--- title: "Efimosfermin Alfa | PepTracker Pro" description: "Efimosfermin alfa (development code BOS-580) is an investigational, long-acting, engineered analog of the metabolic hormone fibroblast growth factor 21 (FGF21) being developed by GSK - which acquired the molecule from Boston Pharmaceuticals in May 2025 for $1.2 billion upfront and up to $800 million in milestones (potential ~$2 billion total) - for steatotic liver disease, principally metabolic dysfunction-associated steatohepatitis (MASH, formerly NASH). Its defining feature is a very long half-life engineered to allow once-monthly subcutaneous dosing - the least frequent schedule among the leading FGF21 analogs, contrasting with the once-weekly or every-two-weeks dosing of efruxifermin (an Fc-FGF21 fusion) and pegozafermin (a glycoPEGylated FGF21). Like the rest of the class, it activates FGF receptors (FGFR1c/2c/3c) together with the co-receptor beta-Klotho to cut liver fat, improve insulin sensitivity, lower triglycerides, and drive direct anti-inflammatory and anti-fibrotic effects in the liver. In a 24-week Phase 2 trial in biopsy-confirmed F2-F3 MASH, once-monthly efimosfermin achieved at least one-stage fibrosis improvement without worsening of MASH in about 45% of patients and MASH resolution without worsening of fibrosis in about 68%, both significantly better than placebo (published in The Lancet, 2025). It holds FDA Breakthrough Therapy designation and EMA PRIME (Priority Medicines) status for MASH, and has advanced into the Phase 3 ZENITH program (ZENITH-1 and ZENITH-2 in F2-F3 MASH), with a Phase 3 program in compensated (F4) MASH cirrhosis also underway; GSK has guided to a first potential launch around 2029." lang: en json-ld: | [ { "@context": "https://schema.org", "@type": "Organization", "name": "PepTracker Pro", "url": "https://peptrackerpro.com", "logo": "https://peptrackerpro.com/favicon.png", "description": "Evidence-based educational resource dedicated to improving peptide research literacy.", "contactPoint": { "@type": "ContactPoint", "email": "hello@peptrackerpro.com", "contactType": "customer support" }, "sameAs": [] }, { "@context": "https://schema.org", "@type": "MedicalWebPage", "name": "Efimosfermin Alfa", "description": "Efimosfermin alfa (development code BOS-580) is an investigational, long-acting, engineered analog of the metabolic hormone fibroblast growth factor 21 (FGF21) being developed by GSK - which acquired the molecule from Boston Pharmaceuticals in May 2025 for $1.2 billion upfront and up to $800 million in milestones (potential ~$2 billion total) - for steatotic liver disease, principally metabolic dysfunction-associated steatohepatitis (MASH, formerly NASH). Its defining feature is a very long half-life engineered to allow once-monthly subcutaneous dosing - the least frequent schedule among the leading FGF21 analogs, contrasting with the once-weekly or every-two-weeks dosing of efruxifermin (an Fc-FGF21 fusion) and pegozafermin (a glycoPEGylated FGF21). Like the rest of the class, it activates FGF receptors (FGFR1c/2c/3c) together with the co-receptor beta-Klotho to cut liver fat, improve insulin sensitivity, lower triglycerides, and drive direct anti-inflammatory and anti-fibrotic effects in the liver. In a 24-week Phase 2 trial in biopsy-confirmed F2-F3 MASH, once-monthly efimosfermin achieved at least one-stage fibrosis improvement without worsening of MASH in about 45% of patients and MASH resolution without worsening of fibrosis in about 68%, both significantly better than placebo (published in The Lancet, 2025). It holds FDA Breakthrough Therapy designation and EMA PRIME (Priority Medicines) status for MASH, and has advanced into the Phase 3 ZENITH program (ZENITH-1 and ZENITH-2 in F2-F3 MASH), with a Phase 3 program in compensated (F4) MASH cirrhosis also underway; GSK has guided to a first potential launch around 2029.", "url": "https://peptrackerpro.com/peptides/efimosfermin", "lastReviewed": "2026-07-13", "reviewedBy": { "@type": "Organization", "name": "PepTracker