Trevogrumab 1mg
Trevogrumab 1mg
Trevogrumab (REGN1033, SAR-391786) is a fully human monoclonal antibody engineered for high-affinity, selective neutralisation of myostatin (GDF-8), a TGF-beta superfamily ligand that functions as a primary negative regulator of skeletal muscle mass.
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Overview
Trevogrumab (REGN1033, SAR-391786) is a fully human monoclonal antibody engineered for high-affinity, selective neutralisation of myostatin (GDF-8), a TGF-beta superfamily ligand that functions as a primary negative regulator of skeletal muscle mass. Research interest centers on its specificity for myostatin without cross-reactivity to other ActRIIB-binding ligands such as activins or GDF-11.
Research applications include myostatin pathway antagonist research, antibody-based ligand neutralisation studies, and comparative ActRIIB pathway inhibitor pharmacology.
- High Purity – 99% Purity Guaranteed
- Independently Lab Tested
- Research Grade Quality
- For Laboratory Research Use Only
Properties
| Chemical Formula | C6374H9884N1696O2018S46 |
|---|---|
| Synonyms | REGN-1033 (REGN1033), Anti-GDF8/Myostatin antibody, SAR-391786 |
| CAS Number | 1429201-24-0 |
| PubChem CID | 384585220 |
| Available formats | 1 vial · KIT (10 vials) |
| Shelf Life | 36 months |
Research
Trevogrumab is a monoclonal antibody studied for its high-affinity, selective binding to myostatin (GDF-8), neutralising its capacity to engage the activin receptor type IIB (ActRIIB) and downstream Smad2/3 signalling cascade that suppresses skeletal muscle hypertrophy pathways. Its specificity profile distinguishes it from broader-spectrum ActRIIB ligand traps (such as soluble ActRIIB-Fc fusion proteins), which neutralise myostatin alongside activins, GDF-11, and BMP-9/10, making trevogrumab a research tool for isolating myostatin-specific pathway contributions without confounding activin or BMP pathway effects. In vitro Smad2/3 reporter assays and rodent muscle-mass studies are standard experimental approaches for characterising trevogrumab's neutralising potency and downstream functional effects. Independently third-party HPLC-tested; COA available per batch.FAQ
How does Trevogrumab's myostatin selectivity distinguish it from broad-spectrum ActRIIB ligand traps in research?
Trevogrumab is engineered as a highly specific anti-myostatin (GDF-8) antibody, binding myostatin directly to prevent its engagement of ActRIIB, with minimal cross-reactivity to other TGF-beta superfamily ligands. This contrasts with soluble ActRIIB-Fc fusion protein ligand traps, which sequester myostatin alongside activins, GDF-11, and BMP-9/10 indiscriminately.
For research questions requiring isolation of myostatin-specific pathway contributions — without confounding effects from co-inhibited activin or BMP signalling — trevogrumab's selective mechanism is the appropriate experimental tool.
What assay formats are used to confirm Trevogrumab's neutralizing potency against myostatin-induced signaling?
Cell-based Smad2/3 reporter assays — using myoblast cell lines such as C2C12 transfected with a Smad-responsive luciferase construct — are standard for quantifying trevogrumab's capacity to block myostatin-induced Smad2/3 transcriptional activation in a dose-dependent manner, typically expressed as an IC50 or neutralising dose. Surface plasmon resonance (SPR) or other direct binding-affinity methods are used in parallel to characterise trevogrumab's intrinsic binding kinetics (Kd, on/off rates) to recombinant myostatin independent of the cell-based functional readout.
What rodent model endpoints are used to evaluate Trevogrumab's functional effects on skeletal muscle mass?
Rodent studies investigating myostatin pathway antagonists typically measure lean body mass and individual muscle wet weight (e.g. gastrocnemius, quadriceps) following a defined dosing period, alongside functional measures such as grip strength or treadmill exercise capacity. These studies often include muscle fiber cross-sectional area histology to confirm hypertrophy at the cellular level, and serum myostatin/antibody pharmacokinetic sampling to correlate systemic drug exposure with the magnitude of the observed muscle-mass phenotype.
