Antimuscarinics For Urinary Incontinence

Written by Megan Boucher

Last updated 2nd January 2026
8 Revisions

There are several different drug classes available to treat urinary incontinence. Antimuscarinic drugs for urinary incontinence include oxybutynin, darifenacin, fesoterodine, propiverine, solifenacin, tolterodine and trospium chloride. 

The following article will cover the antimuscarinic pharmacotherapy available for urinary incontinence, mechanism of action, cautions and contraindications, side effects and clinically significant interactions. Other treatment options include duloxetine and mirabegron

Mechanism Of Action

The urinary bladder is innervated by parasympathetic cholinergic nerves. Acetylcholine contracts the detrusor smooth muscle through activation of muscarinic receptors (mainly M3 receptors which control urinary bladder muscle contraction). 

Urinary antimuscarinics antagonise muscarinic receptors and block acetylcholine from binding, leading to relaxation of smooth muscle, helping to alleviate symptoms of urgency, frequency, and incontinence.

Selective M3 antagonists:

  • Darifenacin, solifenacin, tolterodine and Fesoterodine are all selective muscarinic M3 receptor antagonists. Fesoterodine is also a prodrug which is rapidly and extensively hydrolysed to its primary active metabolite.

Non-selective M3 antagonists:

  • Oxybutynin: competitive antagonist at muscarinic receptors which is active at M3 and M2 receptors. Direct antispasmodic effect on the detrusor muscle of the bladder → reduces incidence of spontaneous contraction of the detrusor muscle in the bladder. 
  • Propiverine: non-selective muscarinic receptor antagonist. Also inhibits calcium influx and modulates intracellular calcium in urinary bladder smooth muscle cells causing musculotropic spasmolysis. 
  • Trospium chloride: high affinity to M1, M2 and M3 muscarinic receptors, competes concentration dependently with acetylcholine to do so. 

Fig 1: Mechanism of action: antimuscarinics for overactive bladder. Muscarinic antagonists such as solifenacin bind the M3 receptor and prevent acetylcholine from binding. This leads to inhibition of voluntary contraction of the bladder.

Pharmacokinetics

The following table describes the key pharmacokinetic properties of urinary antimuscarinic drugs:

Antimuscarinic drug Bioavailability  Tmax/steady state Metabolism  Excretion
Oxybutynin (tablets) F = 6% Tmax = 0.5 – 1 hour CYP3A4 Two phases: 40 minutes & 2-3 hours.

Increased in elderly 

Darifenacin (MR tablets) F = 15-19% Tmax = 7 hours

Steady state by day 6

Extensively metabolised in the liver by CYP3A4 and CYP2D6 (saturable).

CYP2D6 is saturable therefore doubling the dose led to 150% increase in steady state exposure

t½ = 13–19 hrs.

Minimal renal excretion

Fesoterodine (MR tablets) F = 52% (active metabolite) Tmax = 5 

hours. 

Full treatment effect is observed between 2 and 8 weeks

CYP3A4 t½  = 7 hours.

The active metabolite is eliminated via hepatic and renal excretion; exposure increased in moderate renal/hepatic impairment. 

Propiverine (tablets) F = 40.5%

Bioavailability ↑ with high-fat meals.

Tmax = 2.3 hours.  Weak CYP3A4 inhibitor/substrate

Three active metabolites, all elicit pharmacological effect.

t½  = 14-22 hours
Solifenacin (tablets) F = 90% Tmax = 3-8 hours

Maximum effect can be determined after 4 weeks of treatment 

Extensively metabolised by CYP3A4 Terminal half life = 45-68 hours
Tolterodine (tablets) F = 17% (extensive metabolisers (EM)) – 65% (poor metabolisers (PM)) Tmax = 1-3 hours

Effect of treatment can be expected within 4 weeks.

CYP2D6  T½ = 2-3 hours (EM) – 10 hours (PM)

2x↑exposure of tolterodine in hepatic impairment, and 12x ↑ in renal impairment

Trospium chloride (tablets) F~9.6%

Bioavailability ↓ with high-fat meals.

Tmax = 4-6 hours Limited hepatic metabolism T½ = 10-20 hours. 

