Publications and Posters Related to KEVEYIS® (dichlorphenamide)

Publications and Posters

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About KEVEYIS

  • Randomized, placebo-controlled trials of dichlorphenamide. Sansone VA, Burge J, McDermott MP, et al. Randomized, placebo-controlled trials of dichlorphenamide in periodic paralysis. Neurology. 2016;86:1408-1416.
    • Abstract:
      • Objective: To determine the short-term and long-term effects of dichlorphenamide (DCP) on attack frequency and quality of life in hyperkalemic (HYP) and hypokalemic (HOP) periodic paralysis.
      • Methods: Two multicenter randomized, double-blind, placebo-controlled trials lasted 9 weeks (Class I evidence), followed by a 1-year extension phase in which all participants received DCP. Forty-four HOP and 21 HYP participants participated. The primary outcome variable was the average number of attacks per week over the final 8 weeks of the double- blind phase.
      • Results: The median attack rate was lower in HOP participants on DCP than in participants on placebo (0.3 vs 2.4, p = 0.02). The 9-week mean change in the Physical Component Summary score of the Short Form–36 was also better in HOP participants receiving DCP (treatment effect = 7.29 points, 95% confidence interval 2.26 to 12.32, p = 0.006). The median attack rate was also lower in HYP participants on DCP (0.9 vs 4.8) than in participants on placebo, but the difference in median attack rate was not significant (p = 0.10). There were no significant effects of DCP on muscle strength or muscle mass in either trial. The most common adverse events in both trials were paresthesia (47% DCP vs 14% placebo, both trials combined) and confusion (19% DCP vs 7% placebo, both trials combined).
      • Conclusions: DCP is effective in reducing the attack frequency, is safe, and improves quality of life in HOP periodic paralysis.
      • Classification of evidence: These studies provide Class I evidence that DCP significantly reduces attack frequency in HOP but lacked the precision to support either efficacy or lack of efficacy of DCP in HYP. To read more, click here.
  • Randomized trials of dichlorphenamide. Tawil R, McDermott MP, Brown R, et al. Randomized trials of dichlorphenamide in the periodic paralyses. Working Group on Periodic Paralysis. Ann Neurol. 2000;47:46-53.
    • Abstract: Although the carbonic anhydrase inhibitors have been used in the treatment of the primary periodic paralyses (PPs), their efficacy has not been demonstrated in double-blind, placebo-controlled trials. Therefore, we tested the efficacy of dichlorphenamide (DCP; Daranide), a potent carbonic anhydrase inhibitor, in the treatment of episodic weakness in the primary PPs. We performed two multicenter, randomized, double-blind, placebo-controlled crossover trials, one involving 42 subjects with hypokalemic periodic paralysis (HypoPP) and the other involving 31 subjects with potassium- sensitive periodic paralysis (PSPP). In each trial, two 8-week treatment periods were separated by an active washout period of at least 9 weeks. The primary outcome variable in the HypoPP trial was the occurrence of an intolerable increase in attack severity or frequency (end point). The primary outcome variable in the PSPP trial was the number of attacks per week. In the HypoPP trial, there were 13 subjects who exhibited a preference (in terms of the end point) for either DCP or placebo, and 11 of these preferred DCP. In the PSPP trial, DCP significantly reduced attack rates relative to placebo. DCP also significantly reduced attack rates relative to placebo in the HypoPP subjects. We conclude that DCP is effective in the prevention of episodic weakness in both HypoPP and PSPP. To read more, click here.
  • Newly approved drug for periodic paralysis. Fontaine B, Phillips LH. A newly approved drug for a rare group of diseases: dichlorphenamide for periodic paralysis. Neurology. 2016;86:1366-1367.
    • Abstract: Two randomized, double-blind, placebo-controlled crossover trials were performed with 42 patients with hypokalemic periodic paralysis and 31 patients with potassium-sensitive periodic paralysis. A washout period separated the two 8-week-long treatments. Dichlorphenamide reduced attacks or episodic weakness in both forms of periodic paralysis. The authors describe the results of randomized, placebo- controlled, double-blind, and multicenter international phase III trials. To read more, click here.
  • A review of dichlorphenamide. Greig SL. Dichlorphenamide: a review in primary periodic paralyses. Drugs. 2016;76:501-507.
    • Abstract: Oral dichlorphenamide (Keveyis) is a carbonic anhydrase inhibitor that is approved in the USA for the treatment of primary hyperkalaemic and hypokalaemic periodic paralysis and related variants. The efficacy and safety of dichlorphenamide in patients with primary periodic paralyses have been evaluated in four 9-week, randomized, double-blind, placebo-controlled, phase III trials [two parallel-group trials (HOP and HYP) and two cross-over trials]. In two trials in patients with hypokalaemic periodic paralysis, dichlorphenamide was associated with a significantly (eightfold) lower paralytic attack rate and fewer patients with acute intolerable worsening compared with placebo. In two trials in patients with hyperkalaemic periodic paralysis, the attack rate was lower with dichlorphenamide than placebo, with this comparison reaching statistical significance in one trial (crossover) but not the other (HYP), although the attack rate was approximately fivefold lower with dichlorphenamide than placebo in the HYP trial. In 52-week, open-label extensions of the HOP and HYP trials, dichlorphenamide provided sustained efficacy in patients with hypokalaemic or hyperkalaemic periodic paralysis. Dichlorphenamide was generally well tolerated in all four phase III trials and during the extension trials; the most common adverse events were paraesthesia, cognitive disorders, and dysgeusia. As the first agent to be approved in the USA for this indication, dichlorphenamide is a valuable treatment option for patients with primary hyperkalaemic or hypokalaemic periodic paralysis. To read more, click here.
  • KEVEYIS for periodic paralysis. Dichlorphenamide (KEVEYIS) for periodic paralysis. Med Lett Drugs Ther. 2016;58(1492):50.
    • Abstract: Dichlorphenamide (Keveyis – Taro), an oral carbonic anhydrase inhibitor, has been approved by the FDA for treatment of primary hypokalemic and hyperkalemic periodic paralysis and related variants. Dichlorphenamide is the first drug to be approved in the US for this indication. It was approved as Daranide in 1958 for treatment of glaucoma, but had not been marketed since 2002. To read more, click here.

