Pemvidutide Research, Specifications & Scientific Information

Introduction

Pemvidutide is a glucagon and GLP-1 receptor dual agonist developed by Altimmune, and its programme is aimed at the liver rather than at the scale. That focus is deliberate and mechanistically argued: agonists at the GLP-1 receptor reduce body mass by central and peripheral routes, while agonists at the glucagon receptor act directly on hepatocytes to stimulate fatty acid oxidation and inhibit lipogenesis. The claim the compound's investigators make is that the second route reduces liver fat by more than the first route's effect on body mass would account for ^[2].

Its most substantial result, the phase 2b IMPACT trial, is also the reason this page reads the way it does. IMPACT had two primary endpoints. It met one and missed the other, clearly and by a wide margin on the second ^[4]. Both are reported below at the same length.

This page is a reference record. It sets out what has been published about pemvidutide's structure, its receptor pharmacology, and the preclinical and clinical literature, with every source resolved against PubMed, Crossref or ClinicalTrials.gov at the time the page was built. It describes research. It does not describe use in people or animals, and it carries no guidance of any kind on handling the material.

What Is Pemvidutide?

Pemvidutide is an investigational synthetic peptide developed by Altimmune under the code ALT-801. It is not an approved medicine in the United States and has not been approved by the U.S. Food and Drug Administration for any indication.

Structurally it belongs to the glucagon–secretin peptide superfamily. Functionally it is a dual receptor agonist at the GLP-1 receptor and the glucagon receptor — the same pair engaged by survodutide and mazdutide, and a different pair from tirzepatide's GIP and GLP-1 receptors.

One naming caution belongs at the top rather than buried in a footnote. The development code ALT-801 was also used, by a different sponsor in an earlier decade, for an unrelated interleukin-2 and T-cell receptor fusion protein studied in oncology. A literature search on that code alone returns both compounds, and the two have nothing in common. Every citation on this page has been checked against the compound it actually describes.

Pemvidutide Specifications

The 29-residue string above is the backbone recorded for pemvidutide in the FDA/NCATS Global Substance Registration System under UNII A35F525WBG. The letter X is the register's placeholder for a residue with no single-letter representation — at position 2, the position dipeptidyl peptidase-4 cleaves after — so the string cannot be read as if every letter stood for a standard amino acid. The register also carries structural modifications for this substance that the sequence does not express, and the formula and mass shown here are the register's values for the recorded backbone rather than for the complete molecule; the mass of the finished compound is greater. No PubChem compound identifier resolves for the name pemvidutide or for the development code ALT-801, so that field is published as unknown rather than estimated. A caution on the development code: ALT-801 was also used, by a different sponsor and in a different decade, for an unrelated interleukin-2 / T-cell receptor fusion protein studied in oncology. A literature search on that code alone returns both compounds. Any figure on this page is a reference value: the certificate of analysis supplied with a laboratory order is the record for a given lot.

Values that a public register does not carry are shown as not publicly characterised rather than estimated. Identifiers are reference values; the certificate of analysis supplied with a laboratory order is the record for a given lot.

How Does Pemvidutide Work?

Both of pemvidutide's targets are class B1 G protein-coupled receptors and both couple through Gs to raise intracellular cyclic AMP. What differs is where they are expressed and what they do there.

The GLP-1 receptor arm is the familiar incretin pharmacology: receptors on pancreatic islet cells and at central nervous system sites, whose activation modulates glucose-dependent insulin secretion and reduces calorie intake.

The glucagon receptor arm is the one this programme is built around. Glucagon receptor agonism acts on the hepatocyte directly, stimulating fatty acid oxidation and inhibiting lipogenesis. In a liver-disease indication that is not an incidental property — it is a second, independent route to reducing hepatic fat, working alongside rather than through any change in body mass ^[2]. Whether the two contributions can be separated in practice is a question the published trials do not settle, and the compound's own results in body mass and in liver fat move together.

A gap in the published record is worth naming here rather than passing over. No primary in vitro characterisation of pemvidutide's relative potencies at its two receptors appears in the peer-reviewed literature indexed on this page — the equivalent of the receptor-potency tables published at discovery for survodutide and retatrutide. What is published begins at the whole-animal level. This page therefore carries no in vitro evidence section, because there is none to carry.

What Is Pemvidutide Being Researched For?

