Novo, Are You Listening? Vikingtide is Your Chance to Compete with Tirzepatide.

Original posted at obesity.news/ on Jan 11, 2026

Viking Therapeutics appears to have timed this week’s “Vikingtide” data release deliberately, dropping the long awaited VK2735 Phase 2 data just ahead of JPM 2026 in what many investors are calling a classic “put the tape out” moment.

These data have existed in pieces for years. What changed this week is that they are now fully published, peer reviewed, and available for annotation by anyone trying to decide whether VK2735 is merely promising or a legitimate heavy-weight (reducing) contender.

The top-line weight loss signal was already circulating, given this trial ended in early 2024. What matters now is that we have the full accounting, including who tolerated the drug, who did not, and why VK2735 behaves the way it does biologically.

In the 13 week Phase 2 study, patients on the highest 15 mg dose lost an average of 14.7% of their body weight. That places VK2735 squarely in the same conversation as semaglutide at its maximum dose and tirzepatide at lower doses, but achieved in just three months vs. more than a year with tirz and sema.

Per the usual with obesity injectables, the study population skewed heavily female, roughly 66% to 77% depending on dose group, with starting BMIs clustered between 36 and 39. This was not a borderline obesity cohort, these were patients with high BMI’s. The signal held across groups.

Viking has also shared data that helps explain why VK2735 hits as hard as it does. Scientists measure how strongly a drug works by looking at how easily it turns on switches in the body called receptors. If you think of the peptide like a key, our body’s receptors are the lock. The GLP-1 and GIP receptors (the lock) help control hunger and metabolism. The numbers reported, called IC50 values, show how much drug (the key) it takes to “open” half of those receptors.

For VK2735, it takes 188 nM (a measurement of drug concentration) to activate half of the GLP-1 receptors and 325 nM to do the same for GIP. For those of us without a pharmacology degree, VK2735 is not necessarily about grabbing receptors tighter than tirzepatide. Instead, it appears to stay active longer and keep those locks open on for more time. That longer and stronger signal might help explain the rapid weight loss seen in Phase 2, and it also helps explain why side effects increase as doses rise.

On cardiometabolic measures, the drug also delivered. In the 15 mg group, systolic blood pressure fell by 11 points and diastolic by 5 points. Those are notable changes in a population where hypertension is often part of the underlying disease.

The tolerability trade-off

At doses of 5 mg and above, VK2735 produced higher rates of nausea and vomiting than what has been reported historically for tirzepatide. Diarrhea appeared somewhat less frequent. That nuance matters, but the more important signal was discontinuation.

At the 15 mg dose, about 20% of participants stopped treatment due to treatment emergent adverse events. In lower dose cohorts, discontinuation was closer to 10%. That still compares a bit unfavorably with Lilly’s SURMOUNT-1 data, where tirzepatide discontinuation ranged from 4% to 7%. Perhaps something that could be addressed in phase 3 titration schedules.

Defining the current boundary

What is striking, though, is how this asset is positioned relative to the broader market conversation.

VK2735 has (unlike semaglutide / tirzepatide / retatrutide) not yet become a gray market peptide staple, not because it lacks potency, but because it lacks name recognition and viral fanfare. Tirzepatide and retatrutide dominate those channels because they are familiar, searchable, and already embedded in the zeitgeist of obesity medicine. VK2735, despite being discussed on our channels for years, has not crossed that cultural threshold yet. Given the data now on the table, that gap feels temporary.

On paper, VK2735 compares favorably to tirzepatide in ways that matter early in development. The signaling strength is real. The speed of weight loss is real. While Phase 3 will ultimately determine durability and long term tolerability, the Phase 2 signal is strong enough to place VK2735 firmly on the list of assets that will be copied, discussed, and eventually mimicked once awareness catches up.

Not just a peptide story

Lilly’s obesity pipeline is deep, layered, and moving toward market domination with the momentum of a freight train. Novo Nordisk’s is beginning to resemble cable TV in a Netflix and Hulu world, familiar, entrenched, and increasingly constrained. Beyond squeezing more life out of semaglutide, Novo’s near term strategy hinges on GLP-1 plus amylin agonism as a counter to GLP-1 plus GIP, a combination that still lacks any real world proof.

Novo’s failed attempt to acquire Metsera only sharpened this reality. They tried to buy future relevance and ultimately lost out to Pfizer. The fact that regulators were already uncomfortable with that bid suggests any future move would need to be cleaner, more focused, and easier to defend.

VK2735 fits that profile unusually well. It is a single asset with a clear mechanism, strong early data, and an obesity focus that aligns directly with Novo’s core franchise. It does not require platform integration. It does not dilute strategy. It offers something Novo currently lacks: a credible, real world tested next wave injectable that may slow or reverse Lilly’s accelerating capture of market share.

That does not mean a deal is imminent, or even inevitable. It does mean VK2735 now occupies a different strategic category than it did before this data release.

It is no longer just a promising up and coming molecule. It is an injectable asset in phase 3 with an oral version right behind it. It has enough signal to attract copycats, enough data to attract buyers, and so far enough differentiation to matter in the current obesity duopoly where Novo’s pipeline is starting to look a little… Thin.

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