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Pemvidutide

ALT-801 · 1:1 Balanced GLP-1 / Glucagon Dual Agonist · Altimmune · EuPort half-life domain

"Altimmune's GLP-1/glucagon dual agonist with FDA Breakthrough Therapy Designation for MASH. Same dual mechanism as survodutide but with a 1:1 balanced receptor ratio, the proprietary EuPort half-life domain for tolerability, and class-leading lean-mass preservation data. MOMENTUM Phase 2 obesity (2023): 15.6% weight loss at 48 weeks on 2.4 mg. IMPACT Phase 2b MASH (Dec 2025): up to 34.5% fibrosis improvement without MASH worsening. Phase 3 MASH launching 2026. Additional Phase 2 programmes in alcohol use disorder and alcohol-associated liver disease."

Type
1:1 balanced GLP-1 + glucagon receptor dual agonist
MOMENTUM Phase 2 result
15.6% weight loss · 48 weeks · 2.4 mg SubQ weekly
Status
UK: not illegal to buy or possess · WADA: not specifically listed · US FDA: investigational · Breakthrough Therapy Designation (MASH, Jan 2026) · Fast Track (MASH + AUD) · Phase 3 MASH launching 2026
MASH track
IMPACT Phase 2b 48-wk · up to 34.5% fibrosis improvement · Best of EASL 2026
Protocol summary
Clinical status
Phase 2b done · Phase 3 launching 2026
Trial dose
Once-weekly SubQ · 1.2 / 1.8 / 2.4 mg
Trial duration
48 weeks (MOMENTUM, IMPACT)
Trial-stage
Once-weekly SubQ · 1.2 → 1.8 → 2.4 mg (MOMENTUM/IMPACT protocol)
Altimmune escalation regimen · EuPort domain improves tolerability vs other class
Community-reported
Grey-market self-administration follows trial doses · 1.2 mg start · 1.8 mg maintenance · 2.4 mg target for max weight loss
Altimmune holds IP · counterfeit risk meaningful · published Phase 2 protocol is the reference
How we read the evidence
Late Phase 2 / pre-Phase 3 · Breakthrough Therapy Designation for MASH · class-leading lean mass preservation · multiple indications in active development
Animal evidence

Preclinical mouse MASH work showed pemvidutide producing greater weight loss and greater reductions in liver fat, inflammation and fibrosis than the GLP-1 monotherapy semaglutide — the basis for taking it forward into both obesity and MASH programmes in parallel. The 1:1 GLP-1/glucagon ratio and the EuPort half-life domain are Altimmune's design decisions; the EuPort element is intended to slow absorption into circulation, which the company argues improves tolerability compared with faster-acting GLP-1 class members.

Community & clinical practice

Pemvidutide is not commercially available and not prescribable. A grey-market research-peptide supply does exist — some users source vials labelled as pemvidutide or ALT-801 and self-administer subcutaneously, typically following the published MOMENTUM and IMPACT trial doses: 1.2 mg starting, escalating to 1.8 mg or 2.4 mg weekly for maintenance over 12–16 weeks. The community pattern tracks Altimmune's protocol because that's the only published dose data. As with survodutide, counterfeit risk is meaningfully higher than for established research peptides — Altimmune holds the IP, there's no legitimate research-grade supply chain, and vendor-sourced material is unverified by definition. Anyone going this route is treating the published Phase 2 protocol as the reference and operating without third-party verification of vial content.

