Antiobesity

"Antiobesity" is not the name of a specific molecule, protein, receptor, enzyme, transporter, or gene. Instead it refers broadly to any agent—typically pharmaceutical—that is used in the treatment and management of obesity. The term encompasses multiple classes of drugs that act via diverse mechanisms including inhibition of fat absorption in the gut (e.g., orlistat), modulation of appetite-regulating neurocircuits in the brainstem/hypothalamus through incretin mimetics like GLP‑1 receptor agonists (e.g., liraglutide/semaglutide/tirzepatide), stimulation/inhibition at adrenergic/serotonergic/dopaminergic synapses in the CNS to suppress appetite or increase energy expenditure. Because "antiobesity" does not refer to one discrete molecular entity but rather an entire therapeutic category targeting obesity through various pathways and targets—including receptors like GLP‑1R—it cannot be mapped onto structured fields intended for individual molecular targets.

Other names

Anti-obesityAntiobesity agentAnti-obesity drugWeight-loss drug

Mechanisms vary by drug and may include: - Inhibition of gastrointestinal lipases to reduce fat absorption (e.g., orlistat) - Appetite suppression via central nervous system pathways, including modulation of neurotransmitters such as serotonin and norepinephrine, or activation of GLP‑1 receptors in the brainstem/hypothalamus to increase satiety and decrease appetite (e.g., liraglutide, semaglutide, tirzepatide) - Increased energy expenditure through beta‑adrenergic agonism or other mechanisms