Bimagrumab: an investigational human monoclonal antibody against activin type II receptors for treating obesity.

Autor: Kaur M; Department of Pharmacology, Kalpana Chawla Government Medical College, Karnal, India., Misra S; Department of Pharmacology, Kalpana Chawla Government Medical College, Karnal, India.
Jazyk: angličtina
Zdroj: Journal of basic and clinical physiology and pharmacology [J Basic Clin Physiol Pharmacol] 2024 Oct 10. Date of Electronic Publication: 2024 Oct 10.
DOI: 10.1515/jbcpp-2024-0065
Abstrakt: Bimagrumab is a human monoclonal antibody that prevents activin type II receptors (ActRII) from functioning. This antibody has a higher affinity for muscle activin-2 receptors than natural ligands such as activin and myostatin, which act as negative muscle growth regulators. Blocking the activin receptor with bimagrumab could be a new pharmaceutical approach for managing patients with obesity and type 2 diabetes mellitus (T2DM). Bimagrumab has anabolic effects on skeletal muscle mass by preventing myostatin binding and other negative muscle growth regulators. Preclinical animal models have also shown that ActRII blockade promotes actions beyond skeletal muscle, including effects on brown adipose tissue (BAT) differentiation and activity. In a phase 2 randomized clinical trial, ActRII blockade with bimagrumab led to significant loss of total body fat mass (FM), lean mass (LM) gain, and metabolic improvements over 48 weeks in overweight or obese patients with type 2 diabetes. The trial involved [number of participants], and the results showed [specific findings]. Currently, Bimagrumab is being evaluated for its potential to treat muscle wasting, functional loss in hip fractures and sarcopenia, as well as obesity. However, it is essential to note that Bimagrumab also blocks the effects of other ActRII ligands, which play a role in the neurohormonal axes, pituitary, gonads, and adrenal glands. These observations suggest that bimagrumab might represent a new approach for treating patients with obesity and related metabolic disturbances.
(© 2024 Walter de Gruyter GmbH, Berlin/Boston.)
Databáze: MEDLINE