Human trial data

Substantial for an unapproved compound. 12-week MASLD trial (NCT05006885): 94 patients, 1.2 / 1.8 / 2.4 mg vs placebo; maximal effect on weight (-4.3%), ALT (-13.8 IU/L) and cT1 (-75.9 ms) at 1.8 mg. 24-week MASLD extension (NCT05292911): sustained reductions in liver fat and weight. MOMENTUM Phase 2 obesity (2023, n=320, 48 weeks): 15.6% weight loss at 2.4 mg, 11.2% at 1.8 mg, 10.3% at 1.2 mg vs 2.2% placebo, with weight still falling at end of treatment. >30% of 2.4 mg subjects reached ≥20% loss. MRI sub-study (n=67): 21.9% lean loss ratio — class-leading lean mass preservation, particularly in subjects aged 60+. IMPACT Phase 2b MASH (Dec 2025, 48 weeks): 1.2 mg and 1.8 mg vs placebo in F2/F3 fibrosis patients; up to 34.5% fibrosis improvement without MASH worsening (ITT); cT1 reductions -124 ms (1.2 mg) and -140 ms (1.8 mg) vs -21 ms placebo (p<0.0001 both doses). Continued weight loss at 48 weeks with no plateau on 1.8 mg. RECLAIM Phase 2 AUD: ongoing. ALD Phase 2: launched Q3 2025. EASL Congress 2026: 48-week IMPACT data selected as "Best of EASL 2026".

Regulatory status

Investigational. FDA Breakthrough Therapy Designation for MASH (January 2026) — significantly accelerates the regulatory path versus standard timelines. Fast Track designations for both MASH and Alcohol Use Disorder. End-of-Phase 2 FDA meeting completed; Phase 3 MASH registrational parameters aligned in meeting minutes. Phase 3 MASH launches 2026 with submission likely 2027–28. Not approved by MHRA or any regulator. Anyone obtaining pemvidutide outside trials is buying counterfeit or misidentified material.

Convergence

Pemvidutide is genuinely differentiated within the GLP-1/glucagon dual-agonist class. The headline weight-loss number (15.6% at 48 weeks) is comparable to survodutide (16.6% at 76 weeks) but reached in less time and with notably better body-composition preservation (21.9% lean loss ratio — class-leading). The MASH programme has Breakthrough Therapy Designation, which survodutide does not, suggesting FDA views the antifibrotic signal as material. The expanding indications (AUD, ALD) are a plausible extension — GLP-1 receptor activation reduces alcohol craving via mesolimbic reward pathway modulation, and the glucagon component addresses alcohol-related hepatic fat. The supply-chain caveat is the same as survodutide: no legitimate research-grade chain, counterfeit risk real. Established GLP-1 options (semaglutide, tirzepatide) cover the weight-loss mechanism with approved access today.

Origin & What It Is

A balanced 1:1 dual agonist, built for the liver

Pemvidutide is a synthetic peptide developed by Altimmune, Inc. (Nasdaq: ALT), a Maryland-based clinical-stage biotech focused on peptide therapeutics for liver and cardiometabolic disease. The development code is ALT-801. Like survodutide, it's a GLP-1/glucagon dual receptor agonist — but Altimmune's design choices distinguish it. The receptor ratio is engineered to be balanced 1:1, where most competitors lean more heavily toward GLP-1 with the second receptor as accent. And the molecule incorporates Altimmune's EuPort half-life domain, proprietary technology that slows the rate of entry into circulation. The slow-absorption profile is intended to soften the peak plasma levels associated with GI adverse events — which has translated, in the published trials, into a tolerability profile with discontinuation rates lower than placebo in the IMPACT MASH data.

The development strategy is multi-indication. Pemvidutide is being run in parallel through obesity (MOMENTUM Phase 2 completed 2023), MASH (IMPACT Phase 2b completed late 2025, Phase 3 launching 2026), alcohol use disorder (RECLAIM Phase 2 underway), and alcohol-associated liver disease (Phase 2 launched Q3 2025). The AUD application is mechanistically novel — GLP-1 receptor activation modulates mesolimbic reward signalling, reducing alcohol craving in early clinical work, and the glucagon component addresses the hepatic fat that often accompanies heavy drinking. If the AUD programme delivers, pemvidutide becomes one of the few peptides with a credible addiction-medicine indication.

