AT673 dosage and evidence
Written by Aaron CuhaReviewed Sep 2026
The short answer
AT673 is a drug that blocks the GIP receptor, being added to semaglutide in a mid-stage trial of 150 people. It is the exact mirror of NNC0480-0389, which adds a GIP switch-on drug to the same base drug.
Evidence grade for AT673: Limited. The rule: people have taken it in a published study, but fewer than 100 of them. The sum on this page: 1 completed trial, none stating how many people. A grade counts how much has been done to people, not whether it works.
- People given it
- 0
- Human studies
- 1
- Found nothing
- 0
Dose
No human dose established
Amounts that were given in studies sit in Human evidence on this page. None of them is a personal dose.
1 completed trial, 0 people given it
1 effects reported, 1 unwanted, by people using it, not a trial
Goal pages: Fat loss and metabolism
In plain English
In plain English, from Aaron
This is how I would explain it to a friend. The evidence, with the numbers, is further down the page.
AT673 is a test drug that blocks the GIP receptor. It is being added to semaglutide. That is the opposite of NNC0480-0389, which switches the same receptor on. It is not approved anywhere.
What people take it for
- More weight loss on top of semaglutide.
- Better blood sugar in people with type 2 diabetes and extra weight.
What studies in people showed
Nothing has been reported for this drug. A mid-stage trial of 150 people is recruiting and should end in March 2027. The idea has some support from a different drug. Maridebart cafraglutide blocks GIP and switches on GLP-1. In a study of 592 people, those with obesity lost about 12 to 16 percent of their weight in a year. On a dummy they lost about 2.5 percent. That supports the idea, not this drug.
What people report
Reports, not study results
The good
- We have not collected user reports on this one yet.
The bad
- There is no safety data on this drug at all.
Where these come from: From the trial records on this page. We have no user reports.
My bottom line
My opinion: there is nothing to know yet. A recruiting trial is not a result. Check back in 2027.
An opinion, not a finding. I am a coach, not a doctor.
What it has been measured to do
Measured in people
Goals AT673 has been tested for in people, biggest studies first. We count only what the studies on this page say, so the real numbers may be higher.
- Losing weightno headcount stated · 1 study
35 of the 36 indexed goals have no study of any kind behind AT673
No study in people, animals or cells on this page reports a result for these. That does not prove AT673 does nothing for them. It does mean anything you have heard about AT673 and one of these did not come from a study cited here.
Show full evidence
What is AT673?
AT673 is a drug that blocks the GIP receptor, being added to semaglutide in a mid-stage trial of 150 people. It is the exact mirror of NNC0480-0389, which adds a GIP switch-on drug to the same base drug.
If you want one fact that shows how unsettled this field is, it is this pair. Two companies are running mid-stage trials that add opposite actions at the same receptor to the same base drug, for the same purpose, at the same time. One switches GIP on alongside semaglutide. This one blocks it.
AT673 comes from Antag Therapeutics. It is recruiting a mid-stage trial of 150 people, given with semaglutide. No results are published. A search for an earlier company code, AT-7687, found no trial records.
The case for blocking rests on two things. In people, maridebart cafraglutide pairs GLP-1 with a GIP blocking antibody, and it caused weight loss in a mid-stage trial against a dummy. In mice, losing the GIP receptor protects against weight gain on a fatty diet. So there is a human example for this direction. That is what makes the puzzle real, not just theory.
How does AT673 work?
It blocks the GIP receptor instead of switching it on the way tirzepatide does. It is given alongside a GLP-1 drug. In people, a natural shortened piece of GIP blocks its own receptor. In mice, those without the GIP receptor are protected from weight gain on a fatty diet. How blocking causes weight loss when switching on also does is not known.
What have studies in people found about AT673?
No published human data for this drug. One mid-stage trial with semaglutide is recruiting. The approach has human support from a different drug.
- Mid-stage trial, 150 people, given with semaglutide, recruiting as of this review.
- No results, no paper, and no data on blood levels or safety found for AT673 itself.
- A search for an earlier company code, AT-7687, found no ClinicalTrials.gov records.
- The approach has a human example in maridebart cafraglutide. That different molecule pairs GLP-1 with a GIP blocker, and it caused weight loss in a mid-stage trial against a dummy.
What this does not tell you: Nothing about this drug has been measured in public. The page exists because the trial exists, and because its pairing with a switch-on programme at the same stage is worth recording. Do not read the maridebart result as evidence for AT673. It supports the approach, not this molecule.