Pro Research Team", "url": "https://peptrackerpro.com" }, "isPartOf": { "@type": "WebSite", "name": "PepTracker Pro", "url": "https://peptrackerpro.com" } }, { "@context": "https://schema.org", "@type": "BreadcrumbList", "itemListElement": [ { "@type": "ListItem", "position": 1, "name": "Home", "item": "https://peptrackerpro.com" }, { "@type": "ListItem", "position": 2, "name": "Peptides", "item": "https://peptrackerpro.com/peptides" }, { "@type": "ListItem", "position": 3, "name": "Efimosfermin Alfa", "item": "https://peptrackerpro.com/peptides/efimosfermin" } ] }, { "@context": "https://schema.org", "@type": "FAQPage", "mainEntity": [ { "@type": "Question", "name": "People with MASH/NASH or advanced fibrosis tracking non-incretin, liver-directed drug candidates - especially those interested in a once-monthly option.?", "acceptedAnswer": { "@type": "Answer", "text": "Efimosfermin Alfa is a research peptide studied in preclinical models. Efimosfermin alfa (development code BOS-580) is an investigational, long-acting, engineered analog of the metabolic hormone fibroblast growth factor 21 (FGF21) being developed by GSK - which acquired the molecule from Boston Pharmaceuticals in May 2025 for $1.2 billion upfront and up to $800 million in milestones (potential ~$2 billion total) - for steatotic liver disease, principally metabolic dysfunction-associated steatohepatitis (MASH, formerly NASH). Its defining feature is a very long half-life engineered to allow once-monthly subcutaneous dosing - the least frequent schedule among the leading FGF21 analogs, contrasting with the once-weekly or every-two-weeks dosing of efruxifermin (an Fc-FGF21 fusion) and pegozafermin (a glycoPEGylated FGF21). Like the rest of the class, it activates FGF receptors (FGFR1c/2c/3c) together with the co-receptor beta-Klotho to cut liver fat, improve insulin sensitivity, lower triglycerides, and drive direct anti-inflammatory and anti-fibrotic effects in the liver. In a 24-week Phase 2 trial in biopsy-confirmed F2-F3 MASH, once-monthly efimosfermin achieved at least one-stage fibrosis improvement without worsening of MASH in about 45% of patients and MASH resolution without worsening of fibrosis in about 68%, both significantly better than placebo (published in The Lancet, 2025). It holds FDA Breakthrough Therapy designation and EMA PRIME (Priority Medicines) status for MASH, and has advanced into the Phase 3 ZENITH program (ZENITH-1 and ZENITH-2 in F2-F3 MASH), with a Phase 3 program in compensated (F4) MASH cirrhosis also underway; GSK has guided to a first potential launch around 2029." } }, { "@type": "Question", "name": "Clinicians and researchers comparing FGF21 analogs (efimosfermin vs efruxifermin vs pegozafermin) and weighing them against incretin and other MASH mechanisms.?", "acceptedAnswer": { "@type": "Answer", "text": "Efimosfermin Alfa is a research peptide studied in preclinical models. Efimosfermin alfa (development code BOS-580) is an investigational, long-acting, engineered analog of the metabolic hormone fibroblast growth factor 21 (FGF21) being developed by GSK - which acquired the molecule from Boston Pharmaceuticals in May 2025 for $1.2 billion upfront and up to $800 million in milestones (potential ~$2 billion total) - for steatotic liver disease, principally metabolic dysfunction-associated steatohepatitis (MASH, formerly NASH). Its defining feature is a very long half-life engineered to allow once-monthly subcutaneous dosing - the least frequent schedule among the leading FGF21 analogs, contrasting with the once-weekly or every-two-weeks dosing of efruxifermin (an Fc-FGF21 fusion) and pegozafermin (a glycoPEGylated FGF21). Like the rest of the class, it activates FGF receptors (FGFR1c/2c/3c) together with the co-receptor beta-Klotho to cut liver fat, improve insulin sensitivity, lower triglycerides, and drive direct anti-inflammatory and anti-fibrotic effects in the