving ground for recovery biology in humans
Acute injury that doesn't fully resolve drives continued nephron loss and progression to chronic kidney disease (CKD) — a trajectory MARY1 is designed to interrupt
$38k is the incremental cost per CSA-AKI episode in dialysis, intensive care unit (ICU), and readmissions — now accountable to hospitals under the Centers for Medicare & Medicaid Services (CMS) Transforming Episode Accountability Model (TEAM)
OUR SOLUTION: MARY1
MARY1 is designed to re-engage the kidney’s own mitochondrial repair program — before an anticipated injury, and after one occurs.
Unlike supportive care, which manages injury after the fact, MARY1 targets the upstream mitochondrial reset switch — the same mechanism
that accelerates recovery after injury.
WHAT MAKES MARY1 DIFFERENT
FUNCTIONAL RECOVERY AND INJURY PREVENTION BIOLOGY
MARY1 targets the mitochondrial repair machinery that both prevents and reverses injury — with preclinical data supporting activity both before and after injury occurs. A therapeutic thesis built on activating recovery, not blocking a single injury signal.
A CAUSAL, CONFIRMED MECHANISM
5HTR2B antagonism re-engages PGC-1α–linked mitochondrial repair. Receptor knockdown and signaling pathway inhibition confirm this is causal — not correlative. Validated in human proximal tubule cells.
A MEASURABLE PHARMACODYNAMIC BRIDGE
A panel of injury, repair, and functional recovery biomarkers — validated preclinically, being qualified as clinical assays — designed to confirm target engagement in humans.
PATIENTS & CLINICIANS
An active recovery tool, not more waiting
MARY1 is designed to give clinicians a pharmacological tool to drive tubular repair, reduce dialysis dependence, shorten ICU stays, and protect long-term kidney function — in patients who currently have no disease-modifying option.
PAYERS & HEALTH SYSTEMS
Recovery economics, directly measurable
Under CMS TEAM (January 2026), ~741 hospitals are accountable for 30-day coronary artery bypass graft (CABG) episode costs, with health economics and outcomes research prewired from day one.
INVESTORS
Decision-grade data at every gate
Each development stage produces the evidence standard needed for the next financing/partnering event — exposure, PD, and recovery trajectory are the defined targets.
STRATEGIC PARTNERSHIPS
A renal platform with earned expansion
CSA-AKI is the capital-efficient clinical entry point for a broader renal franchise — DGF and platform expansion are earned through clinical data, not assumed.
MARY1 AT A GLANCE
ASSET
MARY1 — selective 5HTR2B antagonist
LEAD INDICATION
Cardiac Surgery Associated-Acute Kidney Injury (CSA-AKI)
THERAPEUTIC APPROACH
Reestablish mitochondrial homeostasis — injury prevention and severity reduction, and functional recovery.
ADMINISTRATION
IV, perioperative — prophylactic or intervention dosing
DEVELOPMENT STAGE
Toward IND-enabling Studies
PRECLINICAL FOUNDATION
Rodent ischemia-reperfusion injury AKI and AKI to CKD durability models — the core evidence behind CSA-AKI, DGF and AKI to CKD Prevention. Translational bridge planned to extend this toward human physiology.
PLATFORM EVIDENCE
Additional data in CKD, diabetic kidney disease (DKD), and aging-kidney, pain & peripheral neuropathy, neurodegeneration, and rare kidney disease models to be pursued clinically only as near term data earns expansion.
REGULATORY STATUS
Preclinical — IND submission planned; no clinical data yet in any indication
COMPOSITION OF MATTER & METHOD OF USE
IP with exclusive worldwide license
PEER REVIEWED PUBLICATIONS
Covering MARY1, its pharmacology, effect on mitochondrial homeostasis & renal function recovery
SEED/SERIES A FUND MILESTONES
IND-enabling, first-in-human PK/PD, and interim CSA-AKI proof-of-concept (Phase 1b/2a)
If kidney recovery has been on your list of unsolved problems,
we'd welcome the conversation.
Payer incentives now reward recovery. The mechanism is proven causal. And this team already spans the scientist who built the biology and the operator executing the plan — that convergence is why now.
We're actively engaged with investors and strategic partners who understand the AKI field — its history, its potential, and what it takes to succeed where others haven't.
Everything here is in service of patients living with kidney disease, and the people who care for them. If that’s you and you’d like to share your experience, to inform our efforts developing medicines, reach out through the contact page.