Vibegron, sold under the brand name Gemtesa, is a medication for the treatment of overactive bladder.
Routes of administration By mouth
Drug class Beta3 adrenergic receptor agonist
Protein binding 49.6 to 51.3% is bound to plasma proteins.
Metabolism Predominantly oxidation and glucuronidation.
Elimination half-life 60 to 70 hours.
Excretion 59% feces (54% of this is in the unchanged parent drug form), 20% urine (19% of this is in the unchanged parent drug form)
Its most common side effects include headache, urinary tract infection, common cold, diarrhea, nausea, and upper respiratory tract infection.
Vibegron, once daily 75 mg provided significant reduction in micturition, urgency episodes and urge incontinence, and increased the volume per micturition.
Vibegron is indicated for the treatment of overactive bladder with symptoms of urge urinary incontinence, urgency, and urinary frequency in adults.
β3 adrenergic receptors agonists such as vibegron has improved overactive bladder (OAB) management by minimizing anticholinergic-related adverse effects.
β3 adrenergic agonist monotherapy may be preferred in older patients, those with high anticholinergic burden, and older adults with multiple comorbidities.
Treatment with vibegron was not associated with clinically meaningful effects on blood pressure or heart rate.
Treatment with vibegron is associated with improvements in patient-reported measures of quality of life.
Vibegron was generally effective, safe and well tolerated, thus represents a valuable treatment option for patients with OAB.
The most common side effects of vibegron are dry mouth, constipation, headache, nasopharyngitis, diarrhea, nausea, bronchitis, urinary tract infection and upper respiratory tract infection. In case of urinary retention.
Risk in pregnant people has yet to be evaluated.
Vibegron compared with other OAB drugs, is very selective and leads to a lesser degree of unwanted side effects.
Vibegron is a substrate for CYP3A4 in vivo, but does not actually induce or inhibit any of the cytochrome P450 enzymes and is thus less likely to take part in drug–drug interactions.
Vibegron differs from the previous overactive bladder drug mirabegron, which was known to be associated in various drug–drug interactions by inhibiting CYP2D6 or inducing CYP3A4, CYP2D6 and CYP2C9 in the liver.
Dose combinations of vibegron and tolterodine showed increased bladder capacity, the effects of both drugs at low doses strengthened each other, known as synergism.
The addition of darifenacin to vibegron created greater bladder relaxation only when used at high doses.
The co-administration with imidafenacin shows an increase in bladder capacity and voided volume in comparison to monotherapy.
The combination of beta-3-adrenergic agonist with a nonselective M2/M3 antagonist as the most prevalent option.
There is no significant drug–drug interaction, aside from a serum concentration increase of digoxin when taken with vibegron.
It does not cross the blood-brain barrier and therefore does not induce cognitive impairment.
Vibegron can be taken with or without food.
Vibegron is a selective agonist for the beta-3 adrenergic receptor, with receptors located in the kidneys, urinary tract and bladder tissue.
Upon binding, the β3 receptor undergoes a conformational change, inducing the activation of adenylate cyclases via G proteins and thereby promotes the formation of cyclic adenosine monophosphate (cAMP).
This cascade is an increases intracellular cAMP concentration, which triggers activation of cAMP-dependent protein kinase A and causes a reduction of Ca2+ concentration in the cytoplasm.
The kinase then phosphorylates myosin chains and thereby inhibits muscle contraction: the final effect of vibegron is muscle relaxation in the bladder. Due to this muscle relaxation, bladder capacity increases and symptoms of overactive bladder are relieved.
The two main metabolic pathways are the oxidation and glucuronidation.
CYP3A4 is the enzyme responsible for the metabolism of vibegron, facilitating oxidative metabolism.
A large part of the unmodified drug is excreted through feces and urine.
The adverse effect rates in participants treated with vibegron were comparable to those in participants who received a placebo.Oncogenic gene fusions are hybrid genes that result from structural DNA rearrangements, leading to deregulated activity.
It is effective and safe for longer use.