What is it?
Efocipegtrutide is an investigational, long-acting medicine designed to influence three metabolic hormone signals involved in appetite, blood sugar, and liver energy handling.
Gathering the record
Relay is organizing the evidence and source boundaries.
Long-acting glucagon / GIP / GLP-1 triple receptor agonist
Efocipegtrutide, formerly HM15211, is a long-acting glucagon/GIP/GLP-1 triple agonist developed primarily for fatty-liver and MASH research. Early human results show liver-fat and weight signals, but no Phase 3 obesity or clinical-outcomes evidence exists.
60-Second Overview
Start with what it is, why it matters, what research has shown, and what remains unknown. The science follows after the orientation.
Start here. These four answers explain why the compound matters before the page introduces the deeper science.
Efocipegtrutide is an investigational, long-acting medicine designed to influence three metabolic hormone signals involved in appetite, blood sugar, and liver energy handling.
Its development has focused on fatty-liver disease and metabolic dysfunction-associated steatohepatitis, or MASH. Researchers want to know whether changing several signals together can reduce liver fat and eventually improve liver injury or scarring.
A small randomized program reported early liver-fat and weight signals, but the outcome report available to Relay is a sponsor conference poster. Peer-reviewed publications and official trial records mainly describe the later biopsy-based study design rather than completed benefit.
Verified biopsy outcomes, fibrosis improvement, clinical liver outcomes, long-term safety, blood-sugar tradeoffs, and broader weight effects remain unresolved. No approved product or transferable preparation standard exists.
The research depth, routes, studies, and primary sources below explain how Relay knows—and where the evidence stops.
Research context
Published research has investigated this compound using the following study designs.
These records explain what researchers did. They are not instructions, recommendations, or a transferable protocol.
Peer-reviewed and official records describe a biopsy-based trial in adults with MASH and fibrosis, but Relay's verified record does not contain a complete peer-reviewed efficacy report from that program.
Reported study administration—not a recommendation.
Research at a glance
Evidence depth, confidence, and route context explain how Relay knows—not what anyone should do.
Phase 1b/2a signals and a biopsy-based Phase 2 program.
Research depth describes how large and mature the overall record is. It does not tell you whether the results were positive.
The main efficacy signal comes from a small sponsor poster.
Confidence describes how reliable and consistent the conclusions are. It can be high for one outcome and low for another.
The strongest evidence type shows what the best-supported conclusions are actually based on.
Human findings are more directly relevant than animal or laboratory results, but they still apply only to the populations and outcomes studied.
Route-specific record
These are exposures used in cited research for a specific route and population—not an instruction for an individual.
Half-life describes how long it takes the measured amount in the body to fall by half. It is not a dosing recommendation.
Evidence can change by administration method. Findings from one route should not automatically be applied to another.
Evidence boundary: A trial-design paper explains what researchers planned to measure; it does not show that the intervention worked. Sponsor-poster findings are kept separate from independently reviewed outcomes, and no generic-vial preparation claim is supported. Amounts shown describe cited research exposure—not a dosage recommendation.
Detailed evidence
Start with the strongest supported conclusion and its main uncertainty. Claim-level records below show how the evidence changes by question, population, route, formulation, and study design.
A randomized 12-week Phase 1b/2a NAFLD study reported dose-dependent liver-fat and weight signals in up to 60 participants.
This is the strongest supported conclusion in the current human evidence—not a summary of every claim made about the compound.
Biopsy-confirmed Phase 2 efficacy, fibrosis and clinical liver outcomes, glycemic tradeoffs from glucagon agonism, long-term safety, weight durability, and comparative performance.
Keeping the main uncertainty visible prevents an early or promising finding from looking more settled than it is.
Questions people bring to the evidence
Research questions—not promises of benefit.
It shares receptor labels with retatrutide but not molecular design, receptor balance, or evidence.
The highest group reached an 88% reduction in the sponsor poster.
Placebo-corrected mean weight change reached about 5.1% at 12 weeks.
Two early-study cases resolved after treatment discontinuation.
No outcomes were publicly available at the cutoff.
Mechanisms
Efocipegtrutide is an Fc-linked, long-acting triple agonist targeting glucagon, GIP, and GLP-1 receptors. In a sponsor-presented 12-week Phase 1b/2a study of adults with obesity and NAFLD, dose-dependent liver-fat reductions reached 88% in the highest group and placebo-corrected weight reduction reached about 5.1%. Mild gastrointestinal events were common, and two hyperglycemia cases resolved after discontinuation. A biopsy-confirmed MASH Phase 2b program was designed to evaluate histologic endpoints, but public completed efficacy results were not located at the cutoff. Fast-track and orphan designations indicate development interest, not approval.
A plausible mechanism can explain why a study was attempted. It does not prove that the compound improves a human outcome.
Studies
Study arms are reported for transparency. They describe what researchers did in a defined record and do not transfer across identities, routes, formulations, or populations.
A later trial phase can ask a more mature question, but it does not guarantee a positive result, regulatory approval, or relevance outside the studied population.
Peer-reviewed description of a randomized biopsy-confirmed MASH trial
Adults with biopsy-confirmed MASH and fibrosis
The design targets histologic endpoints needed to move beyond imaging-only liver-fat changes.
Study administration: Weekly efocipegtrutide dose groups or placebo
Limitations: A design paper contains no efficacy result.
Randomized, double-blind, placebo-controlled trial registry
Adults with biopsy-confirmed MASH
The registry confirms the intended biopsy-based Phase 2 program.
Study administration: Weekly HM15211 or placebo
Limitations: No public completed outcomes were located at the cutoff.
Official program description
Investigational development program
The sponsor positions the molecule as an Fc-linked weekly glucagon/GIP/GLP-1 triple agonist.
Study administration: Long-acting triple-receptor agonism
Limitations: Sponsor mechanism and design descriptions do not establish efficacy.
Randomized, placebo-controlled dose-ranging study
Adults with obesity and nonalcoholic fatty liver disease
The sponsor poster reported dose-dependent liver-fat reduction up to 88% and placebo-corrected weight reduction up to 5.1%.
Study administration: Once-weekly subcutaneous HM15211 dose groups or placebo
Limitations: Small, short sponsor-poster evidence is preliminary and not a clinical liver-outcomes result.
Safety snapshot
No source-qualified adverse-event pattern is represented in the current record.
Evidence boundaryHuman exposure is present, but the record is not detailed enough to characterize a reliable adverse-event pattern.
The current record does not support a reliable common-versus-uncommon frequency split.
Evidence boundaryUnder-detected or under-reported events must not be described as rare.
No source-qualified compound-specific warning or contraindication is encoded in the current record.
Evidence boundaryInvestigational — early MASH-focused human development Biopsy-confirmed Phase 2 efficacy, fibrosis and clinical liver outcomes, glycemic tradeoffs from glucagon agonism, long-term safety, weight durability, and comparative performance.
The current record does not identify a reliable compound-specific pattern of events that caused study discontinuation.
Evidence boundaryThis is an evidence gap, not proof that discontinuations did not occur.
No compound-specific patient-facing urgent-action threshold is established in the current Relay record.
Evidence boundaryRelay does not infer emergency guidance from study discontinuations, mechanism, or incomplete adverse-event reporting.
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2026-07-31
2023-04-01 · PMID 37028504 · DOI 10.1016/j.cct.2023.107095
2020-08-01 · NCT04505436
2020-08-01