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1489 Drugs for Tobacco Dependence ...Sonidegib Odomzo for Basal Cell Carcinoma ...p 27p 31 Clarifi cation: Half-Life of Heroin ...p 32 Olaparib Lynparza for Advanced Ovarian Cancer ...o

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IN THIS ISSUE

ISSUE

1433

Volume 56

Published by The Medical Letter, Inc • A Nonprofi t Organization

ISSUE No

1489

on Drugs and Therapeutics

Elbasvir/Grazoprevir (Zepatier) for Hepatitis C p 25

Drugs for Tobacco Dependence p 27

Sonidegib (Odomzo) for Basal Cell Carcinoma p 31

Clarifi cation: Half-Life of Heroin p 32

Olaparib (Lynparza) for Advanced Ovarian Cancer online only

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25

on Drugs and Therapeutics

ISSUE

1433

Volume 56

ISSUE No

1489 Drugs for Tobacco Dependence Sonidegib (Odomzo) for Basal Cell Carcinoma p 27p 31

Clarifi cation: Half-Life of Heroin p 32

Olaparib (Lynparza) for Advanced Ovarian Cancer online only

ALSO IN THIS ISSUE

Elbasvir/Grazoprevir (Zepatier)

for Hepatitis C

The FDA has approved Zepatier (Merck), a fi

xed-dose combination of two direct-acting antiviral

agents — elbasvir, an NS5A inhibitor, and grazoprevir,

an NS3/4A protease inhibitor — for oral treatment

of chronic hepatitis C virus (HCV) genotype 1 or 4

infection

Pronunciation Key Elbasvir : elb' as veer Zepatier : zep' ah teer

Grazoprevir : graz oh' pre veer

HCV GENOTYPES — Genotype 1 is responsible for

70-80% of HCV infections in the US Genotype 4

is uncommon in the US and Canada; it is the most

prevalent strain of HCV in Central sub-Saharan Africa,

North Africa, and the Middle East.1

FIXED-DOSE COMBINATIONS — Zepatier is the third

all-oral, interferon-free, fi xed-dose combination to

be approved for treatment of infections with HCV genotypes 1 and 4 The combination of ledipasvir/

sofosbuvir (Harvoni) was approved for HCV genotype

1 infection in 20142 and for genotypes 4, 5, and 6 in

paritaprevir/ritonavir copackaged with dasabuvir

(Viekira Pak) was approved for HCV genotype 1

infection in 2014.4 Ombitasvir/paritaprevir/ritonavir

(Technivie) coadministered with ribavirin was

approved for genotype 4 the following year.5

TREATMENT OF HCV GENOTYPE 1 — Current

guidelines recommend that patients with chronic HCV

genotype 1 infection receive either Harvoni, Viekira

Pak, sofosbuvir (Sovaldi) plus simeprevir (Olysio),

or daclatasvir (Daklinza) plus sofosbuvir, all with or

Table 1 Oral Regimens for HCV Genotype 1 Infection

Brand Name Formulation Usual Dosage Tablets Cost 1

Harvoni (Gilead) 90/400 mg ledipasvir/sofosbuvir tabs 1 tab once/day x 12 wks 2,3 1/day 4 $94,500

Sovaldi (Gilead) 400 mg sofosbuvir tabs 1 sofosbuvir 3 tab and 1 daclatasvir 2/day 4 147,000

+ Daklinza (BMS) + 60 mg daclatasvir tabs tab once/day x 12 wks 5

Sovaldi (Gilead) 400 mg sofosbuvir tabs 1 sofosbuvir 3 tab and 1 simeprevir 6 2/day 4 150,360

+ Olysio (Janssen) + 150 mg simeprevir caps cap once/day x 12 wks 7

(Abbvie) ombitasvir/paritaprevir/ritonavir tabs tabs qAM and 1 dasabuvir

+ 250 mg dasabuvir tabs tab bid x 12 wks 8,9

Zepatier (Merck) 50/100 mg elbasvir/grazoprevir tabs 1 tab once/day x 12 wks 9,10 1/day 4 54,600

1 Approximate WAC for 12 weeks’ treatment WAC = wholesaler acquisition cost or manufacturer’s published price to wholesalers; WAC represents a published catalogue or list price and may not represent an actual transactional price Source: AnalySource® Monthly February 5, 2016 Reprinted with permission by First Databank, Inc All rights reserved ©2016 www.fdbhealth.com/policies/drug-pricing-policy.

2 24 weeks for treatment-experienced patients with compensated cirrhosis 8 weeks may be considered for treatment-naive patients without cirrhosis with baseline HCV RNA <6 million IU/mL Patients with decompensated cirrhosis should also receive ribavirin 1000 mg/day (1200 mg/day for those weighing ≥75 kg).

3 Not recommended for use in patients with severe or end-stage renal disease.

4 Patients requiring ribavirin would also take 4-7 tablets or capsules of ribavirin 200 mg each day A 12-week supply of ribavirin for a 70-kg patient costs about $500.

5 Patients with decompensated cirrhosis or post-transplant should also receive ribavirin 1000 mg/day

6 Not recommended for use in patients with moderate or severe hepatic impairment.

7 24 weeks for patients with cirrhosis Whether treatment-experienced patients or those with HCV genotype 1a should also receive ribavirin 1000 mg/day (1200 mg/day for those weighing ≥75 kg) in two divided doses is unclear

8 24 weeks for patients with HCV genotype 1a and cirrhosis (12 weeks may be considered in this population, except in prior non-responders to peginterferon/ribavi-rin) All patients with HCV genotype 1a or cirrhosis should also receive ribavirin 1000 mg/day (1200 mg/day for those weighing ≥75 kg) in two divided doses.

9 Contraindicated for use in patients with moderate or severe hepatic impairment.

10 Patients with HCV genotype 1a with baseline NS5A polymorphisms should also take ribavirin and should be treated for 16 weeks Patients who have failed

to respond to peginterferon, ribavirin and a protease inhibitor should also receive ribavirin, but can be treated for 12 weeks Ribavirin should be given in two divided doses (for those with CrCl >50 mL/min; <66 kg = 800 mg/day, 66-80 kg = 1000 mg/day, 81-105 kg = 1200 mg/day, >105 kg = 1400 mg/day).

