Quick Comparison
| AT7687 | VK2735 | |
|---|---|---|
| Half-Life | Approximately 7-10 days, supporting once-weekly dosing | Approximately 144-168 hours (6-7 days), supporting once-weekly dosing |
| Typical Dosage | Phase 1 first-in-human trial: ascending single and multiple subcutaneous doses. Dose ranges and Phase 2 protocols still being established. The mechanism does not require dose escalation for tolerability the way GLP-1 drugs do — appetite is not the primary target. | Phase 2 (subcutaneous): doses of 2.5, 5, 10, and 15 mg once weekly with stepwise escalation. The 15 mg arm produced the maximum weight loss of 14.7% at 13 weeks. Oral formulation in Phase 1: 30-100 mg daily, dose escalation ongoing. |
| Administration | Subcutaneous injection (likely once weekly based on pharmacokinetics) | Subcutaneous injection (once weekly); oral tablet formulation in earlier development |
| Research Papers | 1 papers | 1 papers |
| Categories |
Mechanism of Action
AT7687
AT7687 is a long-acting GIP receptor antagonist designed to reduce fat storage rather than suppress appetite — a fundamentally different mechanism from every other obesity drug currently on the market or in late-stage development. The rationale is grounded in human genetics: loss-of-function variants in the GIP receptor are associated with lower body mass index and reduced cardiometabolic risk, suggesting that pharmacologically blocking GIP signalling should reproduce these protective effects.
GIP (glucose-dependent insulinotropic polypeptide) normally functions as a fat-storage signal — released from intestinal K-cells in response to food intake, it instructs adipose tissue to take up and store circulating fatty acids. By blocking the GIP receptor specifically on adipocytes, AT7687 prevents this fat-storage signal from being transmitted, leading to reduced lipid uptake into fat cells and a metabolic shift favouring fat oxidation in muscle and liver. Because the mechanism does not depend on suppressing hunger or slowing gastric emptying, the gastrointestinal side effects that limit GLP-1 drug tolerability are largely absent.
This mechanism is the conceptual mirror of MariTide (which combines GLP-1 agonism with GIP antagonism in a single molecule) — AT7687 isolates the GIP-antagonist component to test whether it can produce meaningful weight loss alone or in future combination with GLP-1 agonists. Antag Therapeutics' first-in-human Phase 1 results in 2026 showed acceptable tolerability with mild GI symptoms, plus reductions in LDL cholesterol and resting heart rate — early signals consistent with the predicted cardiometabolic benefit profile. Phase 2 trials are expected to define the magnitude of weight loss achievable in obese patients.
VK2735
VK2735 is a once-weekly subcutaneous dual GLP-1/GIP receptor agonist with a structure optimised for high potency and a clean tolerability profile. Dual incretin receptor activation produces complementary effects on appetite, glucose handling, and energy expenditure: GLP-1 receptor agonism delivers central appetite suppression through hypothalamic arcuate-nucleus signalling, slows gastric emptying, and triggers glucose-dependent insulin secretion, while GIP receptor activation amplifies the insulin response, supports beta-cell function, and modulates adipose tissue lipid handling.
The molecule's pharmacokinetic profile delivers sustained receptor exposure across a one-week dosing interval, achieved through structural modifications that enable albumin binding and resistance to proteolytic degradation. In the Phase 2 VENTURE trial, the 15 mg dose produced 14.7% mean body weight loss at 13 weeks — the fastest early weight loss observed for any obesity drug, with the loss curve still descending steeply at trial end. This rapid trajectory suggests substantially greater total weight loss would be achievable with longer dosing, and Phase 3 VANQUISH trials launched in 2026 are testing 68-week treatment durations to characterise the full magnitude of effect.
Viking is also developing an oral tablet formulation of VK2735 in parallel, which entered Phase 1 in 2024-2025. If both formulations succeed, Viking would have one of the most flexible GLP-1/GIP product profiles on the market — though as a small biotech company it faces significant manufacturing and commercial scaling challenges relative to Lilly and Novo Nordisk.
Risks & Safety
AT7687
Common
mild gastrointestinal symptoms (notably milder than GLP-1 agonists in early data), injection site reactions.
Serious
long-term effects on bone health unknown — GIP signalling has roles in bone metabolism.
Rare
limited human safety data so far. Cardiovascular profile in Phase 1 included reductions in LDL cholesterol and resting heart rate, suggesting a metabolically favourable safety signal.
VK2735
Common
nausea, vomiting, diarrhea, constipation, decreased appetite, injection site reactions. Discontinuation rates in Phase 2 were broadly similar to other GLP-1/GIP dual agonists.
Serious
pancreatitis, gallstones, possible muscle mass loss.
Rare
thyroid C-cell tumour class warning, severe allergic reactions. Long-term safety being established in Phase 3.
Full Profiles
AT7687 →
A novel obesity drug from Danish biotech Antag Therapeutics that takes a completely different approach — instead of suppressing appetite like all the GLP-1 drugs, it stops fat from being stored in the first place by blocking the GIP receptor in fat cells. First-in-human Phase 1 trial completed in 2026 showed it is well tolerated, with mild GI side effects, and produced reductions in LDL cholesterol and resting heart rate alongside weight loss signals.
VK2735 →
Viking Therapeutics' once-weekly weight loss injection that, like tirzepatide, hits both the GLP-1 and GIP receptors. In a 13-week Phase 2 trial it produced 14.7% mean body weight loss — the steepest early loss curve recorded for any obesity drug — and Phase 3 VANQUISH trials began in 2026. An oral tablet version is also in earlier development. Viking is one of the only small biotech companies competing directly with Lilly and Novo Nordisk in the GLP-1 space.