About Primary Periodic Paralysis

  • Therapeutic approaches and drug discovery. Imbrici P, Liantonio A, Camerino GM, et al. Therapeutic approaches to genetic ion channelopathies and perspectives in drug discovery. Front Pharmacol. 2016;7(121):1-28
    • Abstract: In the human genome more than 400 genes encode ion channels, which are transmembrane proteins mediating ion fluxes across membranes. Being expressed in all cell types, they are involved in almost all physiological processes, including sense perception, neurotransmission, muscle contraction, secretion, immune response, cell proliferation, and differentiation. Due to the widespread tissue distribution of ion channels and their physiological functions, mutations in genes encoding ion channel subunits, or their interacting proteins, are responsible for inherited ion channelopathies. These diseases can range from common to very rare disorders and their severity can be mild, disabling, or life-threatening. In spite of this, ion channels are the primary target of only about 5% of the marketed drugs suggesting their potential in drug discovery. The current review summarizes the therapeutic management of the principal ion channelopathies of central and peripheral nervous system, heart, kidney, bone, skeletal muscle and pancreas, resulting from mutations in calcium, sodium, potassium, and chloride ion channels. For most channelopathies the therapy is mainly empirical and symptomatic, often limited by lack of efficacy and tolerability for a significant number of patients. Other channelopathies can exploit ion channel targeted drugs, such as marketed sodium channel blockers. Developing new and more specific therapeutic approaches is therefore required. To this aim, a major advancement in the pharmacotherapy of channelopathies has been the discovery that ion channel mutations lead to change in biophysics that can in turn specifically modify the sensitivity to drugs: this opens the way to a pharmacogenetics strategy, allowing the development of a personalized therapy with increased efficacy and reduced side effects. In addition, the identification of disease modifiers in ion channelopathies appears an alternative strategy to discover novel druggable targets. To read more, click here.
  • Channelopathies. Cannon SC. Channelopathies of skeletal muscle excitability. Compr Physiol. 2015;5:761-790.
    • Abstract: Familial disorders of skeletal muscle excitability were initially described early in the last century and are now known to be caused by mutations of voltage-gated ion channels. The clinical manifestations are often striking, with an inability to relax after voluntary contraction (myotonia) or transient attacks of severe weakness (periodic paralysis). An essential feature of these disorders is fluctuation of symptoms that are strongly impacted by environmental triggers such as exercise, temperature, or serum K+ levels. These phenomena have intrigued physiologists for decades, and in the past 25 years the molecular lesions underlying these disorders have been identified and mechanistic studies are providing insights for therapeutic strategies of disease modification. These familial disorders of muscle fiber excitability are “channelopathies” caused by mutations of a chloride channel (ClC-1), sodium channel (NaV1.4), calcium channel (CaV1.1) and several potassium channels (Kir2.1, Kir2.6, Kir3.4). This review provides a synthesis of the mechanistic connections between functional defects of mutant ion channels, their impact on muscle excitability, how these changes cause clinical phenotypes, and approaches toward therapeutics. To read more, click here.
  • Hyperkalemic periodic paralysis. Weber F, Jurkat-Rott K, Lehmann-Horn F. Hyperkalemic periodic paralysis. In: Pagon RA, Adam MP, Ardinger HH, et al., editors. GeneReviews® [Internet]. Seattle, WA: University of Washington; 1993-2016. http://www.ncbi.nlm.nih.gov/books/NBK1496/; Accessed November 23, 2016.