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without ribavirin.6 Harvoni has produced sustained

virologic response (SVR) rates >90% in various patient

populations, with minimal adverse effects Viekira Pak

with or without ribavirin for 12 or 24 weeks appears

to be similar in effi cacy to Harvoni, but has a higher

pill burden and has a greater potential for adverse

drug interactions The level of evidence supporting

use of simeprevir plus sofosbuvir is the same as that

for Harvoni and Viekira Pak for treatment-naive

pa-tients, but lower for treatment-experienced patients

Daclatasvir plus sofosbuvir was recently approved by

the FDA for treatment of HCV genotype 1 infection; the

level of evidence supporting its use is lower than that

for the other three regimens in both treatment-naive

and treatment-experienced patients

Harvoni, simeprevir plus sofosbuvir, and daclatasvir

plus sofosbuvir are not recommended for patients

with severe or end-stage renal disease because serum

concentrations of sofosbuvir and its metabolite are

signifi cantly increased in these patients

CLINICAL STUDIES — Approval of elbasvir/grazoprevir

was based on the results of trials in both

treatment-naive and treatment-experienced patients infected

with HCV genotype 1, 4, or 6

In one double-blind trial (C-EDGE) in 306

treatment-naive patients with HCV genotype 1 or 4 infection with

or without cirrhosis, 95% of patients (273/288) with

genotype 1 and 100% (18/18) of those with genotype

4 who were treated with elbasvir/grazoprevir achieved

a sustained virologic response 12 weeks after stopping

treatment (SVR12); there were no signifi cant differences

between cirrhotic and non-cirrhotic patients.7

In a single-arm trial in 218 treatment-naive

patients co-infected with HCV and HIV (C-EDGE

CO-INFECTION), 210 (96%), including all 35 patients

with cirrhosis, achieved an SVR12.8

In an unpublished, 4-arm, open-label trial (C-EDGE

TE), 420 patients with HCV genotype 1, 4, or 6

infection that had previously failed to respond to

peginterferon and ribavirin were randomized to

receive elbasvir/grazoprevir for 12 or 16 weeks, with

or without ribavirin Patients treated with ribavirin

in addition to elbasvir/grazoprevir for 16 weeks had

slightly higher SVR12 response rates (97%) than

those treated with the combination alone for 12 or 16

weeks (92%) or with the combination plus ribavirin

for only 12 weeks (94%).9

In an open-label trial in 79 patients with HCV genotype

1 infection that did not respond to previous treatment

with peginterferon and ribavirin in combination with boceprevir, telaprevir, or simeprevir (C-SALVAGE), 96% of patients treated with elbasvir/grazoprevir in combination with ribavirin for 12 weeks achieved an SVR12.10 Virologic response rates were maintained 24 weeks after stopping treatment.11

In a trial in 122 naive and treatment-experienced patients with HCV genotype 1 infection and stage 4-5 chronic kidney disease, including 92 patients

on hemodialysis (C-SURFER), 94% of patients treated with elbasvir/grazoprevir achieved an SVR12.12

In a small cohort of patients with HCV genotype 1a infection who had a pre-existing NS5A resistance-associated polymorphism, an SVR12 occurred in only 70% of patients (39/56) treated with elbasvir/ grazoprevir for 12 weeks compared to 100% (6/6) with

a 16-week course of elbasvir/grazoprevir plus ribavirin

ADVERSE EFFECTS — Fatigue, headache, and nausea

were the most frequent adverse effects reported in clinical trials in patients treated with elbasvir/grazoprevir for 12 weeks; similar adverse event rates were reported

in patients taking placebo Anemia has developed in patients treated for 16 weeks with elbasvir/grazoprevir and ribavirin ALT elevations to >5 times the upper limit of normal occurred in 1% of patients in clinical trials In non-HCV-infected subjects with severe hepatic impairment, grazoprevir levels rose to 12 times the levels found in

those with no hepatic impairment Like Viekira Pak,

Table 2 Results of Some Zepatier Clinical Trials

Treatment-Naive Patients with or without Cirrhosis

C-EDGE (double-blind; 316 patients with genotype 1, 4, or 6)

Zepatier x 12 weeks 95%

C-EDGE CO-INFECTION (open-label; 218 patients with genotype 1,

4, or 6 and HIV)

Zepatier x 12 weeks 96%

Treatment-Experienced Patients with or without Cirrhosis

C-EDGE TE (open-label; 420 patients with genotype 1, 4, or 6 with

or without HIV) 1

Zepatier x 12 weeks 92%

Zepatier x 16 weeks 92%

Zepatier + ribavirin x 12 weeks 94%

Zepatier + ribavirin x 16 weeks 97%

C-SALVAGE (open-label; 79 patients with genotype 1) 2

Zepatier + ribavirin x 12 weeks 96%

Patients with Severe Renal Impairment including Hemodialysis 3

C-SURFER (double-blind; 122 patients with genotype 1)