Excreted renally; ↑ AUC and t½ in renal impairment. 

 

Cautions and Contraindications

The following cautions and contraindications are applicable for antimuscarinic drugs for urinary incontinence:

Cautions Contraindications 
  • In whom fast heart rates are undesirable e.g. cardiac history or hyperthyroidism
    • QT prolongation (fesoterodine, solifenacin, tolterodine)
  • Autonomic neuropathy.
  • Angle-closure glaucoma
  • Pyrexia
  • Anticholinergic CNS effects – hallucinations, agitation, confusion, somnolence
  • Gastrointestinal conditions 
    • Ulcerative colitis
    • Diarrhoea
    • Gastro-oesophageal reflux disease
    • Hiatus hernia with reflux oesophagitis.
  • Parkinson’s disease 
  • Renal and/or hepatic impairment and propiverine, tolterodine, trospium chloride, solifenacin
  • Myasthenia gravis
  • Severe hepatic impairment  (darifenacin, fesoterodine, propiverine, tropsium chloride)
  • Significant bladder outflow obstruction/urinary retention 
  • Toxic megacolon
  • Antimuscarinics may decrease gastric motility: gastrointestinal obstruction, intestinal atony, paralytic ileus, pyloric stenosis, severe ulcerative colitis.
  • Narrow angle glaucoma or shallow anterior chamber (oxybutynin, darifenacin, fesoterodine)
  • Concomitant treatment with potent CYP3A4 inhibitors (darifenacin, tolterodine), alongside hepatic or renal impairment (fesoterodine, solifenacin) 
  • Haemodialysis and solifenacin 
  • Solifenacin and trospium chloride with galactose intolerance/Lapp lactase deficiency/glucose-galactose malabsorption 

Adverse Effects 

General, dose-dependent antimuscarinic effects include:

System Adverse Effects
Gastrointestinal Dry mouth, constipation, nausea, vomiting, dyspepsia
Central Nervous System Drowsiness, dizziness, confusion, headache
Cardiovascular Palpitations, tachycardia
Urinary Tract Urinary retention
Visual / Ocular Dry eyes, blurred vision, angle-closure glaucoma
Dermatological / Others Flushing, skin reactions, rash, angioedema

Interactions 

Class-wide interactions:

  • Potentiation of anticholinergic effects with other anticholinergic agents e.g. amantadine, levodopa, antihistamines, antipsychotics, quinidine, TCAs, atropine, dipyridamole, baclofen, clozapine (constipation)
  • Antagonise the effects of prokinetic therapies e.g. metoclopramide 

Drug-specific interactions

Oxybutynin

  • Medicinal products that can cause or exacerbate oesophagitis – bisphosphonates 
  • Caution with concomitant administration with a CYP3A4 inhibitor → inhibit oxybutynin metabolism.

Darifenacin

  • Potent CYP2D6 inhibitors (paroxetine, cimetidine, quinidine) or moderate CYP3A4 inhibitors (fluconazole, clarithromycin, grapefruit juice) – start at 7.5mg daily, can increase to 15mg daily if required and tolerated 
  • Contraindicated with potent CYP3A4 inhibitors (e.g. rontinavir, ketoconazole, itraconazole)
  • Contraindicated with PGP inhibitors (e.g. ciclosporin, verapamil)
  • Caution with CYP2D6 substrates with a narrow therapeutic window (e.g. flecainide and imipramine) 

Fesoterodine 

  • Metabolised by CYP2D6 and CYP3A4
  • Max dose 4mg with potent CYP3A4 inhibitors e.g. ketoconazole, clarithromycin, itraconazole, ritonavir (unless also has moderate-severe renal/hepatic impairment then contraindicated) 
  • Not recommended with potent CYP3A4 inducers e.g. rifampicin, phenobarbital, carbamazepine, phenytoin, St Johns Wort
  • Max dose 4mg with potent CYP2D6 inhibitor 

Propiverine

  • Potent inhibitors of CYP3A4 combined with methimazole should start with a dose of 15 mg per day.
  • With isoniazid: reduced BP

Trospium chloride

  • Enhancement of the tachycardic action of ß -sympathomimetics
  • Inhibition of absorption with cholestyramine and colestipol 

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