Registered clinical research on pemvidutide has covered:

• Metabolic dysfunction-associated steatohepatitis — a phase 2b trial with liver biopsies at 24 weeks within an ongoing 48-week protocol ^[4].
• Metabolic dysfunction-associated steatotic liver disease — a 12-week randomised trial with imaging endpoints ^[2] and its 12-week extension ^[3].
• Obesity — a completed phase 2 trial, registered but not reported in the sources cited on this page ^[8].
• Safety and tolerability in healthy volunteers with overweight or obesity — a phase 1 trial ^[5].

Each of those is research into a pharmaceutical product candidate, conducted by its sponsor under a registered protocol. None of it is research into, or evidence about, research-grade material supplied for laboratory use.

Human Research on Pemvidutide

Human clinical research

Results from pharmaceutical clinical trials describe the investigational material and populations used in those studies and should not be interpreted as establishing the effects of research-grade materials offered for laboratory use.

IMPACT — phase 2b in biopsy-confirmed steatohepatitis

Population. 212 participants randomised from 1,557 screened, with biopsy-confirmed metabolic dysfunction-associated steatohepatitis and fibrosis stage F2 or F3, at 83 sites in the United States and Australia, between July 2023 and April 2025 ^{[4, 9]}.

Endpoint and duration. Two primary endpoints, both at 24 weeks in the intention-to-treat population: resolution of steatohepatitis without worsening of fibrosis, and improvement of liver fibrosis by at least one stage without worsening of steatohepatitis. Randomised 1:2:2 to once-weekly subcutaneous pemvidutide at 1.2 mg or 1.8 mg, administered without titration, or placebo, within an ongoing 48-week trial ^[4].

Result, first primary endpoint. Resolution of steatohepatitis without worsening of fibrosis occurred in 18 of 86 participants (20%) on placebo, 24 of 41 (58%) at 1.2 mg — difference 38%, 95% CI 21 to 56, p < 0.0001 — and 45 of 85 (52%) at 1.8 mg, difference 32%, 95% CI 19 to 46, p < 0.0001 ^[4].

Result, second primary endpoint. Fibrosis improvement without worsening of steatohepatitis occurred in 24 of 86 participants (28%) on placebo, 13 of 41 (33%) at 1.2 mg — difference 5%, 95% CI −13 to 22, p = 0.59 — and 30 of 85 (36%) at 1.8 mg, difference 8%, 95% CI −6 to 22, p = 0.27. Neither comparison reached significance, and both confidence intervals cross zero ^[4].

Adverse events. Reported in 32 of 41 participants (78%) at 1.2 mg, 69 of 85 (81%) at 1.8 mg and 58 of 86 (67%) on placebo, the majority mild or moderate. Discontinuation for adverse events occurred in none of the 1.2 mg group, one participant (1%) at 1.8 mg and two (2%) on placebo ^[4].

Limitations. The trial met one primary endpoint and missed the other, and the authors say so directly. Fibrosis is the histological feature that determines long-term outcome in liver disease, and it is the endpoint that did not separate from placebo — a placebo arm in which 28% improved by a stage, which is high and which the trial design has to contend with. Twenty-four-week results from a trial designed to run to 48 weeks; the compound was administered without titration, and the low discontinuation rates should be read in that light rather than compared directly with titrated regimens elsewhere.

Twelve-week randomised trial in steatotic liver disease

Population. 94 participants with a body-mass index of 28.0 kg/m² or above and liver fat content of 10% or more by magnetic resonance imaging proton density fat fraction. Median baseline body-mass index 36.2 kg/m² and liver fat content 20.6%; 29% had type 2 diabetes ^{[2, 6]}.

Endpoint and duration. Primary efficacy endpoint the relative percentage reduction from baseline in liver fat content after 12 weeks. Randomised 1:1:1:1 to pemvidutide at 1.2, 1.8 or 2.4 mg or placebo, once weekly, stratified by type 2 diabetes status ^[2].

Result. At week 12, relative reductions in liver fat content were 46.6% (95% CI −63.7 to −29.6), 68.5% (−84.4 to −52.5) and 57.1% (−76.1 to −38.1) for the 1.2, 1.8 and 2.4 mg groups against 4.4% (−20.2 to 11.3) for placebo, p < 0.001 for all. At 1.8 mg, 94.4% reached a 30% reduction, 72.2% a 50% reduction and 55.6% normalisation at 5% or below. Maximal responses for change in body mass (−4.3%, p < 0.001), alanine aminotransferase (−13.8 IU/L, p = 0.029) and corrected cT1 (−75.9 ms, p = 0.002) were all observed at 1.8 mg ^[2].

