AT7687
Also known as: Antag GIP-Receptor Antagonist
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.
Dosage
Phase 1 ascending doses; protocol not yet established
Dosages shown are for research reference only. Always consult a qualified healthcare provider.
Administration
Subcutaneous injection (likely once weekly based on pharmacokinetics)
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Effects
Fat Storage Blockade
Blocks GIP receptor on adipocytes to prevent fat-storage signalling — a novel mechanism vs appetite suppression.
Lipid Profile
Reduced LDL cholesterol observed in Phase 1 first-in-human trial.
Cardiovascular
Resting heart rate reductions seen in early trial data.
GI Tolerability
Notably milder gastrointestinal side effects than GLP-1 class drugs in early data.
Mechanism of Action
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.
Regulatory Status
Not approved. Phase 1 first-in-human trial completed in 2026; Phase 2 in planning (Antag Therapeutics, Denmark).
Risks & Safety
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.
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Research Papers
1Published: October 1, 2024
AI Summary
In obese cynomolgus monkeys, AT-7687 (a GIP receptor antagonist) added to liraglutide produced about 16% weight loss versus 12% with liraglutide alone over 42 days. The combination also improved insulin, glucose and cholesterol; no human trials are published yet.
Frequently Asked Questions
What is 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.
What is AT7687 used for?
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.
What is the dosage for AT7687?
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.
What are the side effects of 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.
How does AT7687 work?
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.
How is AT7687 administered?
AT7687 is administered via subcutaneous injection (likely once weekly based on pharmacokinetics).
What is the half-life of AT7687?
The half-life of AT7687 is Approximately 7-10 days, supporting once-weekly dosing.
Is AT7687 legal?
Not approved. Phase 1 first-in-human trial completed in 2026; Phase 2 in planning (Antag Therapeutics, Denmark).
Sources. This profile is built from peer-reviewed papers indexed on PubMed, FDA-approved labelling where available, and published clinical guidelines. The 1 primary sources used are listed in the Research Papers section above, each linked to its PubMed entry. See our editorial standards for how we research and review peptide profiles.
Last reviewed. by the Peptide Reference Editorial Team. Spot an error? Email a correction.
Not medical advice. Information on this page is for educational and research reference only. Many peptides covered are not approved for human use. See our full medical disclaimer.
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