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Microsoft word - ezetrol pc merck approved moh sugg highlighted 0705.doc

SUMMARY OF PRODUCT CHARACTERISTICS
1.
NAME OF THE MEDICINAL PRODUCT

Ezetrol® 10 mg Tablets

2.

QUALITATIVE AND QUANTITATIVE COMPOSITION

Each tablet contains 10 mg of ezetimibe.
For excipients see 6.1.

3. PHARMACEUTICAL


Tablet.
White to off-white, capsule-shaped tablets debossed with “414” on one side.

4. CLINICAL
PARTICULARS

4.1 Therapeutic

indications

Primary Hypercholesterolaemia

Ezetrol co-administered with an HMG-CoA reductase inhibitor (statin) is indicated as adjunctive therapy to diet for use in patients with primary (heterozygous familial and non-familial) hypercholesterolaemia who are not appropriately controlled with a statin alone. Ezetrol monotherapy is indicated as adjunctive therapy to diet for use in patients with primary (heterozygous familial and non-familial) hypercholesterolaemia in whom a statin is considered inappropriate or is not tolerated.
Homozygous Familial Hypercholesterolaemia (HoFH)
Ezetrol co-administered with a statin, is indicated as adjunctive therapy to diet for use in patients with HoFH. Patients may also receive adjunctive treatments (e.g., LDL apheresis).
Homozygous Sitosterolaemia (Phytosterolaemia)
Ezetrol is indicated as adjunctive therapy to diet for use in patients with homozygous familial sitosterolaemia.
Studies to demonstrate the efficacy of Ezetrol in the prevention of complications of atherosclerosis have
not yet been completed.
4.2
Posology and method of administration
The patient should be on an appropriate lipid-lowering diet and should continue on this diet during Route of administration is oral. The recommended dose is one Ezetrol 10 mg tablet daily. Ezetrol can be administered at any time of the day, with or without food. When Ezetrol is added to a statin, either the indicated usual initial dose of that particular statin or the already established higher statin dose should be continued. In this setting, the dosage instructions for that particular statin should be consulted.
Co-administration with bile acid sequestrants

Dosing of Ezetrol should occur either ≥2 hours before or ≥4 hours after administration of a bile acid Use in the Elderly
No dosage adjustment is required for elderly patients (see section 5.2).
Use in Paediatric Patients
Children and adolescents ≥ 10 years: No dosage adjustment is required (see section 5.2). However,
clinical experience in paediatric and adolescent patients (ages 9 to 17) is limited.
Children < 10 years: No sufficient clinical data are available, therefore, treatment with Ezetrol is not
recommended.

Use in Hepatic Impairment
No dosage adjustment is required in patients with mild hepatic insufficiency (Child Pugh score 5 to 6).
Treatment with Ezetrol is not recommended in patients with moderate (Child Pugh score 7 to 9) or severe
(Child Pugh score > 9) liver dysfunction. (See sections 4.4 and 5.2.)

Use in Renal Impairment

No dosage adjustment is required for renally impaired patients (see section 5.2).
4.3 Contraindications
Hypersensitivity to the active substance or to any of the excipients.

When Ezetrol is co-administered with a statin, please refer to the SPC for that particular statin.
Therapy with Ezetrol co-administered with a statin is contraindicated during pregnancy and lactation.
Ezetrol co-administered with a statin is contraindicated in patients with active liver disease or unexplained
persistent elevations in serum transaminases.

