Pemvidutide

Overview

Pemvidutide is an investigational, lipid-modified peptide that activates both the glucagon-like peptide-1 receptor (GLP-1R) and the glucagon receptor (GCGR). Randomized human studies have evaluated MRI-measured liver fat, body-weight change and biopsy-defined MASH outcomes. The evidence is therefore more substantial than a preclinical lead, but it does not make pemvidutide an approved medicine or establish a self-use regimen.

The most important current result is mixed. In the 212-participant IMPACT phase 2b trial, pemvidutide met the 24-week co-primary endpoint of MASH resolution without worsening fibrosis. It did not meet the other co-primary endpoint of fibrosis improvement without worsening MASH. Both results must travel together.

Verified identity and name collisions

WHO Proposed INN List 126 identifies pemvidutide as CAS 2538014-94-5 with formula C182H275N39O54 and the 29-residue modified sequence HXQGTFTSDYSKYLDEKAAKEFIQWLLQT. In that display, position 2 X is 2-methylalanine, Lys17 carries the glucuronoyl-linked C18 diacid substituent, Glu16 and Lys20 form an amide bridge, and terminal Thr29 is amidated. WHO describes the molecule as an agonist of both the glucagon and GLP-1 receptors. FDA GSRS assigns UNII A35F525WBG to pemvidutide.

No molecular weight is published here. The current FDA GSRS properties expose an estimated 3891.409 Da together with formula C182H283N39O58; that formula does not reproduce the displayed mass and conflicts with WHO's formula and modification mapping. Choosing one value editorially would create false precision, so the discrepancy is documented and the field is withheld.

Those details identify the registered substance record; they do not verify the identity, purity or sterility of an untested product. FDA explicitly notes that a UNII is an identity standard and does not imply regulatory review or approval.

The development code ALT-801 requires context. Altimmune registry records use it for pemvidutide, but older oncology literature uses ALT-801 for an unrelated interleukin-2/T-cell-receptor fusion protein (PMID 21994418). Searching the code without the sponsor, sequence or mechanism can therefore join evidence from two different substances.

Mechanism and structural basis

FDA GSRS records pemvidutide as an agonist target relation for both GLP-1R and GCGR. The human trial papers use the same dual-agonist description. GLP-1 receptor activation is associated with appetite and glucose-regulatory effects, while glucagon-receptor activation provides a research rationale for hepatic lipid metabolism. Clinical endpoints, however, measure the combined investigational product; they do not assign a known share of an outcome to each receptor.

The lipid-related position-17 modification is part of the defined molecule and supports prolonged exposure as a development strategy. It does not by itself prove a particular half-life, dosing interval, clinical benefit or product equivalence. PeptideGuide's shorthand that the half-life is “weekly” confuses a protocol schedule with a pharmacokinetic measurement, so that claim is not promoted.

Pharmacokinetics and dosing boundary

The peer-reviewed human sources reviewed here do not provide a sufficiently clear, directly reported pemvidutide half-life value to protect as an article fact. The studies administered defined products on once-weekly schedules, but once weekly is not a half-life.

Trial amounts are retained only where needed to interpret randomization and outcomes. They cannot be converted into a personal regimen: study eligibility, manufacturing controls, exposure, monitoring and stopping rules are not reproduced by buying or mixing a research material. No oral, compounded or vendor product can be assumed bioequivalent to the trial product.

Evidence map

Randomized MASLD and MASH evidence

Twelve- and 24-week imaging studies

In NCT 05006885, 94 participants with BMI at least 28 kg/m² and MRI liver fat at least 10% were randomized to three pemvidutide arms or placebo for 12 weeks. Mean relative liver-fat reductions were 46.6%, 68.5% and 57.1% in the three active arms, compared with 4.4% with placebo (p<0.001 for each comparison). These are relative MRI-PDFF changes in a short trial, not percentages of participants cured.

The extension NCT 05292911 included 64 completers for 24 total weeks. Relative liver-fat changes from the original baseline were 56.3%, 75.2% and 76.4%, versus 14.0% with placebo; the paper also reported 6.2% body-weight reduction for the strongest active comparison. Because entry required completion and continued treatment in the parent study, the extension is informative but more selected than a fresh 64-person randomization.

IMPACT biopsy endpoints: one met, one not met

IMPACT randomized 212 participants with biopsy-confirmed MASH and F2 or F3 fibrosis: 86 to placebo, 41 to pemvidutide 1.2 mg and 85 to pemvidutide 1.8 mg. At week 24, MASH resolution without fibrosis worsening occurred in 20% (18/86), 58% (24/41) and 52% (45/85), respectively. Differences versus placebo were 38 percentage points and 32 percentage points, both p<0.0001.

