NADI
nah · dee
Early-stage research preview
Shared by invitation only
We found it in the genetics of 500,000 people. We're building the RNA therapeutic that addresses it at the source.
The biology
Your cells replenish NAD+ through a salvage pathway — recycling nicotinamide into the cofactor that powers mitochondria, sirtuin activity, and DNA repair. It works well, until one enzyme intercepts the process.
NNMT — nicotinamide N-methyltransferase — methylates nicotinamide before it can reach the salvage pathway, diverting it into an excretable waste product. In aging liver, visceral fat, and vascular tissue, NNMT is chronically overexpressed. NAD+ levels fall quietly and persistently as a result.
The consequences are familiar: insulin resistance, impaired mitochondrial efficiency, vascular inflammation, accelerated metabolic aging. The upstream cause — this specific enzyme, in these specific tissues — has not been adequately targeted.
NAD+ supplements flood the precursor pool. We target the drain.
NNMT reaction
Downstream consequences
The evidence
We didn't start with a molecule. We started with human genetics — asking what the body's own natural experiments reveal about NNMT. Three independent data sources pointed to the same conclusion.
FinnGen DF13 · 500,348 participants
0
cardiovascular cases · p = 1.3 × 10⁻⁷
NNMT variants associate with broad cardiovascular disease, atrial fibrillation, aortic aneurysm, and cardiometabolic medication use across multiple independent phenotypes.
Human Protein Atlas · tissue expression
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nTPM · liver is NNMT's dominant tissue
NNMT's highest expression is in liver, followed by aorta (15,808 nTPM) and coronary artery (13,041 nTPM) — the exact tissues where cardiometabolic disease originates.
GalNAc-siRNA · clinical precedent
0
approved drugs · same delivery mechanism
Inclisiran, givosiran, lumasiran, vutrisiran — all approved drugs using GalNAc-conjugated siRNA to silence hepatic targets. The delivery infrastructure exists in clinical practice.
The method
Most drug programs begin with a molecule. We begin with a question: what does the body's own genetic architecture tell us about which targets are both causally effective and safe in humans?
01
Genomic validation
Loss-of-function variant data from FinnGen, UK Biobank, and Open Targets identifies genes where genetic reduction is causally linked to cardiometabolic disease and demonstrably safe in the human population. The screen happens before the first experiment.
Mendelian randomization02
RNA therapeutic design
For targets where expression, safety, and delivery profile align, we design GalNAc-siRNA constructs for hepatocyte-selective mRNA knockdown. This modality bypasses the bioavailability failures that have held back every small molecule NNMT program to date.
GalNAc-siRNA03
IP-anchored partnering
We file method-of-treatment patents on validated programs, generate hypothesis packages, and partner with clinical-stage organizations for development execution. Asset-light by design until the data supports building more.
B2B licensingThe team
We are at earliest company formation. Our founding team connects population health analytics and clinical trial methodology with PhD-level expertise in DNA/RNA circuit design.
We are not building a large organization. We are building a discovery engine and an IP portfolio — asset-light, computationally grounded, with experimental work focused on the specific proof points that matter for each program.
A small number of seats remain — as scientific advisors, experimental collaborators, or investors who understand that the most valuable entry point is before the data.
Co-founder · Business
Population health analytics, clinical trial methodology, healthcare data
Co-founder · Scientific
PhD, DNA/RNA circuit design and programming language architecture
CSO · Recruiting
RNA therapeutics postdoc, cardiometabolic or genomics background
Get involved
The right entry point is now — before experimental decisions are fixed, while the IP space is open, and when early contributions carry the most weight.
For scientists
Pressure-test the biology
We want people who will find the holes in the thesis before we spend money on it. If you work on NNMT biology, RNA therapeutics, or cardiometabolic genomics — 30 minutes of honest critique is worth more than enthusiasm.
Start a conversationFor builders
Build the discovery engine
We're building a computational platform running Mendelian Randomization at scale across biobank data. If you work in bioinformatics, data engineering, or computational biology and want equity-primary early involvement — this is early enough to matter.
Tell us what you doFor investors
The right time is before the data
We're raising a small pre-seed round from people who understand that human genetics in 500,000 people is a form of Phase 0 validation — and that AstraZeneca filing NNMT patents in January 2025 is the signal worth paying attention to.
Request the briefContact
We read everything. If you have a perspective on the science, a question about the approach, or want to understand the investment thesis — reach out directly.