

Merck just dropped $400 million on a Chinese biotech's preclinical cancer drug targeting a protein scientists called "undruggable" for 40 years. The KRAS G12D race is on, and Merck's gamble says everything about where Big Pharma is shopping for its next blockbuster.
For decades, scientists called KRAS G12D "undruggable." Merck just bet $400 million that someone finally cracked it.
The pharma giant signed a deal with SciBrunch Therapeutics, a Chinese biotech most people have never heard of, to license a preclinical oral cancer drug called SPR2015. The total deal could be worth up to $2.13 billion with milestones. And the drug hasn't even entered human trials yet.
That's not reckless spending. That's a signal of just how desperate Big Pharma is to own a piece of the hottest target in oncology.
KRAS is a protein that tells cells when to grow. When it mutates, it gets stuck in the "on" position, like a light switch jammed with duct tape. Cells keep dividing and dividing. That's cancer.
The G12D mutation is one of the most common versions of this problem. It shows up in pancreatic, colorectal, and lung cancers, some of the deadliest tumor types on the planet. For 40 years, no one could build a drug that would grab onto this protein and shut it off.
The breakthrough came from a cousin: KRAS G12C. That mutation has a reactive cysteine (think of it as a molecular hook) that chemists could latch onto with a covalent bond. Drugs like sotorasib proved direct KRAS inhibition was possible. The "undruggable" label started peeling off.
But G12D doesn't have that hook. There's no convenient cysteine to grab. Building a drug for G12D is like trying to pick a lock without a keyhole. Scientists had to get creative.
SciBrunch's approach is clever. SPR2015 is described as a molecular glue: it recruits a naturally occurring protein called cyclophilin A to form a three-way complex with mutant KRAS G12D. Picture it like a bouncer who grabs a troublemaker's arm, then calls over a friend to hold the other one. Together, they pin the target down.
Critically, SPR2015 targets KRAS G12D in its , the form that's actually driving cancer. And it's designed to leave normal (wild-type) KRAS alone, which matters because you don't want to shut down healthy cell signaling across the entire body.

Kodiak Sciences failed three consecutive Phase 3 trials and was left for dead. Then its redesigned wet AMD study matched Eylea's efficacy while more than half of patients went six months between injections, nearly tripling the stock overnight.


Join thousands of biotech professionals who start their day with our free, daily briefing.
In preclinical testing, the drug showed nanomolar antiproliferative activity (extremely potent cell-killing at tiny concentrations) across multiple KRAS G12D-mutant cell lines. It also shrank tumors in animal models and looked clean in a 28-day repeat-dose toxicology study in rodents.
Oh, and it's oral. That's a big deal. Many early KRAS G12D drug candidates struggled with the basic medicinal chemistry challenge of turning a potent lab compound into a pill that survives the digestive system and reaches tumors at useful levels. An oral drug with good pharmacokinetics is table stakes for a commercially viable cancer medicine; it's just really hard to pull off for this target.
Merck isn't the only one chasing KRAS G12D. The race has turned into a full sprint, and SPR2015 is actually behind several competitors that are already in human trials.
Astellas has pushed its candidate, setidegrasib, into a Phase 3 study in lung cancer. That's one of the most advanced programs in the field right now. Revolution Medicines is running a Phase 3 trial for zoldonrasib in first-line metastatic pancreatic cancer. Verastem expanded into three Phase 2 registration-directed studies across pancreatic, lung, and colorectal cancers in 2026. Even Incyte has a Phase 3 trial running.
So why would Merck pay $400 million upfront for a drug that's still in the lab? Two reasons.
First, differentiated mechanism. The molecular glue approach and cyclophilin A recruitment could give SPR2015 a different efficacy or safety profile compared to the non-covalent inhibitors already in the clinic. In a crowded field, being different is an asset.
Second, combination potential. Merck already has calderasib (MK-1084), a KRAS G12C inhibitor with Breakthrough Therapy designation in combination with its blockbuster KEYTRUDA. A KRAS G12D drug would let Merck run the same playbook across the broader KRAS-mutant patient population. It's not just buying a drug; it's buying a platform.
This deal is part of a pattern that's now impossible to ignore. U.S. drugmakers have been raiding Chinese biotech pipelines at an accelerating pace. Through just the first half of 2025, American pharma companies signed 14 deals worth $18.3 billion to license drugs from China-based companies. By some estimates, nearly half of all U.S. in-licensing transactions in 2025 were sourced from Chinese partners.
Pfizer paid $1.25 billion upfront for a PD-1/VEGF bispecific antibody from 3SBio, with total deal value reaching roughly $6 billion. Pfizer then followed up with Innovent Biologics on a deal covering 12 early-stage cancer medicines worth up to $10.5 billion. Bristol Myers Squibb and GSK have both done major deals with Hengrui.
The commercial logic is straightforward. Chinese biotechs are producing high-quality assets at valuations that look cheap compared to equivalent Western programs. They often already have preclinical or early clinical data, which means the U.S. buyer gets a head start without paying late-stage prices. It's like shopping at an outlet mall where the brands are just as good but the sticker price is lower.
Merck got global rights to develop, manufacture, and sell SPR2015 anywhere in the world. The deal is already closed. Beyond the $400 million upfront, SciBrunch could earn up to $1.73 billion in milestone payments if the drug hits its development and commercial targets.
That's a big "if" for a preclinical asset. Most drugs that look good in mice never make it through human trials. The history of cancer drug development is littered with spectacular preclinical results that crumbled on contact with actual patients.
But Merck clearly believes the KRAS G12D opportunity is large enough, and SPR2015's mechanism is differentiated enough, to justify the risk. With over 30 registrational studies already running in its oncology pipeline, Merck isn't betting the farm on one molecule. It's adding another card to what's already a strong hand.
The real test comes when SPR2015 enters first-in-human trials. That's when we'll find out whether this molecular glue sticks, or if $400 million just became the most expensive science experiment of 2026.
Novartis's remibrutinib just beat an older MS drug in two large Phase 3 trials, but the real story is *how* it works. Unlike treatments that destroy or trap immune cells, this BTK inhibitor simply tells them to stand down. And in a competitive race littered with safety failures, that distinction could be worth billions.