Zepatier x 12 weeks 94%

SVR12 = HCV RNA <15 or <25 IU/mL 12 weeks after stopping treatment

1 Previously failed to respond to peginterferon and ribavirin

2 Previously failed to respond to boceprevir, simeprevir, or telaprevir in combination with peginterferon and ribavirin

3 Treatment-naive or treatment-experienced patients with or without cir-rhosis

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elbasvir/grazoprevir is contraindicated in patients with

moderate or severe hepatic impairment

PREGNANCY — Use of elbasvir/grazoprevir in

pregnant women has not been studied Studies in

animals using large doses have demonstrated no

adverse effects on fetal development

DRUG INTERACTIONS — Both elbasvir and grazoprevir

are substrates of CYP3A; concomitant use with the

strong CYP3A inhibitor ketoconazole (Nizoral, and

others) increased their serum concentrations and

coadministration with the CYP3A inducer efavirenz

(Sustiva) decreased them Zepatier is contraindicated

for use with efavirenz and strong inducers of CYP3A,

such as rifampin, because of the potential for loss

of effi cacy Grazoprevir is a substrate of organic

anion transporting polypeptide (OATP) 1B1 and 1B3;

coadministration with inhibitors of these transporters

such as cyclosporine (Neoral, and others) can

increase serum concentrations of grazoprevir and

is contraindicated

Grazoprevir is a weak inhibitor of CYP3A; it has

been shown to increase serum concentrations of

midazolam (Versed, and generics) Elbasvir and

grazoprevir are both inhibitors of the drug transporter

breast cancer resistance protein (BCRP) and may

increase plasma concentrations of drugs that are

substrates of this transporter

DOSAGE — Zepatier tablets contain 50 mg of elbasvir

and 100 mg of grazoprevir The recommended dosage

for most patients is one tablet once daily for 12 weeks

Patients with genotype 1a infection who have

high-level NS5A resistance-associated polymorphisms

at baseline should also receive ribavirin and should

be treated for 16 weeks Patients with genotype 1a

or 1b infection previously treated with peginterferon,

ribavirin, and a protease inhibitor should also receive

ribavirin, but can be treated for 12 weeks In patients

with genotype 4 infection previously treated with

peginterferon and ribavirin, addition of ribavirin

is recommended, and their treatment should be

continued for 16 weeks

CONCLUSION — The oral fi xed-dose combination

of the direct-acting antiviral agents elbasvir and

grazoprevir (Zepatier) appears to be highly effective

and well tolerated in patients infected with HCV

genotype 1 or 4 It is less expensive than Harvoni and

may be safer in patients with severe renal impairment

Zepatier, like Viekira Pak, is contraindicated in

patients with moderate or severe hepatic impairment;

Harvoni is not

1 JP Messina et al Global distribution and prevalence of hepatitis

C virus genotypes Hepatology 2015; 61:77.

2 A combination of ledipasvir and sofosbuvir (Harvoni) for hepa-titis C Med Lett Drugs Ther 2014; 56:111.

3 In brief: new indications for Harvoni Med Lett Drugs Ther 2016; 58:6.

4 A 4-drug combination (Viekira Pak) for hepatitis C Med Lett Drugs Ther 2015; 57:15.

5 In brief: Technivie for HCV genotype 4 infection Med Lett Drugs Ther 2015; 57: e162.

6 American Association for the Study of Liver Diseases/Infec-tious Disease Society of America/International Antiviral So-ciety–USA Recommendations for testing, managing, and treating hepatitis C December 11, 2015 Available at www hcvguidelines.org Accessed February 18, 2016.

7 S Zeuzem et al Grazoprevir-elbasvir combination therapy for treatment-naive cirrhotic and noncirrhotic patients with

chron-ic hepatitis C virus genotype 1, 4, or 6 infection: a randomized trial Ann Intern Med 2015; 163:1.

8 JK Rockstroh et al Effi cacy and safety of grazoprevir (MK-5172) and elbasvir (MK-8742) in patients with hepatitis C virus and HIV co-infection (C-EDGE CO-INFECTION): a non-randomised, open-label trial Lancet HIV 2015; 2:e319.

9 P Kwo et al Effi cacy and safety of grazoprevir/elbasvir +/- RBV for 12 or 16 weeks in patients with HCV G1, G4 or G6 infection who previously failed peginterferon/RBV : C-EDGE treatment-experienced EASL - The International Liver Congress 2015 50th Annual Meeting of the European Association for the Study

of the Liver; Vienna, Austria; April 22-26 Available at www.nat-ap.org/2015/EASL/EASL_04.htm Accessed February 18, 2016

10 X Forns et al Grazoprevir and elbasvir plus ribavirin for chronic HCV genotype-1 infection after failure of combination therapy containing a direct-acting antiviral agent J Hepatol 2015; 63:564.

11 M Buti et al Grazoprevir, elbasvir, and ribavirin for chronic hepa-titis C virus genotype 1 infection after failure of pegylated

interfer-on and ribavirin with an earlier-generatiinterfer-on protease inhibitor: fi nal 24-week results from C-SALVAGE Clin Infect Dis 2016; 62:32.

12 D Roth et al Grazoprevir plus elbasvir in treatment-naive and treatment-experienced patients with hepatitis C virus geno-type 1 infection and stage 4-5 chronic kidney disease (the C-SURFER study): a combination phase 3 study Lancet 2015; 386:1537.

Drugs for Tobacco Dependence

▶ Tobacco dependence remains the primary preventable cause of death in the United States It is a chronic disorder that often requires pharmacologic therapy, but counseling may be equally effective and can add to the effectiveness of any treatment for this indication.1,2 Abrupt cessation of smoking appears to be as effective

as gradual reduction.3

NICOTINE — All FDA-approved nicotine replacement

therapies (NRTs) deliver nicotine to nicotinic receptors

in the central nervous system (CNS) in a lower dose and

at a sub stantially slower rate than tobacco cigarettes They increase smoking cessation rates by 50-70% and,

in the short term, may decrease weight gain associated with smoking cessation.4,5 Nicotine undergoes fi rst-pass metabolism, which limits its effectiveness in oral