liver. In a 24-week Phase 2 trial in biopsy-confirmed F2-F3 MASH, once-monthly efimosfermin achieved at least one-stage fibrosis improvement without worsening of MASH in about 45% of patients and MASH resolution without worsening of fibrosis in about 68%, both significantly better than placebo (published in The Lancet, 2025). It holds FDA Breakthrough Therapy designation and EMA PRIME (Priority Medicines) status for MASH, and has advanced into the Phase 3 ZENITH program (ZENITH-1 and ZENITH-2 in F2-F3 MASH), with a Phase 3 program in compensated (F4) MASH cirrhosis also underway; GSK has guided to a first potential launch around 2029." } }, { "@type": "Question", "name": "Patients and caregivers interested in low-frequency dosing schedules for chronic liver disease.?", "acceptedAnswer": { "@type": "Answer", "text": "Efimosfermin Alfa is a research peptide studied in preclinical models. Efimosfermin alfa (development code BOS-580) is an investigational, long-acting, engineered analog of the metabolic hormone fibroblast growth factor 21 (FGF21) being developed by GSK - which acquired the molecule from Boston Pharmaceuticals in May 2025 for $1.2 billion upfront and up to $800 million in milestones (potential ~$2 billion total) - for steatotic liver disease, principally metabolic dysfunction-associated steatohepatitis (MASH, formerly NASH). Its defining feature is a very long half-life engineered to allow once-monthly subcutaneous dosing - the least frequent schedule among the leading FGF21 analogs, contrasting with the once-weekly or every-two-weeks dosing of efruxifermin (an Fc-FGF21 fusion) and pegozafermin (a glycoPEGylated FGF21). Like the rest of the class, it activates FGF receptors (FGFR1c/2c/3c) together with the co-receptor beta-Klotho to cut liver fat, improve insulin sensitivity, lower triglycerides, and drive direct anti-inflammatory and anti-fibrotic effects in the liver. In a 24-week Phase 2 trial in biopsy-confirmed F2-F3 MASH, once-monthly efimosfermin achieved at least one-stage fibrosis improvement without worsening of MASH in about 45% of patients and MASH resolution without worsening of fibrosis in about 68%, both significantly better than placebo (published in The Lancet, 2025). It holds FDA Breakthrough Therapy designation and EMA PRIME (Priority Medicines) status for MASH, and has advanced into the Phase 3 ZENITH program (ZENITH-1 and ZENITH-2 in F2-F3 MASH), with a Phase 3 program in compensated (F4) MASH cirrhosis also underway; GSK has guided to a first potential launch around 2029." } }, { "@type": "Question", "name": "Investors and industry watchers following GSK's MASH strategy, the Boston Pharmaceuticals acquisition, and the competitive FGF21 drug race, including the Phase 3 ZENITH readouts.?", "acceptedAnswer": { "@type": "Answer", "text": "Efimosfermin Alfa is a research peptide studied in preclinical models. Efimosfermin alfa (development code BOS-580) is an investigational, long-acting, engineered analog of the metabolic hormone fibroblast growth factor 21 (FGF21) being developed by GSK - which acquired the molecule from Boston Pharmaceuticals in May 2025 for $1.2 billion upfront and up to $800 million in milestones (potential ~$2 billion total) - for steatotic liver disease, principally metabolic dysfunction-associated steatohepatitis (MASH, formerly NASH). Its defining feature is a very long half-life engineered to allow once-monthly subcutaneous dosing - the least frequent schedule among the leading FGF21 analogs, contrasting with the once-weekly or every-two-weeks dosing of efruxifermin (an Fc-FGF21 fusion) and pegozafermin (a glycoPEGylated FGF21). Like the rest of the class, it activates FGF receptors (FGFR1c/2c/3c) together with the co-receptor beta-Klotho to cut liver fat, improve insulin sensitivity, lower triglycerides, and drive direct anti-inflammatory and anti-fibrotic effects in the liver. In a 24-week Phase 2 trial in biopsy-confirmed F2-F3 MASH, once-monthly efimosfermin achieved