Research library

Key finding

In a phase 2 obesity trial, retatrutide reduced mean body weight by up to 24.2% at 48 weeks versus 2.1% with placebo.

Key finding

In the DXA substudy, retatrutide reduced total fat mass by 15.2% to 26.1% at the 4 mg to 12 mg doses over 36 weeks.

Key finding

This foundational study identified the ovarian activin-binding protein as follistatin, establishing its role as a regulator of activin signalling.

Key finding

Cell experiments showed that follistatin isoforms differ in surface binding and in their neutralization of activin, myostatin and related growth factors.

Key finding

In mice, loss of myostatin caused a large increase in skeletal-muscle mass, establishing the pathway that follistatin-related muscle research seeks to modulate.

Key finding

The study reports that the primary end point was percentage change in weight from baseline to 24 weeks, which ranged from -7.2% to -~18% as the dose of retatrutide increased from 1 mg to 12 mg.

Key finding

Receptor-specific targeting optimizes T2DM treatment, with Semaglutide supporting glycemic control, Tirzepatide enhancing weight loss and glucose regulation, and Retatrutide potentially offering broader metabolic benefits, advancing receptor-targeted, personalized therapy.

Key finding

By recruiting participants with shared disease exposures, the TRIUMPH program will assess the safety and efficacy of retatrutide for the treatment of adults with obesity and two of its common complications-OSA and OA.

Key finding

FST is a novel therapeutic target to improve ovarian cancer response to chemotherapy and potentially reduce recurrence rates.

Key finding

INTRODUCTION: Despite there being a wide range of medicines available for the treatment of type 2 diabetes, the high rate of mortality suggests treatment needs to be improved.

Key finding

Concentrations of circulating activins and follistatins are associated with metabolic parameters and increase after 45 minutes of exercise.

Key finding

Sarcopenia, or age-related loss of muscle mass and strength, is an important contributor to loss of physical function in older adults.

Key finding

We here present evidence that Fst is a potent regulator of insulin action in muscle, and in addition to AKT and p70S6K, we identify TBC1D1, TBC1D4, pyruvate dehydrogenase-E1α, and PAK1 as Fst targets.

Key finding

Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant or digenic disorder linked to derepression of the toxic DUX4 gene in muscle.

Key finding

Follistatin (FST), which was first found in the follicles of cattle and pigs, has been shown to be an essential regulator for muscle development.

Key finding

Follistatin is a member of the TGF-β super family and inhibits the action of myostatin to regulate skeletal muscle growth.

Key finding

Follistatin (FS) inhibits several members of the TGF-beta superfamily, including myostatin (Mstn), a negative regulator of muscle growth.

Key finding

Antagonists of myostatin, a blood-borne negative regulator of muscle growth produced in muscle cells, have shown considerable promise for enhancing muscle mass and strength in rodent studies and could serve as potential therapeutic agents for human muscle diseases.

Key finding

Retatrutide demonstrated significant improvements in body weight and metabolic outcomes among adults with obesity and had an appropriate safety profile.

Key finding

In most cases, pharmacologic strategies to treat genetic muscle disorders and certain acquired disorders, such as sporadic inclusion body myositis, have produced modest clinical benefits.