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pill formulations Nicotine gum, lozenges, and patches

are available without a prescription in the US for

persons ≥18 years old; these products appear to be as

effective as those that require a prescription (nicotine

oral inhaler and nasal spray).Used as monotherapy, a

rapid-onset NRT such as a gum, lozenge, nasal spray,

or oral inhaler should be taken on a regular schedule

to prevent nicotine withdrawal symptoms Combining

the nicotine patch with a rapid-onset formulation

(combination NRT) is more effective than monotherapy

Transdermal – Nicotine patches require 6-8 hours

to achieve peak serum concentrations They deliver

nicotine to the CNS more slowly than any other NRT

Oral – Nicotine from a gum, lozenge, or oral inhaler is

absorbed through the buccal mucosa Serum nicotine

concentrations peak in 20-60 minutes If oral nicotine

is swallowed, fi rst-pass metabolism decreases its

bioavailability

Nasal Spray – Nicotine from nasal spray, the

fastest-acting of all NRTs (but still much slower than

cigarettes), achieves a peak CNS concentration in

5-20 min utes Patients report that relief of nicotine

withdrawal symptoms is faster with the nasal spray

than with other NRT formulations Because it can

irritate the throat and nasal mucosa, the nasal spray

should not be used for more than 3 months

Adverse Effects – The transdermal nicotine patch is

generally well tolerated, but some patients discontinue

it because of insomnia, vivid dreams, or pruritus at the

application site Removing the patch at bedtime can

minimize or eliminate vivid dreams and other sleep

disturbances The nico tine oral inhaler can cause minor

mouth and throat irri tation and cough; tolerance to the

irritating effects usually develops within one or two days

Nicotine gum can cause flatulence, indigestion, nausea,

unpleasant taste, hiccups, and a sore mouth, throat,

and jaw Nicotine lozenges can cause mouth irritation, heartburn, hiccups, and nausea Nicotine nasal spray

causes transient burning and stinging of the nasal mucosa, throat irritation, flushing, coughing, sneezing, lacrima tion, rhinorrhea, and nausea; these symptoms are a common cause of drug discontinuation

Drug Interactions – NRTs are metabolized by CYP2A6,

but do not inhibit or induce CYP enzymes to a clinically signifi cant extent Tobacco smoke, not nicotine itself, induces CYP1A2, CYP2E1, and some uridine diphosphate-glucuronosyltransferases (UGTs); it may increase the metab olism and decrease the effi cacy of drugs that are substrates of these pathways such as

clozapine (Clozaril, and others), theophylline

(Theo-Dur, and others), and propranolol.6,7 Dosages of these drugs may need to be reduced when patients stop smoking

BUPROPION — Used mainly for treatment of

depression, bupropion also has some nicotinic-receptor-blocking activity A sustained-release (SR) formulation of bupropion is FDA-approved for

treat-ment of tobacco dependence (marketed as Zyban)

Bupropion SR should be started 7-14 days before the target quit date to allow for adequate steady-state serum concentrations Immediate-release bupropion

(Wellbutrin, and generics) has also been used

(off-label) to treat tobacco dependence

Effectiveness — Bupropion has doubled smoking

cessation rates compared to placebo in short-term trials It has been as effective as NRT in increasing smoking cessation rates and decreasing weight gain.8

Adverse Effects – Bupropion is generally well tolerated

The most common adverse effects in clinical trials were insomnia and dry mouth Headache, nausea, and anxiety can also occur.9 Bupropion SR has been associated with a seizure incidence of 0.1%; patients with a history of seizure, stroke, brain tumor, brain sur-gery, or severe head injury should not take bupropion

Drug Interactions – Bupropion is primarily metabolized

by CYP2B6 to hydroxybupropion, its most active metabolite Drugs that are inhibitors or inducers of CYP2B6 may interact with bupropion Bupropion and hydroxybupropion inhibit CYP2D6; many antidepres-sants, antipsychotics, beta-blockers, and type 1C antiarrhythmics are CYP2D6 substrates and should be used with caution in patients taking bupropion.6 Use of bupropion with a monoamine oxidase (MAO) inhibitor

or within 2 weeks of stopping one is contraindicated

Recommendations for Treatment of Tobacco Dependence

▶ Tobacco dependence can be safely and effectively

treated with counseling and pharmacotherapy.

▶ All of the nicotine replacement therapies (NRTs) appear

to be about equally effective, but a combination of a

patch and a rapid-onset formulation is generally more

effective than monotherapy

▶ Bupropion has been as effective as NRT

▶ Varenicline appears to be the most effective drug for

treatment of tobacco dependence.

▶ Use of  ≥2 medications has been more effective than

monotherapy.

▶ The optimal duration of treatment is not clear; 3-6

months is probably the minimum, and some patients may

need longer treatment

▶ The effi cacy of electronic cigarettes for smoking

cessation remains to be established.

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Table 1 Some Drugs for Treatment of Tobacco Dependence

Some Available Usual Adult

Nicotinic Receptor Agonists

Nicotine transdermal patch 3 – generic 7, 14, 21 mg/24 hr patches 1 patch/d 4 $40.70 5

NicoDerm CQ (Sanofi ) 84.10 5

Nicotine nasal spray – Nicotrol NS (Pfi zer) 200 sprays/10 mL bottle 1 dose (2 sprays) 8-40x/d 304.90 7

(0.5 mg/spray) (max 5 doses/hr) 4,6

Nicotine oral inhaler – Nicotrol (Pfi zer) 10 mg cartridges 4-16 cartridges/d 290.40 8

(max 16 cartridges/d) 4

Nicotine polacrilex gum 3 – generic 2, 4 mg/piece 8-24 pieces/d 4,9 77.20

Nicorette Gum (GSK) 84.00

Nicotine polacrilex lozenge 3 – generic 2, 4 mg/lozenge 8-20 lozenges/d 4,10 72.00

Nicorette Lozenge(GSK) 11 103.00

Dopaminergic-Noradrenergic Reuptake Inhibitors

Bupropion SR – generic 100, 150, 200 mg SR tabs 12 150 mg bid 13 27.00

Wellbutrin SR (GSK)14 377.20

Zyban (GSK) 150 mg SR tabs 236.00

Nicotinic Receptor Partial Agonist

Varenicline tartrate – Chantix (Pfi zer) 0.5, 1 mg tabs 1 mg bid 15 157.50

1 Dosage reduction may be needed for hepatic or renal impairment.

2 Approximate WAC for 30 days’ treatment at the lowest usual maintenance dosage WAC = wholesaler acquisition cost, or manufacturer's published price to

wholesalers; WAC represents a published catalogue or list price and may not represent an actual transactional price Source: AnalySource® Monthly February

5, 2016 Reprinted with permission by First Databank, Inc All rights reserved ©2016 www.fdbhealth.com/policies/drug-pricing-policy.

