AT673
AT673, GIP receptor antagonist
Written by Aaron CuhaReviewed Sep 2026
Also known as: GIP receptor antagonist, Antag Therapeutics GIPR antagonist
A GIP receptor antagonist being added to semaglutide in a phase 2 trial of 150 people. It is the exact mirror of NNC0480-0389, which adds a GIP agonist to the same drug.
Overview
If you want one fact that captures how unsettled incretin pharmacology is, it is this pair. Two companies are in phase 2 adding opposite interventions at the same receptor to the same background drug, for the same indication, at the same time. One activates GIP alongside semaglutide. This one blocks it.
AT673 comes from Antag Therapeutics and is recruiting a phase 2 of 150 participants in combination with semaglutide. No results are published. An earlier company code, AT-7687, returned no trial records when searched.
The antagonist case rests on mouse genetics, where losing the GIP receptor protects against diet-induced obesity, and on maridebart cafraglutide, which pairs GLP-1 agonism with a GIP antagonist antibody and produced weight loss in a randomised phase 2. So there is a human precedent for the direction, which is what makes the contradiction real rather than theoretical.
Mechanism of action
An antagonist at the GIP receptor, intended to block rather than activate the receptor tirzepatide agonises, given alongside a GLP-1 receptor agonist. The mechanistic case comes from GIP receptor knockout mice being protected against diet-induced obesity, and from the observation that a naturally occurring truncated GIP fragment blocks its own receptor in humans. How blockade produces weight loss when activation also does is unresolved.
Human evidence
No published human data for this compound. One recruiting phase 2 in combination with semaglutide. The direction has human support from a different drug.
- Phase 2, 150 participants, co-administered with semaglutide, recruiting as of this review.
- No results, no publication, and no pharmacokinetic or safety data located for AT673 specifically.
- An earlier company code, AT-7687, returned no ClinicalTrials.gov records.
- The mechanism has human precedent through maridebart cafraglutide, a different molecule pairing GLP-1 agonism with GIP receptor antagonism, which produced weight loss in randomised phase 2.
What this does not tell you: Nothing about this specific compound has been measured in public. The page exists because the trial exists and because the pairing with an agonist programme in the same phase is a fact worth recording. Do not read the maridebart result as evidence for AT673; it supports the mechanism, not the molecule.
Reading the research record
This compound sits inside an unresolved contradiction that runs through the whole incretin field. Activating the GIP receptor produces weight loss, which is how tirzepatide works. Blocking the GIP receptor also produces weight loss, which is how maridebart cafraglutide works. Both results come from randomised human trials. As of this review two drugs are in phase 2 adding opposite GIP interventions to the same background drug, semaglutide: NNC0480-0389 agonises the receptor and AT673 antagonises it. Proposed explanations exist, including receptor desensitisation under sustained agonism producing functional antagonism, and differing central versus peripheral effects, but none is established. This site reports the paradox rather than resolving it, because nobody has resolved it.
The evidence, charted
Fig. 1 · evidence composition
2of 2 citations (100%) are in people
Every citation cited here is Human work; no other study type is cited on this page. This count is of our own citation list and understates any literature larger than the sources we cite.
Fig. 2 · evidence over time
Citations here span just two years, 2025 and 2026.
Too few distinct publication years on this page to plot as a timeline.
Fig. 3 · legal status at a glance
US
Not approved
UK
Approved
AU
Approved
CA
Not approved
Approved in 2 of 4, prescription route in 0, not approved in 2. A jurisdiction's classification is a regulatory fact, not a verdict on the science; see Legal status below for the full text and any notes.
Fig. 4 · dose response
No human dose response curve exists
We draw this figure where the data supports it. For this compound in humans it does not, so the panel stays empty rather than borrowing an animal curve and implying it transfers.
Key studies & citations
- Human2026
A study of AT673 in combination with semaglutide in people with overweight or obesity
Phase 2, 150 participants, GIP receptor antagonist co-administered with semaglutide, recruiting. The mirror image of the NNC0480-0389 programme, which adds a GIP agonist to the same background drug.
ClinicalTrials.gov - Human2025
Once-monthly maridebart cafraglutide for the treatment of obesity: a phase 2 trial
The human precedent for the direction. Maridebart cafraglutide pairs GLP-1 receptor agonism with a GIP receptor antagonist antibody and produced weight loss in a randomised phase 2. Included because without it, GIP antagonism would rest on mouse genetics alone.
New England Journal of Medicine
Frequently asked questions
Blocking GIP and activating GIP are both being tested with semaglutide. How?
That is accurate and unresolved. GIP receptor knockout mice resist diet-induced obesity, which argues for blocking. Tirzepatide activates the receptor and produces large weight loss, which argues for activating. Maridebart cafraglutide blocks it and also produces weight loss. Both directions have human support and nobody has explained why.
Is there any data on AT673 itself?
None published. There is a recruiting phase 2 in 150 people with semaglutide, and no results, safety data or pharmacokinetics located for this compound specifically.
Can I get it?
No. It is investigational and recruiting a trial. There is no other access.