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GLP-1s & incretins · Metabolic & endocrine

AT-7687

An investigational peptide GIP receptor antagonist — it blocks the GIP receptor rather than activating it — in a Phase 2a study combined with semaglutide.

L2Animal / lab studiesIn clinical trialsIn clinical development
How settled this rating is:
very-low confidence in the current evidence rating
Routes studied:
Subcutaneous injection
Also known as:
AT7687, GIP receptor antagonist
Last reviewed:
2026-09-20
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Evidence passport

AT-7687

A one-screen evidence identity for this compound. These fields describe research maturity, confidence and legal status. They are not a safety guarantee, efficacy percentage or recommendation.

Reviewed 2026-09-20
Evidence level
L2Animal / lab studies
Confidence
Very low confidence in rating
Regulatory status
In clinical trials
Development status
In clinical development

Evidence strength

Human efficacy evidence15 of 100 evidence strength

Higher = more and better-quality human evidence. It does not mean the effect is bigger or that the compound works for you.

Human safety evidence12 of 100 evidence strength

Higher = more mature, better-documented human safety data. It does not mean the compound is safer than one with a lower number.

The 0-100 values rate the strength and maturity of evidence, not how effective or safe the compound is.

Evidence base
Includes human studies
Furthest established stage
Phase II
Human research maturity
Phase 2a in combination with semaglutide; first patient dosed 28 July 2026 (sponsor-reported). No results
Source curation
Sources fully curated

Routes recorded

SC injection

Overview

Human efficacy evidence strength15 of 100 evidence strength

Higher = more and better-quality human evidence. It does not mean the effect is bigger or that the compound works for you.

Preclinical (animal / lab) evidence strength40 of 100 evidence strength

Higher = more animal, tissue or cell research. Preclinical results are a starting point, not proof of a human benefit.

Human safety evidence strength12 of 100 evidence strength

Higher = more mature, better-documented human safety data. It does not mean the compound is safer than one with a lower number.

How to read these scores

Every number here rates the evidence, not the compound. They are editorial 0-100 strength ratings, not percentages, and not a rating out of five stars.

  • Human efficacy evidence strength — Higher = more and better-quality human evidence. It does not mean the effect is bigger or that the compound works for you.
  • Preclinical evidence strength — Higher = more animal, tissue or cell research. Preclinical results are a starting point, not proof of a human benefit.
  • Human safety evidence strength — Higher = more mature, better-documented human safety data. It does not mean the compound is safer than one with a lower number. A score of 80 does not mean “80% safe”.
  • Evidence level (L0-L5) — the strongest type of study behind the compound, from anecdote (L0) to large replicated human trials (L5). It is a description of the study evidence, not a quality, safety or recommendation rating.
  • Confidence — how likely we think it is that this rating changes as new research lands. Low confidence means the picture is unsettled, not that the compound is bad.

None of these ratings is medical advice, a safety guarantee, or a recommendation to use anything. How we grade evidence.

How far human research has progressed: Phase 2a in combination with semaglutide; first patient dosed 28 July 2026 (sponsor-reported). No results

Routes & formulations

Studied / approved routes

SC injection

Route availability is not evidence of efficacy, and evidence from one route does not transfer to another. The Registry never provides dosing or sourcing information.

Peptide lifecycle

  1. Discovery

  2. Preclinical

  3. Phase I

  4. Phase II

    Furthest established stage

  5. Phase III

  6. Approved

In clinical development

Active early clinical development. Reaching Phase 2a implies Phase 1 work exists; our record does not establish published Phase 1 outcomes for this molecule.

Last documented development: July 2026 — first patient dosed in the Phase 2a combination study

What it is

A peptide that blocks the GIP receptor. This is the opposite pharmacological direction to GIP agonists such as tirzepatide, and the two must not be read as interchangeable even though both involve the same receptor.

What people claim

  • Blocking GIP is better than activating it
  • Boosts semaglutide weight loss

What the evidence actually says

What people claim: that GIP blockade adds weight loss on top of a GLP-1 medicine. What the evidence actually says: a Phase 2a study combining AT-7687 with semaglutide dosed its first patient on 28 July 2026 and has not reported results. Both GIP agonism and GIP antagonism are being tested clinically, which is itself a sign the biology is unsettled.

Useful next reads based on this compound — not recommendations.

Human evidence

  • Phase 2a study in combination with semaglutide; first patient dosed 28 July 2026, sponsor-reported. No efficacy or tolerability results reported.
  • No published Phase 1 results for this molecule are established in our curated record.

Preclinical evidence

  • GIP receptor antagonism has preclinical support as a weight-management approach, including in combination with GLP-1 receptor agonism; molecule-specific detail is not established in our record.

Animal and cell findings are Level 1–2 evidence.

Mechanism and pathways

Single-targetOne molecule acting at one named receptor.

Receptor targets: GIP receptor (antagonist)

Mechanism class counts the receptors the pharmacology engages and says whether one molecule or several drugs do it. More targets is not the same as more effective, and none of these labels is a receptor name — there is no GLP-3, GLP-4 or GLP-5 receptor.

  • Antagonism blocks signalling at the GIP receptor; agonism activates it. Approved tirzepatide is a GIP agonist, so its evidence says nothing about this molecule.
  • The rationale for combining GIP blockade with a GLP-1 agonist is additional weight loss; the rationale is not a result.

Safety and unknowns

  • No human safety profile is established in our curated record.
  • Combination studies carry the tolerability profile of the GLP-1 component as well as any effect of the antagonist.

Cancer relevance

This section covers questions raised by how the compound works in the body, plus anything regulators and trial teams keep an eye on. It is not a statement that this compound causes cancer — for most compounds here, no human data exist in either direction.

No established human signal

Not established. No human data exist in either direction.

Regulatory status

Regulatory decisions apply to specific jurisdictions, products, formulations and indications. An approval elsewhere is not automatically an approval in your country.

Check the regulatory note and linked primary sources for jurisdiction-specific details.

Not approved anywhere. A Phase 2a study is an early exploratory efficacy and safety study; it does not establish benefit.

Evidence grade

L2Animal / lab studiesVery low confidence in rating

Documented compound-specific animal or laboratory outcome findings, without qualifying human evidence for the assessed benefit.

What would change our rating?

  • Reported Phase 2a results, particularly placebo-controlled comparisons.
  • Published Phase 1 safety and pharmacokinetic data.

References and sources

Source transparency

A provenance snapshot of this profile. Counts show what kinds of sources are cited, not how much scientific weight each source deserves.

Sources fully curated
Last editorial review
2026-09-20
Recently reviewed · 26 days ago
Linked curated sources
1
Sources still pending
0
External specialist reviews
0
None recorded for this profile
Sponsor / official: 1

Review provenance

Registry editorial review: Colin Jackson-White, creator and editor, who is not a doctor or clinician. External specialist review is credited only when a named reviewer has completed a review of this exact profile.

Current linked evidence is sponsor-only. Treat findings as provisional until independent or peer-reviewed documentation is available.

Literature-discovery and AI tools may help locate or challenge candidate evidence, but they are not counted as evidence sources here. Registry judgements are tied to the underlying papers, trial records, regulator documents and official study records.

Source hierarchy: regulatory documents and trial registries first, peer-reviewed work next, sponsor material flagged as non-independent. We never use supplier or clinic marketing as evidence, and where a verified source has not yet been curated we say so rather than inventing one.

Evidence change history

These entries record changes to our assessment of the published evidence — not changes to the compound itself.

No recorded changes yet. Baseline position set on 2026-09-20.