3 Available over the counter (OTC) for persons ≥18 years old Patients should not eat or drink within 15 minutes of using a gum or lozenge.

4 See specifi c label for instructions for dose titration.

5 Cost for 28 transdermal patches.

6 One spray per nostril Maximum of 40 doses/day Should not be used for >3 months

7 Cost of 4 10-mL bottles.

8 Cost of 168 10-mg cartridges; each cartridge delivers 4 mg of nicotine.

9 A second piece of gum can be used within one hour Continuously chewing one piece after another is not recommended.

10 Maximum of 5 lozenges in 6 hours or 20 lozenges/day Do not use more than one lozenge at a time or continuously use one after another.

11 Also available in a mini-lozenge.

12 Only the generic 150-mg SR tablets are FDA-approved for this indication.

13 Initial dosage is 150 mg once/d for 3 days.

14 Not FDA-approved for this indication.

15 Initial dosage is 0.5 mg once/d for 3 days, then bid for 4-7 days.

VARENICLINE — Varenicline tartrate (Chantix), a

nicotinic receptor partial agonist, is FDA-approved

for smoking cessation.10 It binds selectively to 4β2

nicotinic acetylcholine receptors, relieving cravings

and withdrawal symptoms during abstinence

Varenicline binds to the 4β2 receptor with greater

smoking Varenicline should be started 7 days before

the target quit date to allow for adequate

steady-state serum concentrations

Effectiveness – Randomized controlled trials,

including both short-term trials and some for up to

one year, have found varenicline to be more effective

than NRT monotherapy or bupropion and as effective

as combination NRT (nicotine patch plus a

rapid-onset NRT) in increasing smoking cessation rates.11,12

In one randomized, open-label trial in 1086 smokers,

smoking cessation rates with varenicline, combination

NRT, and a nicotine patch alone were similar at 26

and 52 weeks, possibly due to a relatively low level of

Adverse Effects – Varenicline was generally well

tolerated in clinical trials The most common

ad-verse effects were nausea, sleep disturbances, abnormal dreams, headache, constipation, vomiting, flatulence, and xerostomia Neuropsychiatric symp-toms, exacerbations of pre-existing psychiatric illness, suicidal behavior, and an increased rate

of cardiovascular events have been associated with varenicline use in observational studies, but a retrospective cohort study in almost 165,000 patients found no increased risk of any cardiovascular or neuropsychiatric event with varenicline compared

smoking cessation rates in patients with psychiatric illnesses, with no signifi cant psychiatric adverse effects.15,16 Recent analyses of clinical trials have found no increase in suicidal behavior in patients treated with varenicline compared to those treated with NRT, bupropion, or placebo.17

Drug Interactions – Varenicline has no clinically

signifi cant drug interactions Coadministration of varenicline and transdermal nicotine does not affect nicotine pharmacokinetics, but nausea, headache, vomiting, dizziness, dyspepsia, and fatigue may occur more frequently with combined use than with transdermal nicotine alone

Trang 7

COMBINATIONS — Use of ≥2 medications has

generally been more effective than monotherapy in

treating tobacco dependence In one trial, 127 smokers

with comorbid conditions were randomly assigned to

receive a nicotine patch alone or in combination with

a nicotine oral inhaler and bupropion for 10 weeks;

abstinence rates at 26 weeks were 35% with the

combination compared to 19% with the patch alone.18

A randomized, placebo-controlled trial in 446 smokers

that included a week treatment period and a

12-week follow-up found that varenicline plus a nicotine

patch was signifi cantly more effective than varenicline

alone in achieving continuous abstinence at 12 weeks

(55.4% vs 40.9%) and 24 weeks (49.0% vs 32.6%) and

point-prevalence abstinence at 6 months (65.1% vs

46.7%).19 In another trial, a combination of varenicline

and bupropion SR was signifi cantly more effective than

varenicline alone in achieving prolonged abstinence

among 506 smokers at 12 weeks (53.0% vs 43.2%) and

26 weeks (36.6% vs 27.6%), but not at 52 weeks.20

DURATION OF TREATMENT — Longer-duration

pharmacotherapy may improve smoking cessation

of 3-6 months of effective therapy In general, the

dosage of NRTs should be tapered at the end of

treatment; bupropion SR and varenicline can usually

be discontinued without a gradual dosage reduction,

but some clinicians recommend a taper

ELECTRONIC CIGARETTES — Electronic cigarettes,

also called e-cigarettes, are advertised as a safer,

more convenient, and socially acceptable alternative

to tobacco cigarettes They have not been approved

by the FDA as smoking cessation aids E-cigarettes

are battery-operated devices that typically contain a

heating element (atomizer) and a reservoir of liquid

(usually nicotine dissolved in propylene glycol and/or

glycerin) When the user inhales or activates the

device with a button, the liquid nicotine is vaporized

into a visible mist

Clinical Studies – In a clinical trial in adult smokers not

intending to quit, 300 participants were randomized to

e-cigarettes containing 5.4 or 7.2 mg of nicotine or

no nicotine At 12 weeks, complete abstinence from

tobacco cigarettes had occurred in 14% of participants

using a nicotine-containing e-cigarette and in 4% of

those using the nicotine-free device.22

A randomized trial in 657 smokers who wanted to

quit compared a 16-mg nicotine e-cigarette, a

21-mg nicotine patch, and a placebo e-cigarette The

percentage of patients who achieved abstinence from

tobacco cigarettes at 6 months was not signifi cantly higher with the nicotine e-cigarette (7.3%) than with the nicotine patch (5.8%) or placebo device (4.1%).23

A meta-analysis of 38 trials of smokers who used e-cigarettes, including some in smokers who wanted

to quit and others in smokers in general, found that those who used e-cigarettes were actually 28% less likely to quit smoking tobacco cigarettes than smokers who did not use e-cigarettes.24

