Pemvidutide

ALT-801, pemvidutide (INN)

Metabolic & weight

Awaiting medical reviewEN ES DE FR PT ZH+ Follow for updates

Summary

Class: Synthetic dual agonist peptide at the GLP-1 and glucagon receptors, with a lipid (EuPort) modification for albumin binding and weekly dosing; balanced roughly 1:1 between the two receptors
Mechanism: GLP-1 activity suppresses appetite and improves glucose handling while glucagon receptor activity raises energy expenditure and drives fat out of the liver
Routes studied: Subcutaneous once weekly
Half-life: Supports once-weekly dosing; exact human figure not stated here †
Storage: Investigational product supplied and stored under trial protocol
Regulatory status: Not approved anywhere. FDA Fast Track for MASH and alcohol use disorder; Breakthrough Therapy designation for MASH. Phase 3 (PERFORMA) planned from H2 2026 †

Doses are as reported in studies or by the community — never recommendations.

1What it is

Pemvidutide is an investigational weekly injectable peptide that activates two receptors at once: GLP-1, familiar from semaglutide (#3), and the glucagon receptor. Pairing them is deliberate. Glucagon on its own raises blood glucose, which is why it is a rescue drug for hypoglycaemia — but it also increases energy expenditure and acts directly on liver cells to mobilise fat. Combining it with GLP-1, which lowers glucose and appetite, is intended to keep the metabolic benefit while cancelling the glucose penalty.

The main development target is MASH (metabolic dysfunction-associated steatohepatitis), the inflammatory, fibrosing form of fatty liver disease, with obesity, alcohol use disorder and alcohol-associated liver disease as further programmes. It is a clinical-stage molecule only; it has never been marketed and there is no legitimate route to it outside a trial.

2How it's thought to work

GLP-1 receptor arm. appetite suppression via hypothalamic and brainstem circuits, glucose-dependent insulin release, slowed gastric emptying — the established GLP-1 package.

Glucagon receptor arm on the liver. increased fatty acid oxidation and reduced de novo lipogenesis in hepatocytes, which reduces liver fat by a mechanism independent of weight loss. This is the argument for using a dual in liver disease specifically rather than a GLP-1 alone.

Energy expenditure. glucagon receptor agonism raises resting energy expenditure in human physiology studies, adding to the calorie deficit from reduced intake.

Balanced ratio and lipid modification. the roughly 1:1 receptor balance is the design choice that distinguishes it from glucagon-light dual agonists; the lipid modification gives albumin binding and a weekly interval.

A known trade-off. glucagon agonism can raise glucose and heart rate, and has historically caused trouble in this drug class when unbalanced.

A GLP-1 and glucagon receptor agonist designed with a 1:1 balance, aimed at liver fat as much as body weight.Schematic — not to scale

3What the research shows

MASH, Phase 2b (IMPACT)

IMPACT randomised 212 adults with biopsy-confirmed MASH and F2–F3 fibrosis, with or without diabetes, 1:2:2 to weekly pemvidutide 1.2 mg, 1.8 mg or placebo for 48 weeks, with co-primary histological endpoints at week 24 (MASH resolution without worsening fibrosis, or fibrosis improvement without worsening MASH). The sponsor reported that the trial achieved its key measures of success at 24 weeks and presented 48-week data at EASL 2026. Histological response rates should be read from the peer-reviewed publication, not from press summaries, before being quoted. Reported 48-week secondary findings for 1.8 mg versus placebo (company-reported) included weight −7.5% with no plateau, BMI −3.0 kg/m², waist circumference −5.3 cm, systolic/diastolic blood pressure −4.0/−2.2 mmHg, and in participants with elevated values triglycerides −23.7% and total cholesterol −15.4%. A composite non-invasive measure (≥0.5 reduction in ELF score plus ≥30% reduction in liver stiffness) was met by 3.2% on placebo versus 27.8% at 1.2 mg and 32.4% at 1.8 mg. Grade this as A on trial design, while noting that a Phase 2b of 212 patients is not a Phase 3 and that much of the detail is currently sponsor-reported.

Obesity, Phase 2 (MOMENTUM)

A 48-week Phase 2 trial in obesity without diabetes reported dose-dependent weight loss with a high proportion of the loss coming from fat rather than lean mass on body-composition analysis, which is a notable difference from GLP-1 monotherapy where lean-mass loss is a recognised issue (sponsor reports 2024; publication †).

Liver fat content, Phase 1b

Earlier work using MRI-PDFF reported large reductions in liver fat fraction over 12 weeks, consistent with the direct hepatic mechanism.

Graded B (early)

Alcohol use disorder and alcohol-associated liver disease

A Phase 2 trial (RECLAIM) in alcohol use disorder has been run with topline data expected in 2026 †. The rationale follows the broader observation that GLP-1 pathway drugs reduce alcohol intake; nothing is established. Community use: essentially none documented. Because the compound is investigational and appears in "research peptide" marketing, it is worth stating plainly that no human dosing information exists outside the trials, no safety data supports self-directed use, and material sold under this name cannot be assumed to be the molecule tested.

