Phase 2Active, not recruiting

GRK-Biased Activation Via β2-Adrenergic Receptors in Human Skeletal Muscle (GAIN)

G Protein-Coupled Receptor Kinase (GRK)-Biased Signaling Via β2-Adrenergic Receptors and Downstream Activation and Its Role for Protein Synthesis-Regulating Kinases, Function and Receptor Desensitization in Human Skeletal Muscle

Sponsor
Morten Hostrup, PhD (Academic or other)
Enrolment
13 enrolled
Conditions
Overweight and Obesity
Interventions
ATR-258
Ages
adults
Registry
NCT07421024

Full record on ClinicalTrials.gov

From the registry

This longitudinal mechanistic physiological study examines biased β2-adrenergic receptor (β2-AR) signaling in human skeletal muscle, with emphasis on G protein-coupled receptor kinase (GRK)-mediated pathways. Participants will receive daily oral dosing of the GRK-selective long-acting β2-agonist ATR-258 for 8 weeks. Muscle biopsies and physiological measurements will quantify GRK-, cAMP/PKA-, and β-arrestin-related up- and downstream signaling, fiber-type specificity, and potential receptor desensitization with repeated stimulation along with functional read-outs, tissue distribution, cardiovascular response and tolerability.

Primary outcomes

  • Intensity of β2-AR downstream signaling pathways (e.g. GRK, cAMP/PKA, β-arrestin, rpS6) in type I and type II muscle fibers

History

  1. Primary completion expected

  2. Last registry update

  3. Registered

  4. Started