Adverse Effects – There is no evidence to date that

short-term use of e-cigarettes has serious adverse effects.25 The most common adverse effects reported during clinical trials of e-cigarettes were mouth and throat irritation and dry cough Lipoid pneumonia has been reported.26 In non-smokers, repeated exposure

to nicotine in e-cigarettes could lead to nicotine dependence

Toxic Substances – An FDA analysis of 2 different

brands of e-cigarette cartridges found that they contained a number of impurities including polycyclic aromatic hydrocarbons and tobacco-specifi c

e-cigarettes has been found to contain levels of potentially toxic and carcinogenic substances that are lower than those found in cigarette smoke, but higher than those in ambient air.28,29

PREGNANCY — Counseling is the preferred treatment

for pregnant women who smoke Nicotine is classifi ed

as category D (positive evidence of risk) for use during pregnancy However, using NRT during preg-nancy is probably safer for the fetus than smoking, which increases the incidence of low birth weight deliveries and is associated with peri- and post-natal complications NRT can increase smoking cessation rates in late pregnancy by about 40% and,

in one trial that followed infants after birth, it improved developmental outcomes.30 Bupropion and varenicline are classifi ed as category C (no adequate studies in pregnant women; fetal toxicity in animals) for use during pregnancy ■

1 MC Fiore et al Treating tobacco use and dependence: 2008 update U.S Public Health Service Clinical Practice Guideline executive summary Respir Care 2008; 53:1217.

2 AL Siu et al Behavioral and pharmacotherpy interventions for tobacco smoking cessation in adults, including pregnant wom-en: U.S Preventive Services Task Force recommendation state-ment Ann Intern Med 2015; 163:622.

3 N Lindson-Hawley et al Gradual reduction vs abrupt cessation

as a smoking cessation strategy in smokers who want to quit JAMA 2013; 310:91.

4 LF Stead et al Nicotine replacement therapy for smoking ces-sation Cochrane Database Syst Rev 2012; 11:CD000146.

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Sonidegib (Odomzo) for Basal Cell

Carcinoma

Pronunciation Key Sonidegib: soe' ni deg' ib Odomzo: oh dom' zoe

The FDA has approved the hedgehog pathway

inhibitor sonidegib (Odomzo – Novartis) for oral

treatment of locally advanced basal cell carcinoma that cannot be treated with surgery or radiation or has recurred following such treatment Vismodegib

(Erivedge), another oral hedgehog pathway inhibitor,

was approved earlier for the same indication and also for treatment of metastatic basal cell carcinoma.1

STANDARD TREATMENT — Basal cell carcinomas that

cannot be treated effectively with surgery or radiation because of their size or invasion of other organs are uncommon Topical therapies such as 5-fluorouracil, imiquimod, or photodynamic therapy have been used to treat superfi cial lesions Vismodegib is modestly effective for treatment of locally advanced or metastatic basal cell carcinoma.1

MECHANISM OF ACTION — The hedgehog signaling

pathway is important in embryofetal development and

in the regulation of adult stem cells; alterations in the pathway have been implicated in the development

smoothened homolog (SMO) activates the pathway SMO prevalence on the cell surface is regulated by the cell surface receptor patched homolog 1 (PTCH1) Hedgehog ligands inhibit PTCH1, permitting SMO proliferation and activity Mutations in SMO or PTCH1

Table 1 Hedgehog Pathway Inhibitors

Sonidegib (Odomzo) Vismodegib (Erivedge)

Formulation 200 mg capsules 150 mg capsules Route Oral Oral

Metabolism Primarily hepatic by Minimal; 98%

CYP3A4; 36% unchanged unchanged

Elimination Feces (70%); urine (30%) Feces (82%); urine (4%) Half-life 28 days 12 days

Dosage 200 mg once/day 150 mg once/day with

on an empty stomach or without food Cost 1 $335.30 $352.10

1 Approximate wholesale acquisition cost (WAC) for 1 capsule WAC = whole-saler acquisition cost or manufacturer's published price to wholewhole-salers; WAC represents a published catalogue or list price and may not represent an actual transactional price Source: AnalySource® Monthly February 5, 2016 Reprinted with permission by First Databank, Inc All rights reserved ©2016 www.fdbhealth.com/policies/drug-pricing-policy.

5 AC Farley et al Interventions for preventing weight gain

af-ter smoking cessation Cochrane Database Syst Rev 2012;

1:CD006219.

6 Inhibitors and inducers of CYP enzymes and P-glycoprotein

Med Lett Drugs Ther 2013; 55:e44.

7 LA Kroon Drug interactions with smoking Am J Health Syst

Pharm 2007; 64:1917.

8 JR Hughes et al Antidepressants for smoking cessation

Co-chrane Database Syst Rev 2014; 1:CD000031.

9 JT Hays and JO Ebbert Bupropion for the treatment of tobacco

dependence: guidelines for balancing risks and benefi ts CNS

Drugs 2003; 17:71.

10 Varenicline (Chantix) for tobacco dependence Med Lett Drugs

Ther 2006; 48:66.

11 EJ Mills et al Comparisons of high-dose and combination

nicotine replacement therapy, varenicline, and bupropion for

smoking cessation: a systematic review and multiple treatment

meta-analysis Ann Med 2012; 44:588.

12 K Cahill et al Pharmacological interventions for smoking

ces-sation: an overview and network meta-analysis Cochrane

Da-tabase Syst Rev 2013; 5:CD009329.

13 TB Baker et al Effects of nicotine patch vs varenicline vs

com-bination nicotine replacement therapy on smoking cessation at

26 weeks: a randomized clinical trial JAMA 2016; 315:371.

14 D Kotz et al Cardiovascular and neuropsychiatric risks of

var-enicline: a retrospective cohort study Lancet Respir Med 2015;

3:761.