    • Abstract: Hyperkalemic periodic paralysis (hyperPP) is characterized by attacks of flaccid limb weakness (which may also include weakness of the muscles of the eyes, throat, and trunk), hyperkalemia (serum potassium concentration >5 mmol/L) or an increase of serum potassium concentration of at least 1.5 mmol/L during an attack of weakness and/or provoking/worsening of an attack by oral potassium intake, normal serum potassium between attacks, and onset before age 20 years. Although the absence of paramyotonia (muscle stiffness aggravated by cold and exercise) was originally postulated as a means of distinguishing hyperPP from paramyotonia congenita (PMC), approximately 45% of individuals with hyperPP have paramyotonia. In approximately half of affected individuals, attacks of flaccid muscle weakness begin in the first decade of life, with 25% reporting their first attack at age ten years or older. Initially infrequent, the attacks then increase in frequency and severity over time until approximately age 50 years, after which the frequency of attacks declines considerably. Potassium­rich food or rest after exercise may precipitate an attack. A cold environment and emotional stress provoke or worsen the attacks. A spontaneous attack commonly starts in the morning before breakfast, lasts for 15 minutes to one hour, and then disappears. Cardiac arrhythmia or respiratory insufficiency usually does not occur during attacks. Between attacks, approximately half of individuals with hyperPP have mild myotonia (muscle stiffness) that does not impede voluntary movements. More than 80% of individuals with hyperPP older than 40 years report permanent muscle weakness and about one third develop a chronic progressive myopathy. To read more, click here.
  • Hypokalemic periodic paralysis. Vicart S, Sternberg D, Arzel-Hézode M, et al. Hypokalemic periodic paralysis. In: Pagon RA, Adam MP, Ardinger HH, et al., editors. GeneReviews® [Internet]. Seattle, WA: University of Washington; 1993-2016. http://www.ncbi.nlm.nih.gov/books/NBK1338/; Accessed November 23, 2016.
    • Abstract: Hypokalemic periodic paralysis (HOKPP) is a condition in which affected individuals may experience paralytic episodes with concomitant hypokalemia ( <2.5 mmol/L), and occasionally may develop late-onset proximal myopathy. The paralytic attacks are characterized by reversible flaccid paralysis usually leading to paraparesis or tetraparesis but typically sparing the respiratory muscles and heart. Acute paralytic crises usually last at least several hours and sometimes days. Some individuals have only one episode in a lifetime; more commonly, crises occur repeatedly: daily, weekly, monthly, or less often. The major triggering factors are carbohydrate-rich meals and rest after exercise; rarely, cold-induced hypokalemic paralysis has been reported. The interval between crises may vary and may be prolonged by preventive treatment with potassium salts or acetazolamide. The age of onset of the first attack ranges from one to 20 years; the frequency of attacks is highest between ages 15 and 35 and then decreases with age. A variable myopathy develops in at least 25% of affected individuals and may result in a progressive fixed muscle weakness that manifests at variable ages as exercise intolerance predominantly in the lower limbs. It may occur independent of paralytic symptoms and may be the sole manifestation of HOKPP. Individuals with HOKPP are at increased risk for pre- or post-anesthetic weakness and may be at an increased risk for malignant hyperthermia – though not as great a risk as in individuals with true autosomal dominant malignant hyperthermia susceptibility (MHS). To read more, click here.