at least one-stage fibrosis improvement without worsening of MASH in about 45% of patients and MASH resolution without worsening of fibrosis in about 68%, both significantly better than placebo (published in The Lancet, 2025). It holds FDA Breakthrough Therapy designation and EMA PRIME (Priority Medicines) status for MASH, and has advanced into the Phase 3 ZENITH program (ZENITH-1 and ZENITH-2 in F2-F3 MASH), with a Phase 3 program in compensated (F4) MASH cirrhosis also underway; GSK has guided to a first potential launch around 2029." } } ] } ] --- [Skip to main content](#main) **Educational information only.** This site does not provide medical advice. [Read full disclaimer](/disclaimer) [PepTracker Pro](/) [Home](/)[Peptides](/peptides)[Compare](/compare)[Glossary](/glossary)[Blog](/blog)[Calculators](/calculators)[Start Here](/start) [Open the App](https://app.peptrackerpro.com) [Peptides](/peptides)/ Efimosfermin Alfa **Research-only content.** This page is for educational purposes and does not constitute medical advice. [Read full disclaimer →](/research-disclaimer) # Efimosfermin Alfa Low Evidence Efimosfermin alfa (development code BOS-580) is an investigational, long-acting, engineered analog of the metabolic hormone fibroblast growth factor 21 (FGF21) being developed by GSK - which acquired the molecule from Boston Pharmaceuticals in May 2025 for $1.2 billion upfront and up to $800 million in milestones (potential ~$2 billion total) - for steatotic liver disease, principally metabolic dysfunction-associated steatohepatitis (MASH, formerly NASH). Its defining feature is a very long half-life engineered to allow once-monthly subcutaneous dosing - the least frequent schedule among the leading FGF21 analogs, contrasting with the once-weekly or every-two-weeks dosing of efruxifermin (an Fc-FGF21 fusion) and pegozafermin (a glycoPEGylated FGF21). Like the rest of the class, it activates FGF receptors (FGFR1c/2c/3c) together with the co-receptor beta-Klotho to cut liver fat, improve insulin sensitivity, lower triglycerides, and drive direct anti-inflammatory and anti-fibrotic effects in the liver. In a 24-week Phase 2 trial in biopsy-confirmed F2-F3 MASH, once-monthly efimosfermin achieved at least one-stage fibrosis improvement without worsening of MASH in about 45% of patients and MASH resolution without worsening of fibrosis in about 68%, both significantly better than placebo (published in The Lancet, 2025). It holds FDA Breakthrough Therapy designation and EMA PRIME (Priority Medicines) status for MASH, and has advanced into the Phase 3 ZENITH program (ZENITH-1 and ZENITH-2 in F2-F3 MASH), with a Phase 3 program in compensated (F4) MASH cirrhosis also underway; GSK has guided to a first potential launch around 2029. Aliases Efimosfermin Alfa +5 more Evidence Low Evidence Last Updated 2026-07-13 Reading Time 6 min ## Table of Contents 1. [What It Is](#what-it-is) 2. [Regulatory Status](#regulatory-status) 3. [Why Researchers Study It](#why-researchers-study) 4. [Proposed Mechanisms](#proposed-mechanisms) 5. [Evidence Snapshot](#evidence-snapshot) 6. [Commonly Discussed Benefits](#benefits) 7. [Safety & Cautions](#safety) 8. [Comparisons](#comparisons) 9. [Calculator Tools](#calculator) 10. [Citations](#citations) ## What It Is Efimosfermin alfa (BOS-580) is an investigational, long-acting analog of fibroblast growth factor 21 (FGF21), the endogenous hormone the body releases - mainly from the liver - under fasting and metabolic stress to tell liver, fat, and brain tissue to burn fat, sharpen insulin sensitivity, lower circulating triglycerides, and quiet hepatic inflammation and scarring. Native FGF21 is an appealing target for metabolic dysfunction-associated steatohepatitis (MASH), the fibrosing form of fatty liver disease that can progress to cirrhosis, but it is cleared from the body within hours, making it impractical as a drug. Efimosfermin is engineered to dramatically extend that half-life - far enough to