OUR APPROACH
Designed around what the
AKI field has taught us.
MARY1 and its clinical strategy are built on a clear reading of why acute kidney injury has resisted clinical translation — and a disciplined plan to address each of those challenges directly.
The development challenge
Clinical programs in CSA-AKI have consistently failed to demonstrate efficacy in humans. The reasons are multifactorial — mechanistic, translational, and endpoint-related. What the field has established is how difficult it is to prove benefit in this setting without confirmed target engagement in the kidney and recovery endpoints that can be attributed to mechanism.
CSA-AKI remains the most interpretable setting to change this. A predictable, time-anchored injury window. A defined, risk-enriched patient population. Serial plasma and urine sampling. And recovery endpoints that now carry direct payer accountability under CMS TEAM.
The opportunity is not to repeat what has been tried. It is to bring a mechanistically grounded recovery medicine into the setting most likely to produce a clean, attributable signal — and to confirm that signal at every step.
What MARY1 does differently
Recovery and prevention biology
MARY1 activates the kidney's own mitochondrial repair program — reducing injury severity before an anticipated event and driving recovery after one occurs. A dual-window profile that no prior AKI program has entered the clinic with.
A confirmed causal mechanism
The mechanism is not a hypothesis. It is causally established in preclinical science — confirmed by receptor knockdown and pathway inhibition, and validated across species and human proximal tubule cells.
Attribution built in, not retrofitted
Prespecified biomarkers will confirm target engagement at every clinical dose — making it possible to know whether the drug is working in the kidney before reading an endpoint.
A gate-driven clinical path
Each stage produces exactly one deliverable: the evidence standard required for the next financing, regulatory, or partnership decision. CSA-AKI first. Expansion earned by data. No gate is a black box.
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 CABG episode costs. The clinical endpoints are designed to map directly to the economic case, with HEOR prewired from day one.
INVESTORS
Decision-grade data at every gate
Each development stage is designed to produce the evidence standard needed for the next financing event. Preclinical mechanism is confirmed. Exposure, PD, and recovery trajectory are the defined targets of the clinical program.
STRATEGIC PARTNERSHIPS
A renal platform with earned expansion
Preclinical evidence spans CSA-AKI, kidney transplant, diabetic kidney disease, and aging kidney. The CSA-AKI wedge is the capital-efficient entry. Expansion into a broader renal franchise is earned — not assumed — through clinical data.