The fibrosis co-primary endpoint was negative. At least one-stage fibrosis improvement without worsening MASH occurred in 28% (24/86) with placebo, 33% (13/41) with 1.2 mg and 36% (30/85) with 1.8 mg. Differences were 5 percentage points (p=0.59) and 8 percentage points (p=0.27). The trial therefore did not show a statistically significant fibrosis improvement at 24 weeks. A positive MASH-resolution result must not be rewritten as proven fibrosis reversal.

Safety and funding boundary

In the 24-week MASLD extension, drug-related adverse events were reported in 50.0%, 80.0% and 57.1% of the three pemvidutide groups, versus 42.1% with placebo. Nausea was the most common event; two participants in the 1.2 mg group and one in the 1.8 mg group stopped treatment because of adverse events. The paper reported no serious adverse events in this small extension.

In IMPACT, adverse events occurred in 78%, 81% and 67% of the 1.2 mg, 1.8 mg and placebo groups; most were mild or moderate. Treatment discontinuation because of adverse events occurred in 0/41, 1/85 and 2/86. These short, selected trials cannot exclude uncommon or long-latency harms, provide product-quality assurance outside trials or establish safety in people who did not meet their eligibility criteria.

Altimmune funded all three published trials. In the 24-week extension, several authors were employees with financial interests, and company-associated authors designed, collected, analysed and interpreted the data. Sponsor involvement does not invalidate a randomized result, but it is material when weighing replication, endpoint selection and claims that extend beyond the paper.

Current clinical-trial programme

A sponsor-bounded ClinicalTrials.gov query for pemvidutide OR "ALT-801", checked on 21 August 2026, returned 9 records: 8 completed and 1 active, not recruiting. Five were phase 1 and four phase 2; none had posted structured results in the registry snapshot.

The completed records include MOMENTUM for obesity (NCT 05295875, 391 participants), IMPACT for MASH (NCT 05989711, 212), RECLAIM for alcohol use disorder in people with overweight or obesity (NCT 06987513, 100), and earlier MASLD, type 2 diabetes, interaction and first-in-human studies. RESTORE for alcohol-associated liver disease (NCT 07009860, planned 121) was active, not recruiting. Registry status proves that a study exists; it does not supply a positive outcome. In particular, MOMENTUM's “results submitted” label is not a substitute for posted structured results or a peer-reviewed report.

Current regulatory status

Exact-name searches of FDA's public Drugs@FDA data returned no match for pemvidutide or ALT-801 on 21 August 2026. A case-insensitive search of the current European Commission Union Register dataset returned 0 matches for the same names. These are bounded public-data checks for FDA approvals and centrally authorised EU medicines, not proof about every national register or future decision.

The FDA GSRS identity page is not an approval record. Likewise, a trial being listed as involving an “FDA-regulated drug product” describes regulatory oversight of the study; it does not mean the investigational product has an approved indication.

Russian literature

A Russian-origin 2026 Doctor.Ru narrative review by Semikova and colleagues discusses pemvidutide in fatty-liver research. Its pemvidutide section summarises the same 94-participant, 12-week international study and reproduces the 46.6%, 68.5% and 57.1% relative liver-fat changes. The authors reported no external funding.

The review is useful Russian-language secondary context, but it is not a Russian pemvidutide trial, independent replication or new safety dataset. It also does not replace the later IMPACT result, especially the failed 24-week fibrosis endpoint. No Russian-origin primary human pemvidutide study was located in the accessible indexed sources reviewed.

WADA and sport

An exact-name check of the official 2026 WADA Prohibited List produced no named match for pemvidutide or ALT-801. The list is not exhaustive, the ALT-801 code is ambiguous, and absence of a name is not a sport-eligibility decision.

No S0 or other WADA class is inferred. Medicinal approval, trial status and anti-doping classification are separate axes. Athletes remain responsible for product contents and need a current case-specific answer from their anti-doping organisation or Global DRO rather than relying on this name search.

Research-integrity conclusion

The PeptideGuide discovery record cites PMID 33567185. That PMID is the semaglutide STEP 1 obesity trial, not a pemvidutide study, and cannot support pemvidutide efficacy, safety, dosing or pharmacokinetics. Its green safety label, weekly “half-life” and benefit summary are therefore not promoted.

The defensible conclusion is narrower. Pemvidutide is a defined dual GLP-1R/GCGR agonist with randomized human MASLD and MASH evidence. Short imaging studies reported substantial liver-fat changes, and IMPACT reported more MASH resolution without fibrosis worsening. But IMPACT's fibrosis-improvement co-primary endpoint was not met, long-term clinical benefit-risk is unknown, no approved regimen exists, and current registry activity is not regulatory approval.