support once-monthly subcutaneous injection, the longest dosing interval among the front-running FGF21 analogs and its main practical differentiator from once-weekly efruxifermin and once-weekly/every-two-weeks pegozafermin. Mechanistically all three converge on the same pathway: the FGF21 backbone anchors to the co-receptor beta-Klotho and then engages FGF receptors (FGFR1c, FGFR2c, FGFR3c) to trigger the metabolic signaling that reduces liver fat and fibrosis. The molecule originated at Boston Pharmaceuticals and was acquired by GSK in May 2025 in a deal worth up to roughly $2 billion, giving GSK a Phase 3-ready, potential best-in-class entrant in the increasingly crowded MASH field. Its clinical program spans pre-cirrhotic F2-F3 disease (the Phase 3 ZENITH-1 and ZENITH-2 trials) and compensated F4 cirrhosis, positioning efimosfermin as a liver-directed therapy distinct from - and a potential future combination partner for - the incretin (GLP-1/GIP/glucagon) weight-loss drugs. Also known as: Efimosfermin Alfa, Efimosfermin, BOS-580, GSK5073706, long-acting FGF21 analog (GSK), efimosfermin (MASH) ## Regulatory Status ## Why Researchers Study It Efimosfermin is one of the three most advanced FGF21 analogs and the one built around the longest dosing interval - once monthly - making it a key test of whether a convenient, low-burden FGF21 therapy can match the fibrosis-reversing ambitions of once-weekly rivals efruxifermin and pegozafermin. Because it works through a mechanism entirely different from the GLP-1/GIP/glucagon incretin drugs, it is studied both as a standalone MASH therapy across the fibrosis spectrum and as a potential future combination partner for incretin-based weight-loss agents. GSK's ~$2 billion acquisition and the drug's FDA Breakthrough Therapy and EMA PRIME designations have made its Phase 3 ZENITH readouts one of the more closely watched events in the MASH field, and the head-to-head question of monthly efimosfermin versus weekly efruxifermin and pegozafermin is a defining debate for how best to drug the FGF21 pathway. ## Proposed Mechanisms - FGF21 receptor agonism: efimosfermin activates FGF receptor complexes (FGFR1c, FGFR2c, and FGFR3c) together with the obligate co-receptor beta-Klotho in liver, adipose tissue, and other metabolic tissues, reproducing and amplifying the actions of native FGF21. - Direct hepatic effects: reduces hepatic de novo lipogenesis and liver fat and drives anti-inflammatory and anti-fibrotic actions in the liver, aiming to resolve steatohepatitis and improve fibrosis. - Improved insulin sensitivity and lipid handling: enhances peripheral glucose uptake and fat oxidation and lowers circulating triglycerides while improving the cholesterol profile, targeting the metabolic drivers of MASH. - Adipose-tissue signaling: acts on fat tissue to raise adiponectin and promote healthier lipid storage, part of the broader FGF21 metabolic program. - Engineered long half-life: protein engineering greatly extends the very short half-life of native FGF21 - far enough to allow once-monthly subcutaneous dosing, the longest interval among the leading FGF21 analogs and a contrast with efruxifermin's Fc-fusion and pegozafermin's glycoPEGylation weekly approaches. ## Evidence Snapshot Low Evidence Low Medium High Study Type Model Outcome Link RCT (human, Phase 2 - 24 weeks) Biopsy-confirmed F2-F3 MASH; once-monthly subcutaneous efimosfermin alfa (300 mg every 4 weeks) vs placebo At least one-stage fibrosis improvement without worsening of MASH in ~45% of patients and MASH resolution without worsening of fibrosis in ~68%, both significantly greater than placebo, alongside reductions in liver fat and liver-injury markers [Source](https://www.thelancet.com/journals/lancet/article/PIIS0140-6736\(25\)02276-7/abstract) RCT (human, Phase 2a - dose-ranging, 12 weeks) Phenotypic MASH (BMI 30-45), 12 US centers; efimosfermin 75 mg or 150 mg every 2 or 4 weeks, or 300 mg every 4 weeks, vs placebo Favorable