One Idea.
Two Companies. Thirty Years.
Before bexobrutideg had a name, before Nurix had a ticker symbol, before $460 million in pharma partnerships, there was a postdoctoral fellow at Baylor College of Medicine making mice that couldn't repair UV-damaged DNA. Arthur Sands was studying a gene called XPC. The knockout mouse he created became a model organism for skin cancer research. That was 1993. He was 27.
By 1995, he had co-founded a company. The idea: use gene knockout technology at industrial scale to figure out which proteins actually matter enough to become drug targets. It sounds obvious now. It wasn't then. Lexicon Genetics - later Lexicon Pharmaceuticals - spent 19 years proving the concept, generating over $450 million in revenue through alliances with Bristol Myers Squibb, Takeda, and Genentech, and studying nearly 5,000 genes through its Genome5000 program.
When Sands left Lexicon in July 2014, he didn't pause. He joined Nurix Therapeutics as CEO two months later. The thesis had shifted: instead of finding which proteins to target, the question became whether you could simply make unwanted proteins vanish. Targeted protein degradation - using the cell's own trash-disposal machinery to eliminate disease-causing proteins entirely - was the new frontier. Sands had watched drug resistance claim one cancer treatment after another. Degraders offered something inhibitors couldn't: you can't develop resistance to the absence of a protein.
"2025 was a defining year for Nurix, having advanced our potentially best-in-class BTK degrader, bexobrutideg, into pivotal development for patients with relapsed or refractory CLL."
- Arthur T. Sands, CEO, Nurix Therapeutics, January 2026Sands isn't a typical biotech CEO. He holds an M.D. and a Ph.D. in Cell Biology from Baylor, plus a B.A. in Economics and Political Science from Yale. That combination - the molecular biologist who can read a balance sheet, the economist who understands ligase biochemistry - shapes how Nurix operates. The company runs a proprietary DEL-AI drug discovery engine that pairs DNA-encoded library (DEL) screening with machine learning. It's not just a research tool. It's a competitive moat Sands spent years building, and it powers every program in Nurix's portfolio.
Degraders, E3 Ligases,
and the DEL-AI Engine
Every cell contains a system called the ubiquitin-proteasome pathway - a molecular trash disposal that marks proteins for destruction and grinds them down. E3 ubiquitin ligases are the enzymes that do the marking. For most of pharmaceutical history, drug hunters have tried to inhibit proteins: sit in the active site, block the function, hope the effect lasts. Sands and Nurix are playing a different game. They're co-opting the trash disposal to eliminate specific proteins entirely.
DEL-AI: The Discovery Engine
Nurix's proprietary platform starts with DNA-encoded library (DEL) technology - collections containing billions of small molecules, each tagged with a unique DNA barcode. Machine learning algorithms analyze screening data to predict which molecular scaffolds will recruit E3 ligases to target proteins, directing the cell's own degradation machinery. The result: a feedback loop that compresses years of medicinal chemistry into months. Every internal and partnered program at Nurix runs through this engine.
The platform has delivered three major types of molecules: bivalent degraders (small molecules that simultaneously grip a target protein and an E3 ligase, forcing them together for ubiquitin tagging), E3 ligase inhibitors (compounds that block ligases which suppress immune responses, effectively releasing the brakes on T cells and NK cells), and degrader-antibody conjugates (DACs) that use antibodies to deliver degraders directly to tumor cells. It's a toolkit that three of the world's largest pharmaceutical companies - Sanofi, Gilead Sciences, and Pfizer - have each paid to access.
The lead internal asset, bexobrutideg (NX-5948), degrades BTK - Bruton's tyrosine kinase, a signaling protein that B-cell malignancies and autoimmune conditions depend on. Conventional BTK inhibitors like ibrutinib work until they don't: mutations in the BTK active site render them useless. Bexobrutideg sidesteps this entirely by degrading BTK protein rather than blocking it. The data from Phase 1 - an objective response rate of 83% in chronic lymphocytic leukemia patients, including those whose disease had progressed through both a BTK inhibitor and BCL2 inhibitor - drew enough attention that in October 2025, Nurix initiated the DAYBreak CLL-201 pivotal Phase 2 study.
Nurix Clinical Pipeline
A wholly owned portfolio plus partnered programs with Sanofi, Gilead, and Pfizer.
| Asset | Target | Indication | Stage | Partner |
|---|---|---|---|---|
| Bexobrutideg NX-5948 |
BTK degrader | Relapsed/Refractory CLL | Pivotal Ph2 | Wholly owned |
| Bexobrutideg tablet formulation |
BTK degrader | Autoimmune / Inflammatory | Phase 1 | Wholly owned |
| Zelebrudomide NX-2127 |
BTK + IKZF1/3 degrader | B-cell Malignancies | Phase 1 | Wholly owned |
| NX-1607 | CBL-B inhibitor | Solid Tumors / Oncology | Phase 1 | Wholly owned |
| GS-6791 | IRAK4 degrader | Autoimmune | Phase 1 | Gilead Sciences |
| NX-3911 | STAT6 degrader | Autoimmune | Preclinical | Sanofi |
| Multiple programs | Undisclosed | Cancer / Autoimmune | Discovery | Pfizer |
The Long Arc
of Arthur Sands
Three Degrees,
One Thesis
A Yale economics major who ended up with an M.D. and a Ph.D. in Cell Biology. The combination isn't incidental.
Sands continues to serve as adjunct professor in the Department of Human and Molecular Genetics at Baylor College of Medicine - a thread of connection to the lab bench he never fully cut. He is also named as inventor on numerous patents related to the discovery of human genes and their use in therapeutic development.