Adverse events. Tolerated at all three amounts, with no severe or serious adverse events reported ^[2].

Limitations. Twelve weeks, 94 participants, with imaging rather than histology as the endpoint. The response was not monotonic — 1.8 mg outperformed 2.4 mg on every measure reported — which is a real feature of the data in a trial this size and is not explained.

Twenty-four-week extension

Population. 64 participants who completed the 12-week trial above and continued at their originally assigned amount. Baseline mean body-mass index 36.7 kg/m² and liver fat content 22.2%; 26.6% had type 2 diabetes ^{[3, 7]}.

Endpoint and duration. Primary efficacy endpoint the relative percentage reduction from baseline in liver fat content after 24 weeks of treatment, in a double-blind 12-week extension of the earlier trial ^[3].

Result. At 24 weeks, relative reductions in liver fat content were 56.3%, 75.2% and 76.4% for the 1.2, 1.8 and 2.4 mg groups against 14.0% for placebo, p < 0.001 for all. At 1.8 mg, 84.6% reached a 50% reduction and 53.8% reached normalisation at 5% or below. Change in body mass was 6.2% over 24 weeks, p < 0.001 against placebo ^[3].

Limitations. An extension in completers only, which selects for participants who tolerated the compound and so cannot be read as a 24-week result in the original randomised population. Sixty-four participants. The placebo group's liver fat content also fell by 14%, three times its 12-week figure.

Preclinical Research on Pemvidutide

Animal research

The mouse study published in 2022 is the compound's principal preclinical record, and its design is more demanding than most in this field: it ran against two active comparators rather than vehicle alone.

Male C57BL/6J mice were fed an Amylin Liver NASH diet for 32 weeks. Animals with biopsy-confirmed steatosis and fibrosis then received ALT-801, semaglutide, elafibranor or vehicle daily for 12 weeks while the diet continued. Endpoints included body and liver weight, hepatic and plasma cholesterol and triglycerides, plasma aminotransferases, and histological analysis of steatosis, inflammation measured by galectin-3, and fibrosis measured by collagen type 1 alpha 1, together with the composite non-alcoholic fatty liver disease activity score and fibrosis stage ^[1].

ALT-801 produced significant reductions in body mass of approximately 25%, in plasma aminotransferases, in plasma total cholesterol and in hepatic triglycerides and cholesterol, alongside improved hepatic steatosis, with greater reductions than semaglutide and elafibranor, p < 0.05. It significantly reduced galectin-3 and collagen type 1 alpha 1 against vehicle, p < 0.05, and produced greater reductions in galectin-3 than elafibranor. Every animal treated with ALT-801 improved on the composite activity score relative to the active controls ^[1].

Two cautions attach to that comparison, and they matter because it is the comparison most likely to be quoted. The comparators were administered on the same daily schedule as the test compound, which is not how semaglutide is administered in its own trials. And a 25% reduction in body mass in a diet-induced obese mouse is not a quantity that translates to people; the comparative ranking in a rodent model has repeatedly failed to predict the ranking in human trials in this field.

Findings described in this section were observed in animals. Nothing in them establishes anything about humans.

Current Research Status

Status as of September 22, 2026. This block is rendered from maintained fields, not from prose, so it cannot go stale in one place and stay current in another.

Pemvidutide vs Related Compounds

The distinctions between pemvidutide and the compounds it is usually set beside are which receptors each engages and what each programme has measured, and nothing else is stated here.

Receptor agonism

Pemvidutide — GLP-1R and GCGR. Survodutide and mazdutide — the same pair. Tirzepatide — GIPR and GLP-1R, a different pair. Retatrutide — all three. Semaglutide — GLP-1R alone.

Programme emphasis

Pemvidutide's published record is weighted towards liver endpoints — imaging and histology — rather than towards body mass, which is unusual among the dual agonists and reflects the hepatic rationale for glucagon receptor agonism.

Published characterisation

Survodutide and retatrutide have published receptor-potency characterisations from their discovery papers. Pemvidutide's published record begins at the animal model. That is a difference in what has been made public, not necessarily in what was measured.