15 RM Anthenelli et al Effects of varenicline on smoking cessation

in adults with stably treated current or past major depression: a

randomized trial Ann Intern Med 2013; 159:390.

16 AE Evins et al Maintenance treatment with varenicline for

smoking cessation in patients with schizophrenia and bipolar

disorder: a randomized clinical trial JAMA 2014; 311:145.

17 JR Hughes Varenicline as a cause of suicidal outcomes

Nico-tine Tob Res 2016; 18:2.

18 MB Steinberg et al Triple-combination pharmocotherapy for

medically ill smokers: a randomized trial Ann Intern Med 2009;

150:447.

19 CF Koegelenberg et al Effi cacy of varenicline combined with

nicotine replacement therapy vs varenicline alone for smoking

cessation: a randomized clinical trial JAMA 2014; 312:155.

20 JO Ebbert et al Combination varenicline and bupropion SR for

tobacco-dependence treatment in cigarette smokers: a

ran-domized trial JAMA 2014; 311:155.

21 M Siahpush et al Association between duration of use of

phar-macotherapy and smoking cessation: fi ndings from a national

survey BMJ Open 2015; 5:e006229.

22 P Caponnetto et al Effi ciency and safety of an electronic

ciga-rette (ECLAT) as tobacco cigaciga-rettes substitute: a prospective

12-month randomized control design study PLoS One 2013;

8:e66317.

23 C Bullen et al Electronic cigarettes for smoking cessation: a

randomised controlled trial Lancet 2013; 382:1629.

24 S Kalkhoran and SA Glantz E-cigarettes and smoking

cessa-tion in real-world and clinical settings: a systematic review and

meta-analysis Lancet Respir Med 2016; 4:116.

25 H McRobbie et al Electronic cigarettes for smoking

ces-sation and reduction Cochrane Database Syst Rev 2014;

12:CD010216.

26 L McCauley et al An unexpected consequence of electronic

cigarette use Chest 2012; 141:1110.

27 FDA Summary of results: laboratory analysis of electronic

cigarettes conducted by FDA April 22, 2014 Available at www.

fda.gov/NewsEvents/PublicHealthFocus/ucm173146.htm

Ac-cessed February 18, 2016.

28 ML Goniewicz et al Levels of selected carcinogens and

toxi-cants in vapour from electronic cigarettes Tob Control 2014;

23:133.

29 R Goel et al Highly reactive free radicals in electronic cigarette

aerosols Chem Res Toxicol 2015; 28:1675.

30 T Coleman et al Pharmacological interventions for promoting smoking cessation during pregnancy Cochrane Database Syst Rev 2015; 12:CD010078.

Trang 9

1 Vismodegib (Erivedge) for basal cell carcinoma Med Lett Drugs Ther 2012; 54:53.

2 J Rodon et al A phase I, multicenter, open-label, fi rst-in-human, dose-escalation study of the oral smoothened inhibi-tor sonidegib (LDE225) in patients with advanced solid tumors Clin Cancer Res 2014; 20:1900.

3 MR Migden et al Treatment with two different doses of sonidegib in patients with locally advanced or metastatic basal cell carcinoma (BOLT): a multicentre, randomised, double-blind phase 2 trial Lancet Oncol 2015; 16:716.

4 FDA Medical review - sonidegib Available at: www.accessdata fda.gov/drugsatfda_docs/nda/2015/205266Orig1s000MedR pdf Accessed February 18, 2016.

5 C Danial et al An investigator-initiated open-label trial of sonidegib in advanced basal cell carcinoma patients resistant

to vismodegib Clin Cancer Res 2015 Nov 6 (epub).

can cause unchecked hedgehog pathway activity and

have been found in ~10% and >85%, respectively, of

basal cell carcinomas.3 Like vismodegib, sonidegib

binds to and inhibits the signaling activity of SMO

CLINICAL STUDIES — Approval of sonidegib was

based on the results of a double-blind trial (BOLT)

that included 194 patients with locally advanced

basal cell carcinoma who were not candidates for

surgery or radiation Patients were randomized

to receive once-daily treatment with sonidegib

200 mg or 800 mg.3 A 12-month effi cacy analysis

(summarized in FDA review documents) found that

an objective (complete or partial) response occurred

in 58% (38/66) of patients taking 200 mg/day and in

44% (56/128) of those taking 800 mg/day.4

ADVERSE EFFECTS — In an 18-month safety analysis

that included 79 patients who received sonidegib

200 mg/day in the clinical trial, muscle spasms,

alopecia, dysgeusia, fatigue, nausea, diarrhea, and

weight loss were reported at rates >30%, but were

usually mild to moderate (grade 1-2) in severity

Severe (grade 3-4) musculoskeletal adverse effects

and increases in serum creatine kinase levels

occurred in 9% and 8% of patients, respectively Lipase

elevations were severe in 13% of patients Sonidegib

treatment was discontinued in 34% of patients

and interrupted in 20% because of adverse effects

Amenorrhea of ≥18 months’ duration occurred in 2 of

14 premenopausal women who were taking the drug

PREGNANCY — Sonidegib is teratogenic and

embryotoxic, and exposure can occur through seminal

fluid Effective contraception is recommended for

both women and men taking the drug, including men

who have had a vasectomy Women should avoid

pregnancy during treatment and for at least 20 months

following the last dose; men should use condoms

during treatment and for at least 8 months after the

last dose Patients taking sonidegib should not donate

blood or blood products for at least 20 months after

their last dose

DRUG INTERACTIONS — Sonidegib is a substrate of

CYP3A4; the mean AUC of the drug increased 2.2-fold

when it was administered with ketoconazole (Nizoral,

and others), a strong CYP3A inhibitor Use of sonidegib

with strong or moderate CYP3A inhibitors should be

avoided; patients who must take a moderate CYP3A

inhibitor such as fluconazole (Diflucan, and generics)

concurrently should do so for <14 days and should

be monitored for adverse effects Coadministration

of rifampin (Rifadin, and generics), a strong CYP3A

inducer, decreased sonidegib exposure by 72%; use

of sonidegib with strong or moderate CYP3A inducers should be avoided

RESISTANCE — In a single-arm trial, 9 patients

with advanced basal cell carcinoma that had not responded to vismodegib were treated with sonidegib

