

SK Biopharmaceuticals just dropped $315 million on a Parkinson's drug that hasn't even picked its final molecule yet. The dual-target approach is scientifically intriguing, but the timing, right after the field's biggest clinical failure, makes this one of 2026's boldest preclinical bets.
Most preclinical drugs don't have names yet, let alone nine-figure price tags. But SK Biopharmaceuticals just signed a deal worth up to $315 million for 1ST-104, a Parkinson's disease candidate from South Korean biotech 1st Biotherapeutics that hasn't even finished selecting its final drug candidate.
Read that again. The compound is so early that the partner still needs to pick which version of the molecule moves forward. And SK is already writing checks.
The deal includes a $1.8 million upfront payment, another $1.8 million when the drug candidate is formally selected, and then a waterfall of development, regulatory, and sales milestones that could reach $315 million total. SK also made a $2.2 million equity investment in 1st Biotherapeutics, signaling this isn't just a licensing transaction; it's a relationship.
So why would anyone pay this much for something this early? The answer sits at the intersection of two Parkinson's targets that scientists have been chasing for years.
1ST-104 is designed to hit two kinases (enzymes that drive cell signaling) at once: LRRK2 and c-Abl. Both have been linked to Parkinson's disease, but nobody has tried blocking them simultaneously in a single drug before.
Think of it like fixing a leaky house. Most companies are patching one hole at a time. 1st Biotherapeutics wants to patch two holes with the same piece of tape.
LRRK2 is probably the most well-known genetic target in Parkinson's research. Mutations in this gene are among the strongest risk factors for the disease, and overactive LRRK2 signaling messes with the cell's recycling machinery (the endolysosomal system). That leads to a buildup of toxic alpha-synuclein protein, which is the hallmark of Parkinson's.
c-Abl works a different angle. When this kinase gets overactivated, it accelerates neuroinflammation, damages dopamine-producing neurons, and disables parkin, a protein that normally protects the brain. In animal models, blocking c-Abl has reduced neuron loss and improved motor function.

Bristol Myers Squibb just killed a $100 million drug program before its trial even finished, and the fallout goes way beyond one company's balance sheet. The world's only clinical-stage degrader-antibody conjugate is now dead, leaving an entire emerging drug class without proof it works in humans.


Join thousands of biotech professionals who start their day with our free, daily briefing.
The idea behind 1ST-104 is that hitting both pathways could offer broader protection than targeting either one alone. It's a compelling hypothesis. But there's an important caveat: no published data yet proves that dual inhibition actually works better than going after just one target.
1ST-104 is specifically a "Type II" LRRK2 inhibitor, which means it binds the enzyme in its inactive shape rather than its active one. This is more than a technical footnote.
Most LRRK2 drugs in development are Type I inhibitors that grab the enzyme while it's switched on. Type II inhibitors take a different approach, locking onto the off-switch conformation instead. In preclinical work, 1ST-104 has shown it can cross the blood-brain barrier (the protective shield around the brain that blocks most drugs) and hit its intended targets selectively. Those are promising early signs, though the company hasn't published detailed efficacy data from disease models.
This deal didn't happen in a vacuum. It landed just months after the most advanced LRRK2 inhibitor in the world essentially failed.
Biogen and Denali's BIIB122 was the poster child of the LRRK2 field. It reached a Phase 2b trial called LUMA in patients with early Parkinson's. In May 2026, LUMA missed its primary endpoint, meaning the drug didn't show a meaningful benefit on the main measure it was designed to hit. Biogen and Denali pulled the plug on developing BIIB122 for general (idiopathic) Parkinson's, though a smaller study in patients who actually carry LRRK2 mutations is still running.
That failure sent a chill through the LRRK2 community. And yet here's SK, just four months later, betting big on a preclinical LRRK2 program. The dual-target angle with c-Abl is clearly part of the pitch: if LRRK2 alone wasn't enough, maybe LRRK2 plus c-Abl will be.
It's a reasonable argument. But it's also the kind of reasoning that has burned Parkinson's investors many times before. No disease-modifying therapy for Parkinson's has ever been approved. A GCase modulator (another genetically validated target) also posted a negative readout in 2026. The graveyard is getting crowded.
This deal makes more sense when you zoom out and look at SK Biopharmaceuticals' broader strategy. The company is going all-in on neuroscience.
In September 2026 (the same month as this deal), SK reorganized its entire CNS research operation into a dedicated Neuroscience Division reporting directly to the CEO. They hired a new leader, Kim Tae-ho, to run it. They also have an internal Parkinson's program called SKL32276, a GCase activator in preclinical development, plus an AI-driven neuroimmune collaboration with Insilico Medicine.
The pattern is clear: SK isn't making a one-off bet. It's building a Parkinson's and neurodegeneration portfolio through targeted licensing deals, equity investments, and collaborations rather than splashy acquisitions.
Preclinical neurology deals have been getting bigger across the board. In 2025, Novartis paid $200 million upfront (with a total value up to $2 billion) to Arrowhead for a preclinical Parkinson's siRNA asset. GSK struck a deal with ABL Bio worth up to $2.7 billion for preclinical neuroscience programs with blood-brain barrier shuttle technology.
By comparison, SK's $1.8 million upfront is modest. The $315 million total looks large on paper, but the vast majority of that value is locked behind sales milestones. In other words, 1st Biotherapeutics only sees the big money if the drug actually reaches patients and sells.
That's a milestone-heavy structure, which is standard for preclinical deals. It limits SK's downside while giving 1st Biotherapeutics a shot at a transformative payout.
This deal is a bet that two targets are better than one in Parkinson's disease, placed at a moment when the leading single-target approach just stumbled. SK Biopharmaceuticals is paying a small amount now for the option to own a potentially differentiated asset later.
The science is intriguing. The logic is sound. But Parkinson's disease modification remains one of biotech's hardest problems, and no amount of deal engineering changes the fact that 1ST-104 still has to prove it works in actual patients. That proof is years away.
For now, this is a story about conviction: a company willing to write a preclinical check with a lot of commas in it, in a therapeutic area where the biggest players keep striking out. Whether that conviction looks brilliant or foolish will depend on data that doesn't exist yet.
Novartis killed its ALS drug lifonebart after a Phase 2 trial missed every endpoint, adding to a decades-long streak of industry failures against one of neuroscience's most stubborn diseases. But the company's next move tells a different story.