4Reported side effects and interactions

Literature-reported

Gastrointestinal events — nausea, vomiting, diarrhoea — were mostly mild to moderate and concentrated in the first eight weeks, as with the GLP-1 class. Discontinuation for adverse events was reported at about 1% in IMPACT. The sponsor reported no imbalance in cardiac adverse events versus placebo; given the glucagon mechanism this is a specific thing to watch rather than to assume.

Community-reported

none that can be relied on; there is no documented community use and nothing to report.

Class-level considerations from glucagon agonism. potential rise in fasting glucose or worsening glycaemic control, increased heart rate, and in the wider dual/triple-agonist literature occasional hepatic enzyme elevations. These were the failure modes of earlier glucagon-containing .

Class-level considerations from GLP-1 agonism. gallbladder events, pancreatitis (rare, causality debated), delayed gastric emptying with aspiration risk under anaesthesia, lean-mass loss alongside fat loss, and the rodent thyroid C-cell signal that carries across the class.

Interactions. no established human interaction data. On mechanism, expect the GLP-1 class interactions — additive hypoglycaemia risk with insulin or sulfonylureas, and slowed absorption of oral drugs.

Markers researchers commonly monitor

From the trial protocols and the pharmacology of both receptors:

Marker	Why it's watched
Liver histology (biopsy)	still the regulatory standard for MASH resolution and fibrosis stage; the only endpoint that settles the question.
MRI-PDFF liver fat fraction	the non-invasive measure of the direct hepatic effect.
Liver stiffness (FibroScan/VCTE) and ELF or other fibrosis panels	the composite used in the 48-week IMPACT secondary analysis.
ALT, AST, GGT, bilirubin	both as disease markers and because glucagon-containing agonists have historically needed hepatic safety watching.
Fasting glucose and HbA1c	glucagon receptor agonism can push glucose up; the central question for whether the 1:1 balance works.
Resting heart rate	raised by both GLP-1 and glucagon agonism.
Lipid panel and triglycerides	reported to improve; part of the metabolic claim.
Body weight, waist circumference and body composition (DEXA)	the lean-versus-fat mass split is a specific claim made for this molecule.
Blood pressure	reported reductions.
Lipase and amylase	GLP-1 class pancreatitis monitoring.

Free for everyone. Safety information is never behind a paywall.

5Formulation and administration context

Investigational once-weekly injection, supplied and administered under trial protocol. There is no marketed presentation, no approved concentration, and no self-preparation guidance; material offered outside a trial has no established identity, purity or dose. Nothing in the published work supports preparation or dosing by an individual.

6Commonly studied alongside

Compared against, not combined with: semaglutide (#3) and tirzepatide as the established incretin benchmarks. Conceptually grouped with other glucagon-containing agonists — survodutide (GLP-1/glucagon), retatrutide (GIP/GLP-1/glucagon) and cotadutide — and with non-incretin MASH drugs such as resmetirom as comparators in the same indication.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved; investigational. Fast Track designation for MASH and for alcohol use disorder; Breakthrough Therapy designation for MASH. Phase 3 PERFORMA planned from H2 2026 †
European Union	Not authorised; investigational
United Kingdom	Not licensed
Australia	Not approved
South Africa	Not registered
Sport	Not specifically listed by WADA. GLP-1 receptor agonists are not prohibited as of 2026 †; as a non-approved substance it would fall under S0 for athletes

8Open questions

Whether the Phase 2b histological signal holds in a Phase 3 trial with a clinical-outcome follow-on.
Whether the claimed preservation of lean mass versus GLP-1 monotherapy is real and durable, measured properly.
Whether glucagon receptor agonism causes glycaemic or cardiac trouble over years rather than months.
Whether liver benefit is separable from weight loss, as the mechanism predicts.
Whether the alcohol use disorder signal across the incretin class is real.

9References

1Harrison SA et al. (2026). IMPACT: a Phase 2b randomised trial of pemvidutide in MASH with F2–F3 fibrosis. [Publication to be confirmed before citing figures.] PubMed
2Nahra R et al. (2024). Pemvidutide, a GLP-1/glucagon dual receptor agonist, in subjects with overweight or obesity: a randomised Phase 2 trial (MOMENTUM) [verify journal]. PubMed
3Altimmune (2026). 48-week IMPACT Phase 2b data presented at EASL Congress 2026 (company presentation). PubMed
4Boland ML et al. (2020). Resolution of NASH and hepatic fibrosis by the GLP-1R and GCGR dual agonist cotadutide. Nat Metab — class mechanism reference. PubMed · DOI
5Nourredine M et al. (2026). Commentary: dual agonists and direct hepatic targeting in MASH. Am J Manag Care [verify]. PubMed

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

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11Page history

31 Oct 2026Profile published — awaiting medical review

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