The state of the research
This drug sits inside an open puzzle that runs through this whole family of drugs. Switching on the GIP receptor causes weight loss. That is how tirzepatide works. Blocking the GIP receptor also causes weight loss. That is how maridebart cafraglutide works. Both results come from human trials that compared the drug with a dummy. As of this review, two drugs are in mid-stage trials adding opposite GIP actions to the same base drug, semaglutide. NNC0480-0389 switches the receptor on, and AT673 blocks it. There are ideas about why both work. One is that keeping the switch on for a long time wears it out, so it ends up acting blocked. Another is that the brain and the rest of the body respond differently. None is proven. This site reports the puzzle rather than solving it, because nobody has solved it.
The evidence, in charts
Fig. 1a · how many people
2studies in people cited, but none says how many people took part
number of people not stated
We do not draw a total, because none of the studies in people on this page gives one. Read the sources below for what each study measured.
We read the number of people from the source lines on this page. Where a line gives no number, we count nothing for it. We do not guess.
Fig. 1b · evidence mix
All 2 sources here are studies in people.
- Study in people · done in people2100%
Counted from the list of sources on this page. It counts only what we cite, so there may be more studies out there. A review counts once, however many studies it sums up.
Fig. 2 · evidence over time
Sources here come from just two years, 2025 and 2026.
Too few different years on this page to draw a timeline.
Fig. 3 · legal status at a glance
US
Not approved
UK
Not approved
AU
Not approved
CA
Not approved
Not approved in any of the four countries shown. This is what the law says, not a verdict on the science. See Legal status below for the full text and any notes.
Fig. 4 · how much does what
Nobody has tested different amounts in people
This chart would show how the effect changes as the amount goes up. For this compound, nobody has measured that in people. So we leave it empty. We will not borrow an animal chart and pretend it works the same in people.
Fig. 5 · what the molecule is
- Kind of compound
- Peptide
- Molecule weight
- Not asserted. No source loaded states a molecular weight or states whether it is a peptide or an antibody.
- Half-life
- Stated in words, not a numbersee the exact wording below
- Chain length
- None on file
Half-life as stated on file: Not asserted. No pharmacokinetic figure was resolved in the sources loaded.
No amino acid sequence is on file for AT673, so none is drawn rather than guessed from a name.
The studies we cite
- Study in people2026A study of AT673 in combination with semaglutide in people with overweight or obesity
The test of blocking GIP, rather than activating it, is recruiting now. Antag Therapeutics plans to enrol 150 people with type 2 diabetes and extra weight, giving AT673 alongside semaglutide. Completion is estimated for March 2027 and nothing has been reported. It is the mirror image of the NNC0480-0389 programme, which adds a GIP activator to the same background drug. Nobody has yet reported which direction is right.
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.
- Study in people2025Once-monthly maridebart cafraglutide for the treatment of obesity: a phase 2 trial
Blocking GIP while activating GLP-1 produced large weight loss in people. 592 took part, 465 with obesity and 127 who also had type 2 diabetes, split by chance between several doses and a dummy, injected once a month. After a year, people with obesity lost between about 12% and 16% of their body weight, against about 2.5% on the dummy. Losses were smaller in the diabetes group. Stomach and bowel side effects were common. Amgen paid for it.
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.
Where to buy AT673
No seller we track lists AT673 yet. We read sellers’ public product lists every week, and this section fills in as soon as one does. Every seller, graded
Common questions
Has AT673 been tested in people?
Yes. 0 people given it across 1 completed trial cited here, 0 of which found nothing. AT673 is a drug that blocks the GIP receptor, being added to semaglutide in a mid-stage trial of 150 people. It is the exact mirror of NNC0480-0389, which adds a GIP switch-on drug to the same base drug.
What is the AT673 dosage?
No human dose established. Amounts that were given in studies sit in Human evidence on this page. None of them is a personal dose. 1 completed trial, 0 people given it
Is AT673 FDA-approved?
Investigational. Not approved anywhere. A mid-stage study is signing people up.
Blocking GIP and activating GIP are both being tested with semaglutide. How?
That is right, and nobody has explained it. Mice without the GIP receptor resist weight gain on a fatty diet, which argues for blocking. Tirzepatide switches the receptor on and causes large weight loss, which argues for switching on. Maridebart cafraglutide blocks it and also causes weight loss. Both directions have support in people, and nobody knows why.
Is there any data on AT673 itself?
None published. There is a recruiting mid-stage trial in 150 people with semaglutide. No results, safety data or blood level data have been found for this drug itself.
Can I get it?
No. It is a test drug in a trial that is recruiting. There is no other way to get it.