800 mg/day No objective responses occurred In vitro

analyses identifi ed the presence of SMO mutations conveying resistance against hedgehog pathway inhibition in 5 patients, all of whom experienced disease progression.5

DOSAGE AND ADMINISTRATION — The recom-mended dosage of sonidegib is 200 mg once daily

at least 1 hour before or 2 hours after a meal Serum creatine kinase and creatinine levels should

be measured before and during treatment If severe musculoskeletal reactions occur, treatment interruption or discontinuation may be necessary

CONCLUSION — Sonidegib (Odomzo), the second

oral hedgehog pathway inhibitor to be approved by the FDA, is modestly effective for treatment of locally advanced basal cell carcinoma It does not appear to

offer any advantages over vismodegib (Erivedge) and

has not been effective in treating cancers that have not responded to vismodegib ■

Clarifi cation: Half-Life of Heroin

A reader expressed concern that a statement in our article

Naloxone (Narcan) Nasal Spray for Opioid Overdose (Med

Lett Drugs Ther 2016; 58:1) might be misleading We stated that heroin has a half-life of 2-6 minutes, which is correct, but heroin is a prodrug that is rapidly metabolized

to 6-acetylmorphine and morphine The risk of respiratory depression is related to those active metabolites, and it may persist well beyond the clearance of heroin from the blood.

Online Only Article

Olaparib (Lynparza) for Advanced Ovarian Cancer

www.medicalletter.org/TML-article-1489e

Trang 10

e32

The Medical Letter

on Drugs and Therapeutics

The FDA has approved the oral poly (ADP-ribose)

poly-merase (PARP) inhibitor olaparib (Lynparza –

Astra-Zeneca) as monotherapy for treatment of women with

advanced ovarian cancer who have BRCA1/2 germline

mutations and have received at least 3 prior lines of

chemotherapy Olaparib is the fi rst PARP inhibitor to

be approved in the US It is approved outside the US

for maintenance treatment of relapsed BRCA-mutated

ovarian cancer

therapy for treatment of breast cancer and other cancers with defi ciencies in DNA repair mechanisms, including endometrial, prostate, and pancreatic cancers.5

ADVERSE EFFECTS — Olaparib appears to be better

tolerated than other drugs used to treat advanced cancer Nausea, vomiting, fatigue, and anemia are common, but generally have only been mild to moderate (grade 1-2) in severity Fatal pneumonitis has been reported with olaparib; treatment should be interrupted if new or worsening respiratory symptoms occur According to olaparib labeling, myelodysplastic syndrome/acute myeloid leukemia occurred in 22 of 2,618 patients treated with the drug; 17 of these cases were fatal

DRUG INTERACTIONS — Lynparza is primarily

metabolized by CYP3A; concomitant use of strong

or moderate CYP3A inhibitors or inducers should be avoided.6

DOSAGE AND COST — Olaparib is available in

50-mg capsules The recommended dosage is 400 50-mg (8 capsules) twice daily A bottle containing 112 capsules (a 7-day supply) costs $2996.00.7

CONCLUSION — Oral treatment with olaparib

(Lynparza), a poly (ADP-ribose) polymerase (PARP)

inhibitor, can produce a response in some women with advanced ovarian cancer, particularly those with BRCA-mutated cancers, and it is generally well tolerated Whether it improves overall survival is unknown Its effi cacy in the treatment of other cancers remains to be established ■

Olaparib (Lynparza) for Advanced

Ovarian Cancer

1 CC Gunderson and KN Moore Olaparib: an oral PARP-1 and PARP-2 inhibitor with promising activity in ovarian cancer Fu-ture Oncol 2015; 11:747.

2 SM Domchek et al Effi cacy and safety of olaparib monotherapy

in germline BRCA1/2 mutation carriers with advanced ovarian cancer and three or more lines of prior therapy Gynecol Oncol 2016; 140:199.

3 J Ledermann et al Olaparib maintenance therapy in plati-num-sensitive relapsed ovarian cancer N Engl J Med 2012; 366:1382.

4 J Ledermann et al Olaparib maintenance therapy in patients with platinum-sensitive relapsed serous ovarian cancer: a pre-planned retrospective analysis of outcomes by BRCA status in

a randomised phase 2 trial Lancet Oncol 2014; 15:852.

Pronunciation Key Olaparib: oh lap' a rib Lynparza: lin par' zah

MECHANISM OF ACTION — PARP enzymes are involved

in many cellular functions, including DNA

transcrip-tion and repair PARP inhibitranscrip-tion causes breaks in

double-stranded DNA Olaparib is most active against

tumors with a defi ciency in homologous recombination

(DNA repair), such as those with BRCA1/2 mutations,

because it activates an ineffective repair mechanism,

a process known as synthetic lethality It is cytotoxic

for ovarian cancer cells in general, but especially for

those that are BRCA1/2-defi cient.1

CLINICAL STUDIES — FDA approval of olaparib

was based on the results of a single-arm trial that

included 137 women with germline BRCA1/2-mutated

advanced ovarian cancer who had previously received

at least 3 lines of chemotherapy The objective

response rate with olaparib monotherapy was 34%

(partial response 32%; complete response 2%) and the

median duration of response was 7.9 months.2

A randomized, double-blind, placebo-controlled trial

evaluated the effi cacy of olaparib maintenance therapy

in 265 women with platinum-sensitive relapsed

ovarian cancer with or without BRCA1/2 mutations;

progression-free survival was signifi cantly longer with

olaparib than with placebo (8.4 vs 4.8 months).3 In a

subset analysis of 136 women with a BRCA mutation,

progression-free survival was 11.2 months with

olaparib versus 4.3 months with placebo.4

Olaparib and other (investigational) PARP inhibitors

are being tried for use alone and as part of combination

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