The FDA granted Breakthrough Therapy Designation for MASH in January 2026 following 48-week IMPACT data. BTD significantly accelerates the regulatory path — more frequent FDA interactions, rolling review, and priority review at submission. It's a stronger signal than Fast Track alone (which pemvidutide also holds for MASH and AUD). The 48-week IMPACT data was selected as "Best of EASL 2026" for the Barcelona EASL Congress.

Phase 1
First-in-human
✅ Complete
Phase 2
MOMENTUM obesity
✅ 15.6% · 2023
Phase 2b
IMPACT MASH
✅ 34.5% fibrosis · Dec 2025
BTD
MASH designation
✅ Jan 2026
Phase 3
MASH registrational
🔄 Launching 2026
Science & Mechanism

1:1 GLP-1/glucagon — with a slow-release domain

Dual Mechanism — Four Design Choices

1
GLP-1 receptor (appetite, insulin): The same baseline mechanism as semaglutide, tirzepatide and survodutide. Central appetite suppression via hypothalamic GLP-1Rs, glucose-dependent insulin secretion, delayed gastric emptying. The proven core.
2
Glucagon receptor (energy expenditure, hepatic fat): Glucagon-receptor activation drives hepatic fatty-acid oxidation and increases resting energy expenditure. Reduces hepatic lipid accumulation — the rationale for the MASH programme. Same mechanism as survodutide's glucagon arm.
3
Balanced 1:1 receptor ratio: Altimmune engineered pemvidutide for equal potency at GLP-1 and glucagon receptors, where most dual agonists lean more heavily on one arm. The hypothesis: a stronger glucagon contribution drives the lean-mass preservation (glucagon-mediated lipolysis preferentially mobilises fat over muscle) and the hepatic-fat reduction at lower weight-loss magnitudes. Published 21.9% lean loss ratio supports this — class-leading for the GLP-1 family.
4
EuPort half-life extension domain: Proprietary Altimmune technology that extends serum half-life enough for weekly dosing while specifically slowing the rate of entry into circulation. Lower peak plasma concentrations correspond to lower peak GI side effects. The IMPACT MASH 48-week safety data showed lower discontinuation-for-AE rates than placebo, which is unusual in the class.

Key MOMENTUM Phase 2 obesity data (n=320, 48 weeks, doses 1.2 / 1.8 / 2.4 mg vs placebo): 15.6% weight loss at 2.4 mg, 11.2% at 1.8 mg, 10.3% at 1.2 mg, 2.2% placebo. Near-linear continued weight loss at the 2.4 mg dose at the end of treatment — no plateau. Over 30% of 2.4 mg subjects achieved ≥20% body weight reduction. MRI sub-study: 21.9% lean loss ratio with stronger preservation in subjects aged 60 and over. Robust reductions in BMI, triglycerides, LDL cholesterol, blood pressure, with no clinically meaningful heart rate increase.

Key IMPACT Phase 2b MASH data (48 weeks, 1.2 mg and 1.8 mg vs placebo, F2/F3 fibrosis patients): 34.5% fibrosis improvement without MASH worsening (ITT analysis). cT1 reductions: -124 ms at 1.2 mg, -140 ms at 1.8 mg vs -21 ms placebo (both doses p<0.0001). AI-based digital pathology showed statistically significant fibrosis reduction at 24 weeks. Weight loss of up to 6.2% at 24 weeks with continued progression to 48 weeks on 1.8 mg, no plateau. Favourable tolerability — discontinuation-for-AE rate lower than placebo.

How pemvidutide sits against the class: Semaglutide STEP-1 (68 wk): ~14.9% weight loss, no glucagon component, recently MASH-approved. Tirzepatide SURMOUNT-1 (72 wk): ~20.9% weight loss, GLP-1/GIP, no glucagon. Survodutide SYNCHRONIZE-1 (76 wk): 16.6%, GLP-1/glucagon, no BTD. Retatrutide Phase 2 (48 wk): 24.2%, GLP-1/GIP/glucagon triple. Pemvidutide MOMENTUM (48 wk): 15.6% with class-leading lean preservation. The pemvidutide differentiators are body composition, MASH Breakthrough Therapy designation, and the multi-indication scope (AUD, ALD).