safety and tolerability with improvements in hepatic steatosis (liver fat) and metabolic markers; results supported feasibility of every-4-week (once-monthly) dosing and further MASH development [Source](https://www.thelancet.com/journals/langas/article/PIIS2468-1253\(25\)00067-6/abstract) RCT (human, Phase 3 - ZENITH program, ongoing) ZENITH-1 and ZENITH-2 pivotal trials in biopsy-confirmed F2-F3 MASH (e.g., NCT07221227, NCT07221188), plus a Phase 3 program and Phase 2 study (NCT06920043) in compensated F4 MASH cirrhosis Pivotal program designed to confirm fibrosis improvement and MASH resolution across the fibrosis spectrum; no efficacy readouts yet, with a first potential launch guided to around 2029 [Source](https://clinicaltrials.gov/study/NCT07221227) ## Commonly Discussed Benefits [metabolic dysfunction-associated steatohepatitis (MASH/NASH) - fibrosis improvement and MASH resolution in pre-cirrhotic F2-F3 disease (investigational)]()[reductions in liver fat (MRI-PDFF), liver enzymes, and non-invasive fibrosis biomarkers]()[improved insulin sensitivity, glycemic markers, and blood lipids (lower triglycerides, improved cholesterol profile)]()[potential treatment of compensated (F4) MASH cirrhosis (investigational; Phase 3 program underway)]()[once-monthly subcutaneous dosing - the longest interval among leading FGF21 analogs - enabled by an engineered long half-life]() Researching Efimosfermin Alfa ? Track it, set reminders, and keep notes in the free app. [Track in App](https://app.peptrackerpro.com/?add=efimosfermin) ## Safety & Cautions - Investigational and not approved: efimosfermin is in Phase 3 development for MASH and is not available by prescription; its ability to improve fibrosis and clinical outcomes in the pivotal ZENITH trials remains to be confirmed. - No self-sourcing: efimosfermin is a proprietary, engineered FGF21 biologic studied only in controlled trials. Material sold online as 'efimosfermin', 'BOS-580', or 'FGF21' is not the clinical drug and cannot be assumed authentic, pure, or safe. - Gastrointestinal effects and appetite: the most commonly reported adverse effects in trials are diarrhea, nausea, and increased appetite, generally mild-to-moderate and transient. - FGF21-class considerations: agents in this class have been examined for possible effects on bone-turnover markers and other parameters; the long-term significance of these signals is still being studied. - Not a weight-loss or obesity drug: unlike the incretins, efimosfermin is being developed for liver disease (MASH), and it should not be conflated with GLP-1/GIP-based weight-loss therapies. ## Comparisons See how Efimosfermin Alfa compares to related peptides: [Efimosfermin Alfa vs Survodutide](/compare/efimosfermin-vs-survodutide) [Efimosfermin Alfa vs Pemvidutide](/compare/efimosfermin-vs-pemvidutide) [Efimosfermin Alfa vs Efocipegtrutide](/compare/efimosfermin-vs-efocipegtrutide) [Efimosfermin Alfa vs Pegozafermin](/compare/efimosfermin-vs-pegozafermin) [Efimosfermin Alfa vs Efruxifermin](/compare/efimosfermin-vs-efruxifermin) ## Calculator Tools Use our research tools to explore dosing and reconstitution data: [Reconstitution Calculator](/calculators) ## Citations 1. \[1\] Once-monthly efimosfermin alfa (BOS-580) in MASH with F2 or F3 fibrosis: 24-week Phase 2 results - The Lancet (2025) [PubMed](https://www.thelancet.com/journals/lancet/article/PIIS0140-6736\(25\)02276-7/abstract) 2. \[2\] Efimosfermin alfa (BOS-580), a long-acting FGF21 analogue, in phenotypic MASH: Phase 2a trial - The Lancet Gastroenterology & Hepatology (2025) [PubMed](https://www.thelancet.com/journals/langas/article/PIIS2468-1253\(25\)00067-6/abstract) 3. \[3\] GSK to acquire efimosfermin, a Phase III-ready potential best-in-class medicine for steatotic liver disease - GSK (May 2025) [PubMed](https://www.gsk.com/en-gb/media/press-releases/gsk-to-acquire-efimosfermin-a-phase-iii-ready-potential-best-in-class-specialty-medicine-to-treat-and-prevent-progression-of-steatotic-liver-disease-sld/) 