If you’ve been reading the Voyager for any stretch, you know targeted protein degradation is having a moment.
We’ve written about EpiBiologics degrading EGFR from the outside of the cell. Nested hit 38% in melanoma with a pan-RAF/MEK molecular glue. Dewpoint pivoted hard to go after MYC after laying off 70% of staff. Gilead paid Kymera $45M to option a CDK2 glue. Roche is paying C4T up to $1B for DACs.
The field isn’t emerging anymore. It’s here.
Nurix Therapeutics brought three preclinical readouts to AACR 2026, and the package tells you exactly why degraders are beating kinase inhibitors on hard targets.
Nurix AACR 2026 pipeline
NRX-0305 — pan-mutant BRAF degrader
Oral · CNS-penetrant · Class 1, 2, 3 BRAF mutants
NRX-4972 — Aurora Kinase A degrader
CNS-penetrant · Kills enzymatic + scaffolding function
NX-1607 — CBL-B inhibitor (not a degrader)
Oral · Reverses T-cell exhaustion · Synergy with PD-1
Start with NRX-0305, the BRAF degrader.
BRAF inhibitors already exist.
Dabrafenib. Encorafenib. Vemurafenib.
They work, but they work on Class 1 mutations (V600E/K) and patients eventually relapse. Part of the reason is that BRAF doesn’t only signal through its kinase activity. It also acts as a scaffold, holding other proteins in place to drive signaling even when the kinase is blocked. A kinase inhibitor shuts down the enzyme. It can’t touch the scaffold.
A degrader just removes the whole protein. Enzyme gone. Scaffold gone. Problem gone.
NRX-0305 is CNS-penetrant, meaning it can cross into the brain. BRAF-mutant melanoma frequently metastasizes to the CNS, and current therapies struggle there. If preclinical data holds up, this could be a meaningful step forward for patients with brain mets.
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NRX-4972 is the one that shows off the modality. Aurora Kinase A (AURKA) has been a hot target for 20 years. Every kinase inhibitor attempt has underperformed in the clinic. The reason, increasingly, looks like AURKA’s scaffolding role: it stabilizes MYC-family proteins, and that stabilization is arguably more important than its kinase activity for tumor survival.
Kinase inhibitors can’t disrupt scaffolding. Degraders can. This is the clean case for why TPD exists as a modality.
NX-1607 is different. It’s actually not a degrader. It’s an oral small molecule inhibitor of CBL-B, which is itself an E3 ligase that tags T-cell activation proteins for destruction. Inhibit CBL-B, and you prevent those activation signals from getting degraded. T cells stay active longer. In the data, Nurix showed enhanced T-cell activation and synergy with PD-1 blockade.
It’s basically trying to be an oral checkpoint inhibitor. It’s already in Phase 1 in solid tumors.
The strategic read on Nurix: they have a lead program (bexobrutideg, the BTK degrader, in Phase 2 for r/r CLL) that’s the monetization anchor. The three AACR assets are pipeline depth. Sanofi already paid up to $2.5B in milestones across five targets. Gilead extended their IRAK4 deal. Seagen (now Pfizer) is into DACs for up to $3.4B.
Nurix sits on ~$550M in cash. They’re not desperate. They’re building a platform-backed pipeline that big pharma keeps paying to access.
And while everyone else at AACR is showing individual molecules, Nurix showed up with three.Â