Current Management of Primary Periodic Paralysis

  • A review of dichlorphenamide. Greig SL. Dichlorphenamide: a review in primary periodic paralyses. Drugs. 2016;76:501-507.
    • Abstract: Oral dichlorphenamide (Keveyis) is a carbonic anhydrase inhibitor that is approved in the USA for the treatment of primary hyperkalaemic and hypokalaemic periodic paralysis and related variants. The efficacy and safety of dichlorphenamide in patients with primary periodic paralyses have been evaluated in four 9-week, randomized, double-blind, placebo-controlled, phase III trials [two parallel-group trials (HOP and HYP) and two cross-over trials]. In two trials in patients with hypokalaemic periodic paralysis, dichlorphenamide was associated with a significantly (eightfold) lower paralytic attack rate and fewer patients with acute intolerable worsening compared with placebo. In two trials in patients with hyperkalaemic periodic paralysis, the attack rate was lower with dichlorphenamide than placebo, with this comparison reaching statistical significance in one trial (crossover) but not the other (HYP), although the attack rate was approximately fivefold lower with dichlorphenamide than placebo in the HYP trial. In 52-week, open-label extensions of the HOP and HYP trials, dichlorphenamide provided sustained efficacy in patients with hypokalaemic or hyperkalaemic periodic paralysis. Dichlorphenamide was generally well tolerated in all four phase III trials and during the extension trials; the most common adverse events were paraesthesia, cognitive disorders, and dysgeusia. As the first agent to be approved in the USA for this indication, dichlorphenamide is a valuable treatment option for patients with primary hyperkalaemic or hypokalaemic periodic paralysis. To read more, click here.
  • Review of the diagnosis and treatment of primary periodic paralysis. Statland JM, Fontaine B, Hanna MG, Johnson NE, Kissel JT, Sansone VA, Shieh PB, Tawil RN, Trivedi J, Cannon SC, Griggs RC. Review of the diagnosis and treatment of periodic paralysis. Muscle Nerve. 2018;57:522-530.
    • Abstract: Periodic paralyses (PPs) are rare neuromuscular disorders caused by mutations in skeletal muscle sodium, calcium, and potassium channel genes. PPs include hypokalemic paralysis, hyperkalemic paralysis, and Andersen-Tawil syndrome. Common features of PP include autosomal dominant inheritance, onset typically in the first or second decades, episodic attacks of flaccid weakness, which are often triggered by diet or rest after exercise. Diagnosis is based on the characteristic clinic presentation then confirmed by genetic testing. In the absence of an identified genetic mutation, documented low or high potassium levels during attacks or a decrement on long exercise testing support diagnosis. The treatment approach should include both management of acute attacks and prevention of attacks. Treatments include behavioral interventions directed at avoidance of triggers, modification of potassium levels, diuretics, and carbonic anhydrase inhibitors. To read more, click here.
  • Safety and pharmacokinetics of escalating single and multiple doses of dichlorphenamide in healthy individuals. Cohen F. Open‐label, dose‐escalation, phase 1 study of safety and single and multiple‐dose pharmacokinetics of dichlorphenamide in healthy volunteers. Clin Pharmacol Drug Dev. 2018 (online ahead of print). doi: 10.1002/cpdd.464.
    • Abstract: Single‐ and multiple‐dose pharmacokinetics and safety were investigated in this phase 1 study of dichlorphenamide, a carbonic anhydrase inhibitor approved in the United States for treatment of primary periodic paralysis. Dichlorphenamide was administered to 6 cohorts (n = 6 each) of healthy adults. Cohorts A through E received single doses of 25–400 mg followed by 50–800 mg/day in divided doses for 10 total doses. Cohort F (safety analysis only) received up to 28 titrated doses from 100–800 mg/day. Plasma for pharmacokinetics sampling was obtained predose and up to 48 hours postdose. Twenty‐five of 36 enrolled subjects completed. Median time to maximum plasma concentration ranged from 1.5–3 hours, and mean half‐life from 32–68 hours. Mean area under the concentration‐time curve from time 0 to tau (length of the dosing interval estimated using the trapezoidal method) and maximum observed plasma concentration increased dose‐proportionally after multiple doses. The incidence and severity of adverse events (AEs) were dose‐related, with at least one mild AE reported among 17%, 17%, and 67% of patients in cohorts A, B, and C, respectively; and at least one mild‐to‐moderate AE among 100% of subjects in cohorts D, E, and F. One serious AE of rash was reported in cohort F. Eleven subjects discontinued; 10 due to AEs at 400 or 800 mg/day (cohorts E and F), including 100% of cohort F. Hypokalemia contributed to 5 of 6 discontinuations in cohort F (all 800 mg/day). To read more, click here.
  • Treatment for periodic paralysis. Sansone V, Meola G, Links TP, Panzeri M, Rose MR. Treatment for periodic paralysis. Cochrane Database Syst Rev. 2008; Jan 23;(1):CD005045.
