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Catalog/Bimagrumab

Bimagrumab

Also known as BYM338

An antibody that blocks the activin type II receptor itself — shutting off myostatin AND activin signaling at once; famous for adding muscle while cutting fat.

Overview

Bimagrumab is a fully human monoclonal antibody that blocks the activin type II receptors (ActRIIA/ActRIIB) — the receptor every ligand on this axis must use. By acting at the receptor rather than on a single ligand, it shuts down myostatin and activin signaling simultaneously, which is why it produces the axis’s most striking body-composition effect: in trials it has both reduced fat and increased lean mass, an unusual combination for a weight-affecting drug.

Background

Bimagrumab’s history maps the whole field. It was developed (as BYM338, Novartis) for muscle-wasting conditions — sporadic inclusion body myositis (where its pivotal trial failed), sarcopenia, and COPD-related wasting — before a notable Phase 2 in type 2 diabetes showed it cut fat mass substantially while adding lean mass. That fat-down/muscle-up profile made it a centerpiece of the obesity muscle-preservation thesis: Versanis advanced it, and Eli Lilly acquired Versanis for roughly $2 billion in 2023 to pair it with tirzepatide.

The honest update is that the path has not been smooth: a combination Phase 2 with semaglutide showed weight loss with preserved/added lean mass, but Lilly subsequently terminated a mid-stage obesity study pairing bimagrumab with its own incretin therapy. As the receptor-level blocker of the axis, bimagrumab is the broadest-acting and the most-watched — and a reminder that even the most mechanistically compelling agent has to clear real trials. It is investigational for these uses.

Mechanism

Binds ActRIIA/ActRIIB and prevents their natural ligands (myostatin, activins, and related factors) from signaling. Blocking the shared receptor disinhibits muscle growth broadly while reducing fat mass.

Key research findings

  • Receptor-level blockade — targets ActRIIA/B, blocking myostatin and activin signaling together (broadest mechanism on the axis).
  • Fat down, muscle up — Phase 2 in type 2 diabetes reduced fat mass while increasing lean mass, an unusual profile.
  • GLP-1 combination — bimagrumab + semaglutide preserved/added lean mass alongside weight loss in Phase 2.
  • Commercial bet and setback — Lilly acquired Versanis (~$2B, 2023) but later terminated a mid-stage obesity combination study.
  • Muscle-wasting origins — earlier developed for inclusion body myositis (pivotal trial failed), sarcopenia, and COPD.

How Bimagrumab is made

Behind every vial of Bimagrumab is the same exacting pipeline every research peptide runs — but the chemistry plays out differently for this molecule. Here is how Bimagrumab, specifically, is brought into being.

  1. On paper first

    On paper, Bimagrumab weighs in at roughly 150,000 daltons. Before a single bond is made, the target sequence, salt form, and purity threshold are written down as the contract the finished material must meet.

  2. Built residue by residue

    Bimagrumab is assembled by solid-phase peptide synthesis — the chain grows one protected residue at a time on resin, and what you fail to build cleanly here you pay to remove later.

  3. Purity is won here

    The crude mixture — Bimagrumab plus its deletions and side products — is then separated on preparative HPLC, and where the cut is taken decides the difference between a genuinely pure peptide and a barely-passable one.

  4. Proven, then protected

    A real batch of Bimagrumab proves itself: identity confirmed by mass spectrometry against its ~150,000 Da, purity read directly off an analytical HPLC trace, water and counterion content measured. That batch-specific certificate of analysis is the only honest way to know what is actually in a vial of Bimagrumab — and a short, cold, accountable chain of custody is how that purity survives the trip to your bench.

Walk the full synthesis pipeline

Handling, storage & why purity is hard

Bimagrumab is a fully human recombinant monoclonal antibody (~150 kDa) produced in mammalian cell culture, characterized with antibody-grade analytics (glycan/charge-variant profiling, mass spectrometry, receptor-binding/cell-based potency) — not a synthetic peptide.

Storage
Stored refrigerated (2–8 °C), protected from light and freezing, not shaken; investigational handling per trial protocol.
Handling
A large glycosylated antibody sensitive to freezing, heat, and agitation, which can cause aggregation.

Don't judge a vial by its cake. A fluffy, good-looking lyophilized powder reflects bulking agents and freeze-drying parameters — not purity. Insist on a batch-specific certificate of analysis.

How peptides are made — the full pipeline

Research areas

  • Obesity
  • Type 2 diabetes
  • Muscle wasting
  • Body composition

Research-area guides

Latest research

Recent clinical trials and publications mentioning Bimagrumab, pulled automatically from ClinicalTrials.gov and PubMed and refreshed daily. Listings are unfiltered search results, not curated endorsements.

Frequently asked questions

What is bimagrumab?+

A monoclonal antibody that blocks the activin type II receptor, shutting off both myostatin and activin signaling. It is notable for reducing fat while increasing muscle mass, and has been studied in obesity and type 2 diabetes.

How is it different from the myostatin antibodies?+

The myostatin antibodies neutralize a ligand; bimagrumab blocks the shared receptor those ligands use, so it acts more broadly across the whole activin/myostatin axis.

Is bimagrumab approved for obesity?+

No. Despite encouraging body-composition data and a major acquisition, it remains investigational, and at least one mid-stage obesity combination study was terminated.

Is this medical advice?+

No — this is a research and educational reference. Bimagrumab is an investigational antibody, not an approved drug.

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