Benefits & Evidence to Date

What the data shows

⚖️
Weight loss — 15.6% at 48 weeks (Phase 2)
MOMENTUM (n=320, 48 wk): 15.6% at 2.4 mg vs 2.2% placebo. Continued weight loss at end of treatment, no plateau. >30% of high-dose subjects achieved ≥20% reduction.
● Strong — Phase 2 complete · Phase 3 launching 2026
💪
Lean mass preservation (class-leading)
MRI body composition sub-study: 21.9% lean loss ratio across the cohort, with stronger preservation in subjects aged 60+. Best-in-class for the GLP-1 family — typical GLP-1 monotherapy runs higher lean loss percentages.
● Strong — MRI sub-study published
🫀
MASH / hepatic fibrosis
IMPACT Phase 2b (48 wk): up to 34.5% fibrosis improvement without MASH worsening (ITT). cT1 -140 ms at 1.8 mg vs -21 ms placebo (p<0.0001). AI digital pathology confirmed fibrosis reduction at 24 weeks. FDA Breakthrough Therapy Designation Jan 2026.
● Strong — Phase 2b complete · BTD · Phase 3 in 2026
🍷
Alcohol use disorder (AUD)
RECLAIM Phase 2 underway. Mechanism is mesolimbic reward modulation via GLP-1 receptors — emerging evidence that GLP-1 agonism reduces alcohol craving. Fast Track designation granted.
● Limited — Phase 2 ongoing
🫀
Alcohol-associated liver disease (ALD)
Phase 2 launched Q3 2025. Combines AUD craving-reduction mechanism with glucagon-driven hepatic fat reduction — addresses both the behavioural and tissue arms of ALD.
● Limited — Phase 2 recently launched
Safety to Date

Safety profile — tolerability advantage from the EuPort domain

⚠️
IMPACT 48-week data: tolerability profile maintained from 24 weeks, with discontinuation-for-AE rate lower than placebo. GI events consistent with GLP-1 class but blunted in peak severity — Altimmune attributes this to the EuPort slow-absorption domain. Full long-term safety data will accumulate through Phase 3 and post-marketing. Class-warning watch-items (thyroid C-cell, pancreatitis, gallbladder) apply by default until proven otherwise. As with survodutide, the glucagon-receptor component creates additional hepatic considerations the Phase 3 MASH programme should clarify in a larger patient base.
Moderate
GI adverse events — nausea, vomiting, diarrhoea. Most common AE category, mild-to-moderate severity, concentrated during dose escalation. EuPort half-life domain reduces peak plasma concentrations, which Altimmune argues translates to lower peak GI symptoms — and the IMPACT discontinuation data supports the argument.
Unknown
Long-term hepatic safety — glucagon-receptor agonism is biologically active in the liver. The IMPACT MASH programme characterised hepatic effects in fibrosis patients; the Phase 3 MASH trial will extend that to a larger cohort over longer duration. Long-term hepatic safety in non-MASH populations remains incompletely characterised.
Unknown
Class-level GLP-1 cautions — thyroid C-cell tumour risk (boxed warning carried by semaglutide and tirzepatide), pancreatitis, gallbladder disease, diabetic retinopathy progression in T2D. Pemvidutide has not been shown to differ from class on these; all class-level cautions apply by default.
Unknown
Counterfeit risk in research peptide markets — pemvidutide is not commercially available. Any product labelled as such on grey-market peptide sites is by definition unverified. Like survodutide, this is one of the higher counterfeit-risk compounds because the genuine molecule has no legitimate supply route outside trials.