4. \[4\] GSK's investigational liver therapy efimosfermin receives US FDA Breakthrough Therapy and EMA PRIME designations for MASH - GSK [PubMed](https://www.gsk.com/en-gb/media/press-releases/gsk-s-investigational-liver-therapy-efimosfermin-receives-us-fda-breakthrough-therapy/) 5. \[5\] A Pivotal Clinical Study to Investigate Efimosfermin Alfa in Participants With Biopsy-confirmed F2- or F3-stage MASH - ClinicalTrials.gov (NCT07221227) [PubMed](https://clinicaltrials.gov/study/NCT07221227) ### Keep researching in the app - Log Efimosfermin Alfa to your private tracker - Set a dosing reminder - Compare it side-by-side with your stack [Open PepTracker Pro Free](https://app.peptrackerpro.com/?add=efimosfermin) [Browse more peptides](/peptides) ## Related Peptides ### Survodutide Medium Evidence A dual GLP-1/glucagon receptor agonist with FDA Breakthrough Therapy designation for MASH and Priority Review NDA filed February 2026. Phase 3 SYNCHRONIZE-1 reported 16.6% weight loss at 76 weeks; approval possible Q3 2026. [Weight Management](/benefits/weight-management)[Appetite Regulation](/benefits/appetite-regulation)[Metabolism](/benefits/metabolism)[Fat Loss](/benefits/fat-loss) [View Details](/peptides/survodutide) [\+ Compare](/compare?select=survodutide)[](https://app.peptrackerpro.com/?add=survodutide) ### Pemvidutide Medium Evidence A GLP-1/glucagon dual receptor agonist with FDA Breakthrough Therapy Designation for MASH, showing strong weight loss and liver benefits in Phase 2 trials. [Weight Management](/benefits/weight-management)[Fat Loss](/benefits/fat-loss)[Liver Health](/benefits/liver-health)[Metabolism](/benefits/metabolism) [View Details](/peptides/pemvidutide) [\+ Compare](/compare?select=pemvidutide)[](https://app.peptrackerpro.com/?add=pemvidutide) ### Efocipegtrutide Medium Evidence Efocipegtrutide (Hanmi code HM15211) is an investigational, long-acting, once-weekly GLP-1/GIP/glucagon 'triple' receptor agonist being developed primarily for metabolic dysfunction-associated steatohepatitis (MASH, formerly NASH) rather than obesity alone. It is built on Hanmi's LAPSCovery platform as a chemical conjugate of a chimeric tri-agonist peptide (TA15211) fused to a human IgG4 Fc fragment, which extends its half-life via FcRn-mediated recycling and enables weekly subcutaneous dosing. By adding glucagon-receptor activation to the GLP-1/GIP dual mechanism, efocipegtrutide is designed to combine appetite suppression and glycemic control with increased energy expenditure and direct hepatic anti-steatotic, anti-inflammatory, and anti-fibrotic effects. In a Phase 1b/2a study in obese subjects with non-alcoholic fatty liver disease, 12 weeks of treatment reduced liver fat by roughly 20% to 59% (dose-dependent, MRI-PDFF) versus about 6% on placebo. It has FDA Fast Track designation for MASH and orphan-drug designations from the FDA and EMA for primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and idiopathic pulmonary fibrosis (IPF). The 52-week adaptive Phase 2 HM-TRIA-201 study (NCT04505436) in biopsy-confirmed MASH with fibrosis is the pivotal read the field is watching. [Liver Health](/benefits/liver-health)[Weight Management](/benefits/weight-management)[Glycemic Control](/benefits/glycemic-control)[Metabolism](/benefits/metabolism) [View Details](/peptides/efocipegtrutide) [\+ Compare](/compare?select=efocipegtrutide)[](https://app.peptrackerpro.com/?add=efocipegtrutide) ### Pegozafermin Low Evidence Pegozafermin (development code BIO89-100) is an investigational, long-acting analog of fibroblast growth factor 21 (FGF21) being developed for metabolic dysfunction-associated steatohepatitis (MASH, formerly NASH) and for severe hypertriglyceridemia (SHTG). Originally developed by 89bio and acquired by Roche in a deal announced in September 2025 (about $2.4 billion upfront and up to roughly $3.5 billion including a contingent value right), it uses site-specific glycoPEGylation to