OUR PIPELINE
One Molecule, MARY1. A Disciplined Clinical Sequence.
Every Expansion Earned By Data
CSA-AKI, the first clinical wedge, is chosen for interpretability, not market size. MARY1’s drug development is designed to produce clean interpretable proof in CSA-AKI patients. No clinical data exist yet in any indication. That proof earns the broader AKI and kidney franchise plus platform expansion. A second program applies MARY1 to non-opioid pain, gated on its own data.
PIPELINE AT A GLANCE
KIDNEY PROGRAMS
Cardiac Surgery Associated AKI (CSA-AKI)
Kidney Transplant Delayed Graft Function (DGF)
AKI to CKD Prevention
PAIN PROGRAM
Non-Opioid Pain (acute, CIPN, inflammatory)
PLATFORM EXPANSION
CKD, Diabetic Kidney Disease (DKD), Aging
Neurodegeneration
Each indication development is data gated by the ones before it – CSA-AKI proof of concept unlocks DGF; CSA-AKI and DGF proof of concept together unlock AKI to CKD Prevention. Pain is gated on its own data, starting with the focused pain lead indication and expanding to opioid sparing use and chronic neuropathic pain.
CARDIAC SURGERY ASSOCIATED
ACUTE KIDNEY INJURY
Predictable injury window, risk-enriched Kidney Disease: Improving Global Outcomes (KDIGO) stage 2–3 cohort, serial pharmacokinetic (PK)/PD sampling, and utilization-linked endpoints for which hospitals are now accountable under CMS TEAM. Rodent ischemia reperfusion data support both prophylactic and treatment dosing.
KIDNEY TRANSPLANT DGF
Unlocked by CSA-AKI proof of concept. A second time-anchored ischemia reperfusion injury setting where exposure–PD–recovery coherence from CSA-AKI can be replicated in humans. Kidney transplant is the preferred treatment for end-stage kidney disease, improving quality of life and survival compared to dialysis. Ischemia reperfusion injury during cold storage — cold ischemia time — ≥ 19 hours is associated with around 30% DGF, higher kidney discard rates, increased resource utilization, and worse outcomes such as kidney rejection, failure, and death.
AKI TO CKD PREVENTION
Unlocked by CSA-AKI and DGF data together. Day 30 rodent ischemia-reperfusion AKI data show an antifibrotic signature supporting the biological rationale. No clinical data exists yet in this indication. Each year, >1M patients in the US/EU experience AKI; 15–30% progress from AKI to CKD within a year, adding $5–24B in hospitalization, dialysis costs, and profound quality-of-life loss.
PLATFORM EXPANSION
MARY1's biology has preclinical read-across into CKD, DKD, aging, neurodegeneration, and rare kidney diseases. These are chronic and/or metabolically driven conditions — distinct from the shared ischemia-reperfusion (I/R) mechanism across CSA-AKI, DGF, and AKI→CKD prevention — and are pursued only as CSA-AKI and follow-on data earn expansion.
Same molecule, separate clinical path. In mouse models MARY1 produces analgesia in acute, inflammatory, and neuropathic pain, without meaningful opioid receptor binding. The lead pain indication has a predictable onset and validated patient-reported endpoints. No MARY1 clinical data exist yet.
NON-OPIOID PAIN