    • Abstract: Muscle weakness and attacks of paralysis are two important features of periodic paralyses. Paralytic attacks occur in acute episodes and can be incapacitating. Attacks may last from several hours to several days according to the type of muscle channel involved. In some cases permanent muscle weakness can also occur. We are unsure whether such permanent muscle weakness is more likely to develop if the frequency of attacks is high and therefore might be less likely to occur if attacks are fully prevented by treatment. Although the treatment of choice in periodic paralysis is generally considered to be acetazolamide, there is no standardised treatment regimen and no consensus as to when to start treatment. We do not know if acetazolamide treatment prevents any permanent weakness that may occur.
      • We found two small studies demonstrating an improvement of muscle strength with pinacidil and acetazolamide. There was only one trial considering treatment of paralytic attacks, demonstrating a decrease in the severity and frequency of the attacks using diclorophenamide
      • We did not find other randomised or quasi-randomised studies, but only case reports and anecdotal articles using other drugs to reduce paralyses attacks. Further research is needed to determine the best treatment for reducing the frequency and severity of attacks and to treat or prevent permanent muscle weakness To read more, click here.
  • Efficacy and safety of dichlorphenamide in adolescent patients with primary periodic paralysis (poster). E. Ciafaloni, F. Cohen, R. Griggs. Poster presented at 2018 AAN Annual Meeting; April 21—27, 2018; Los Angeles, CA.
    • Abstract:
      • The primary periodic paralyses (PPP) are ion channelopathies of skeletal muscle caused by point mutations in calcium, sodium, or potassium channel genes
      • In adults with PPP, symptoms of muscle weakness and myotonia were often present in childhood
      • PPP may be managed with lifestyle interventions; however, prophylactic drug therapy is often indicated
      • Dichlorphenamide (DCP; Keveyis®, Strongbridge Biopharma) is the only FDA-approved drug for use in adults with PPP
      • 2 multinational, placebo-controlled clinical trials demonstrated that DCP reduced the frequency, severity, and duration of PPP attacks of muscle weakness/paralysis when used daily– One of these studies—the Tawil/Working Group on Periodic Paralysis (WGPP)—enrolled adolescents as well as adults
      • Results from the adolescent subgroup of the Tawil/WGPP have not been previously described
      To view the poster, click here.
  • Efficacy of dichlorphenamide in primary periodic paralysis: Pooled-data analysis of two Phase 3 clinical trials (poster). P. Shieh, F. Cohen, R. Barohn, R. Griggs. Poster presented at the 2018 AAN Annual Meeting; April 21—27, 2018; Los Angeles, CA.
    • Abstract:
      • The primary periodic paralyses (PPP) are ion channelopathies of skeletal muscle caused by point mutations in calcium, sodium, or potassium channel genes
      • Dichlorphenamide (DCP [Strongbridge Biopharma plc, Trevose, PA]) is [an] FDA-approved drug for use in adults with PPP
      • 2 multinational, placebo-controlled clinical trials, each including substudies of hyperkalemic and hypokalemic PPP patients, demonstrated the efficacy and safety of DCP
      • Efficacy was originally reported separately for each substudy within each trial using average on-treatment weekly attack rates over the final 8 wk of the 9-wk, double-blind treatment period
      • An integrated analysis was conducted to evaluate overall efficacy determined by absolute and relative changes from baseline in average weekly attack rates
      To view the poster, click here.
  • Characterization of common adverse events in a Phase 3, placebo-controlled, double-blind and open-label extension study of dichlorphenamide for primary periodic paralysis (poster). M Hanna, F Cohen, R Griggs. Poster presented at the Muscle Study Group Annual Scientific Meeting; September 17—19, 2018; Oxford, UK.
    • Abstract:
      • Primary periodic paralysis (PPP) is a rare condition caused by genetic mutations in skeletal muscle sodium, calcium, and potassium channels, resulting in attacks of muscle weakness.
      • Dichlorphenamide (DCP), administered daily for up to 1 year, has been shown to reduce the frequency, severity, and duration of attacks of PPP and was approved in the United States for the treatment of primary hyperkalemic and hypokalemic periodic paralysis and related variants in 2015
      • The most common adverse events (AEs) observed during clinical trials were paresthesia and cognition-related AEs
        • In the double-blind phase of the HYP/HOP trial (n=65), compared with placebo, DCP-treated patients had higher rates of paresthesia (placebo, 14% vs DCP, 47%) and cognitive disorder (placebo, 7% vs DCP, 19%)
      • To further consider the safety profile of DCP, additional characterization of these AEs was conducted.
      To view the poster, click here.