Regulatory position

Pemvidutide, survodutide and retatrutide are investigational. Mazdutide is approved in China and not in the United States. Semaglutide and tirzepatide are active ingredients of products approved in the United States. Approval is specific to a jurisdiction, a product and an indication.

No comparison of effect between these compounds is made on this page. Where head-to-head trials exist they are registered, and their results belong to the papers that report them.

Chemical & Molecular Characteristics

The FDA/NCATS Global Substance Registration System records pemvidutide under UNII A35F525WBG with a 29-residue backbone written HXQGTFTSDYSKYLDEKAAKEFIQWLLQT.

Three points qualify that record.

The X is not an amino acid. It is the register's placeholder for a residue with no single-letter representation, and it sits at position 2 — the position dipeptidyl peptidase-4 cleaves after, and the position this family of peptides protects by substituting a non-standard residue. Reading the string as though every letter were a standard amino acid would misdescribe the molecule exactly where its stability comes from.

The figures shown are the backbone's, not the molecule's. The formula C182H283N39O58 and the mass of approximately 3,891 g/mol are the register's values for the recorded backbone. The register carries structural modifications for this substance in addition, so the complete molecule is heavier. No PubChem compound identifier resolves for pemvidutide or for ALT-801, so no second register is available to check the finished molecule's formula against — and the field is published as unknown rather than filled with a plausible figure.

The development code is ambiguous, and the ambiguity is a real hazard. ALT-801 also designates an interleukin-2 and T-cell receptor fusion protein from a different sponsor, studied in advanced malignancies and published in 2011. Any identifier, catalogue entry or paper found under the bare code ALT-801 should be checked against the compound it describes before being relied on. CAS registry number 2538014-94-5 is unambiguous and is the identifier to use.

Frequently Asked Questions

Scientific References

1. Nestor JJ, Parkes D, Feigh M, et al.. Effects of ALT-801, a GLP-1 and glucagon receptor dual agonist, in a translational mouse model of non-alcoholic steatohepatitis Scientific reports; 2022. PMID 35461369 doi:10.1038/s41598-022-10577-2
2. Harrison SA, Browne SK, Suschak JJ, et al.. Effect of pemvidutide, a GLP-1/glucagon dual receptor agonist, on MASLD: A randomized, double-blind, placebo-controlled study Journal of hepatology; 2025. PMID 39002641 doi:10.1016/j.jhep.2024.07.006
3. Browne SK, Suschak JJ, Tomah S, et al.. Safety and efficacy of 24 weeks of pemvidutide in metabolic dysfunction-associated steatotic liver disease: A randomized, controlled clinical trial JHEP reports : innovation in hepatology; 2025. PMID 41113119 doi:10.1016/j.jhepr.2025.101483
4. Noureddin M, Harrison SA, Loomba R, et al.. Safety and efficacy of weekly pemvidutide versus placebo for metabolic dysfunction-associated steatohepatitis (IMPACT): 24-week results from a multicentre, randomised, double-blind, phase 2b study Lancet (London, England); 2025. PMID 41237796 doi:10.1016/S0140-6736(25)02114-2
5. ALT-801 (Pemvidutide) in Healthy Overweight and Obese Volunteers to Study Safety and Tolerability 2020. NCT04561245
6. ALT-801 in Diabetic and Non-Diabetic Overweight and Obese Subjects With Non-alcoholic Fatty Liver Disease (NAFLD) 2021. NCT05006885
7. Extension of ALT-801 in Diabetic and Non-Diabetic Overweight and Obese Subjects With (NAFLD) 2022. NCT05292911
8. Efficacy and Safety of ALT-801 in the Treatment of Obesity 2022. NCT05295875
9. IMPACT TRIAL: Efficacy and Safety of Pemvidutide in Subjects With Nonalcoholic Steatohepatitis (NASH) 2023. NCT05989711

Every identifier above is resolved against PubMed, Crossref or ClinicalTrials.gov at build time, and the title returned by the register is compared with the title stored here. A page does not publish if a reference fails to resolve.

Research-Use Information

For in vitro research use only. This material is a laboratory reagent. It is not a drug, food, dietary supplement, or cosmetic and is not for human or veterinary use, including ingestion, injection, or any other administration. No information on this page describes or implies any effect in humans or animals. Sold only to researchers under our Terms of Sale.