extend the very short half-life of native FGF21 to roughly 55-100 hours, enabling once-weekly or once-every-two-weeks subcutaneous dosing. FGF21 is a metabolic hormone that acts on liver, fat, and other tissues to improve insulin sensitivity, lower triglycerides, and exert direct anti-fibrotic and anti-inflammatory effects. In the Phase 2b ENLIVEN trial in biopsy-confirmed F2-F3 MASH, the 44 mg every-two-weeks dose produced at least a one-stage fibrosis improvement without worsening of MASH in about 27% of patients versus 7% on placebo, and MASH resolution without worsening of fibrosis in about 26% versus 2% on placebo, with benefits sustained through week 48. Pegozafermin holds FDA Breakthrough Therapy designation and EMA PRIME status for MASH and has advanced into the Phase 3 ENLIGHTEN program (ENLIGHTEN-Fibrosis in non-cirrhotic F2-F3 MASH and ENLIGHTEN-Cirrhosis in compensated F4 cirrhosis), plus the Phase 3 ENTRUST trial in SHTG. [metabolic dysfunction-associated steatohepatitis (MASH/NASH) - fibrosis improvement, MASH resolution, and reduced liver fat (investigational)]()[severe hypertriglyceridemia (SHTG) - large reductions in blood triglycerides (investigational; Phase 3 ENTRUST)]()[improved insulin sensitivity and glycemic markers]()[improvements in non-invasive markers of liver injury and fibrosis (liver fat by MRI-PDFF, liver enzymes, fibrosis biomarkers)]()+1 more [View Details](/peptides/pegozafermin) [\+ Compare](/compare?select=pegozafermin)[](https://app.peptrackerpro.com/?add=pegozafermin) ### Efruxifermin Low Evidence Efruxifermin (development codes EFX, AKR-001; originally AMG 876) is an investigational, once-weekly, subcutaneously injected analog of the metabolic hormone fibroblast growth factor 21 (FGF21) being developed by Akero Therapeutics for metabolic dysfunction-associated steatohepatitis (MASH, formerly NASH), including both pre-cirrhotic fibrosis and compensated (F4) cirrhosis. It is a bivalent Fc-FGF21 fusion protein - two engineered FGF21 sequences fused to a human immunoglobulin (IgG1) Fc domain - a design distinct from the glycoPEGylation used by its main FGF21-class rival, pegozafermin. The Fc fusion extends the very short half-life of native FGF21 to support once-weekly dosing while preserving agonism at FGF receptors (FGFR1c/2c/3c) together with the co-receptor beta-Klotho. In the 96-week Phase 2b HARMONY trial in biopsy-confirmed F2-F3 MASH, at least a one-stage improvement in fibrosis without worsening of MASH was reached by about 75% of patients on 50 mg and 46% on 28 mg versus 24% on placebo (published in The Lancet, August 2025). In the Phase 2b SYMMETRY trial in compensated MASH cirrhosis, about 39% of 50 mg patients with paired week-96 biopsies achieved reversal of cirrhosis without worsening of MASH versus 15% on placebo (published in the New England Journal of Medicine). Efruxifermin holds FDA Breakthrough Therapy designation and has advanced into the Phase 3 SYNCHRONY program (SYNCHRONY Histology in F2-F3 MASH, SYNCHRONY Outcomes in F4 compensated cirrhosis, and SYNCHRONY Real-World in non-invasively diagnosed MASH/MASLD, whose double-blind portion completed enrollment with safety results expected in 2026). [metabolic dysfunction-associated steatohepatitis (MASH/NASH) - fibrosis improvement and MASH resolution in pre-cirrhotic F2-F3 disease (investigational)]()[reversal of compensated (F4) cirrhosis due to MASH without worsening of MASH (investigational; Phase 2b SYMMETRY, Phase 3 SYNCHRONY Outcomes)]()[reductions in liver fat (MRI-PDFF), liver enzymes, and non-invasive fibrosis biomarkers]()[improved insulin sensitivity, glycemic markers, and blood lipids (lower triglycerides, improved cholesterol profile)]()+1 more [View Details](/peptides/efruxifermin) [\+ Compare](/compare?select=efruxifermin)[](https://app.peptrackerpro.com/?add=efruxifermin) [PepTracker Pro](/) Educational peptide information and research tracking tools. 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