Health and Economic Burden From Primary Periodic Paralysis

  • Impact of periodic paralysis on quality of life. Cavel-Greant D, Lehmann-Horn F, Jurkat-Rott K. The impact of permanent muscle weakness on quality of life in periodic paralysis: a survey of 66 patients. Acta Myol. 2012;31:126-133.
    • Abstract: The periodic paralyses are hereditary muscle diseases which cause both episodic and permanent weakness. Permanent weakness may include both reversible and fixed components, the latter caused by fibrosis and fatty replacement. To deter- mine the degree of handicap and impact of permanent weakness on daily life, we conducted a 68-question online survey of 66 patients over 41 years (mean age, 60 ± 14 years). Permanent weakness occurred in 68%, muscle pain in 82% and muscle fatigue in 89%. Eighty-three percent of patients reported themselves as moderately to very active between ages 18-35. At the time of the survey only 14% reported themselves as moderately to very active. Contrary to the literature, only 21% of patients reported decreased frequency of episodic weakness with increased age. Sixty-seven percent had incurred injuries due to falls. Mobility aids were required by 49%. Strength increased in 49% of patients receiving professional physiotherapy and in 62% performing self-managed exercise routines. A decline of strength was observed by 40% with professional and by 16% with self-managed exercise routine, suggesting that overworking muscles may not be beneficial. There is an average of 26 years between age at onset and age at diagnosis indicating that diagnostic schemes can be improved. In summary our data suggests that permanent muscle weakness has a greater impact on the quality of life of patients than previously anticipated. To read more, click here.

Important Safety Information for KEVEYIS

What is KEVEYIS?

KEVEYIS (pronounced keh-VAY-iss) (dichlorphenamide) is a prescription drug used to treat primary hyperkalemic periodic paralysis, primary hypokalemic periodic paralysis, and other similar diseases.

What should you tell your healthcare provider before taking KEVEYIS?

Tell your doctor if you are allergic to dichlorphenamide or other sulfa drugs; if you take high doses of aspirin, or if you have lung or liver disease; if you are pregnant, plan to become pregnant, or are breastfeeding or plan to breastfeed.

What should you know about KEVEYIS?

  • Severe allergic and other reactions have happened with sulfonamides (drugs such as KEVEYIS) and have sometimes been fatal. Stop taking KEVEYIS at the first sign of skin rash, swelling, difficulty breathing, or any other unexpected side effect or reaction, and call 911 right away.
  • Tell your healthcare provider if you take aspirin or if another healthcare provider instructs you to begin taking aspirin. High doses of aspirin should not be taken with KEVEYIS.
  • KEVEYIS can cause your body to lose potassium, which can lead to heart problems. Your healthcare provider will measure the potassium levels in your blood before you start treatment and at certain times during treatment.
  • Tell your healthcare provider about all other prescription and over-the-counter medicines you take, including supplements, as some medicines can interact with KEVEYIS.
  • While taking KEVEYIS, your body may produce too much acid or may not be able to remove acid from the body. Your healthcare provider may run tests on a regular basis to check for signs of acid buildup.
  • KEVEYIS may increase your risk of falling. Tell your healthcare provider right away if you experience a fall while taking KEVEYIS.
  • The risks of falls and acid buildup are greater in elderly patients.
  • It is not known whether KEVEYIS is safe or effective for people younger than 18 years of age.

What are the most common side effects with KEVEYIS?

The most common side effects are a feeling of numbness, tingling or burning (“pins and needles”) in the toes, feet, hands or fingers; trouble with memory or thinking; feeling confused; and unpleasant taste in the mouth.

These are not all of the possible side effects of KEVEYIS. Call your healthcare provider for medical advice about side effects. You are encouraged to report negative side effects of prescription drugs to the FDA. Visit www.fda.gov/medwatch/ or call 1-800-FDA-1088.

Please see KEVEYIS Important Safety Information and Full Prescribing Information.

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STRONGBRIDGE BIOPHARMA® is a registered trademark of the Strongbridge Biopharma plc. companies, which include Strongbridge Ireland Limited and Strongbridge U.S. Inc.
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