4.4

Special warnings and precautions for use

When Ezetrol is co-administered with a statin, please refer to the SPC for that particular statin.
Liver Enzymes
In controlled co-administration trials in patients receiving Ezetrol with a statin, consecutive transaminase
elevations (≥ 3 X the upper limit of normal [ULN]) have been observed. When Ezetrol is co-administered
with a statin, liver function tests should be performed at initiation of therapy and according to the
recommendations of the statin. (See section 4.8.)
Skeletal Muscle
In post-marketing experience with Ezetrol, cases of myopathy and rhabdomyolysis have been reported.
Most patients who developed rhabdomyolysis were taking a statin concomitantly with Ezetrol. However,
rhabdomyolysis has been reported very rarely with Ezetrol monotherapy and very rarely with the addition
of Ezetrol to other agents known to be associated with increased risk of rhabdomyolysis. If myopathy is
suspected based on muscle symptoms or is confirmed by a creatine phosphokinase (CPK) level >10
times the ULN, Ezetrol, any statin, and any of these other agents that the patient is taking concomitantly
should be immediately discontinued. All patients starting therapy with Ezetrol should be advised of the
risk of myopathy and told to report promptly any unexplained muscle pain, tenderness or weakness (see
section 4.8).
Hepatic Insufficiency
Due to the unknown effects of the increased exposure to ezetimibe in patients with moderate or severe
hepatic insufficiency, Ezetrol is not recommended (see section 5.2).
Fibrates
The safety and efficacy of Ezetrol administered with fibrates have not been established; therefore,
co-administration of Ezetrol and fibrates is not recommended (see section 4.5).

Ciclosporin
Caution should be exercised when initiating Ezetrol in the setting of ciclosporin. Ciclosporin
concentrations should be monitored in patients receiving Ezetrol and ciclosporin (see section 4.5).
Warfarin
If Ezetrol is added to warfarin, the International Normalised Ratio (INR) should be appropriately monitored
(see section 4.5).
Excipient
Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-
galactose malabsorption should not take this medicine.

4.5

Interaction with other medicaments and other forms of interaction

In preclinical studies, it has been shown that ezetimibe does not induce cytochrome P450 drug
metabolising enzymes. No clinically significant pharmacokinetic interactions have been observed
between ezetimibe and drugs known to be metabolised by cytochromes P450 1A2, 2D6, 2C8, 2C9, and
3A4, or N-acetyltransferase.
In clinical interaction studies, ezetimibe had no effect on the pharmacokinetics of dapsone,
dextromethorphan, digoxin, oral contraceptives (ethinyl estradiol and levonorgestrel), glipizide,
tolbutamide, or midazolam, during co-administration. Cimetidine, co-administered with ezetimibe, had no
effect on the bioavailability of ezetimibe.
Antacids: Concomitant antacid administration decreased the rate of absorption of ezetimibe but had no
effect on the bioavailability of ezetimibe. This decreased rate of absorption is not considered clinically
significant.
Cholestyramine: Concomitant cholestyramine administration decreased the mean area under the curve
(AUC) of total ezetimibe (ezetimibe + ezetimibe glucuronide) approximately 55 %. The incremental
low-density lipoprotein cholesterol (LDL-C) reduction due to adding Ezetrol to cholestyramine may be
lessened by this interaction (see section 4.2).
Fibrates: Concomitant fenofibrate or gemfibrozil administration increased total ezetimibe concentrations
approximately 1.5- and 1.7-fold respectively, however these increases are not considered clinically
significant.
Fibrates may increase cholesterol excretion into the bile, leading to cholelithiasis. In a preclinical study in
dogs, ezetimibe increased cholesterol in the gallbladder bile (see section 5.3). Although the relevance of
this preclinical finding to humans is unknown, co-administration of Ezetrol with fibrates is not
recommended until use in patients is studied (see section 4.4).
Statins: No clinically significant pharmacokinetic interactions were seen when ezetimibe was co-
administered with atorvastatin, simvastatin, pravastatin, lovastatin, fluvastatin, or rosuvastatin.

Ciclosporin:
In a study of eight post-renal transplant patients with creatinine clearance of > 50 mL/min on
a stable dose of ciclosporin, a single 10-mg dose of Ezetrol resulted in a 3.4 fold (range 2.3 to 7.9-fold)
increase in the mean AUC for total ezetimibe compared to a healthy control population, receiving
ezetimibe alone, from another study (n=17). In a different study, a renal transplant patient with severe
renal insufficiency who was receiving ciclosporin and other multiple medications demonstrated a 12-fold
greater exposure to total ezetimibe compared to concurrent controls receiving ezetimibe alone. In a two-
period crossover study in twelve healthy subjects, daily administration of 20 mg ezetimibe for 8 days with
a single 100-mg dose of ciclosporin on Day 7 resulted in a mean 15 % increase in ciclosporin AUC
(range 10 % decrease to 51 % increase) compared to a single 100-mg dose of ciclosporin alone. A
controlled study on the effect of co-administered ezetimibe on ciclosporin exposure in renal transplant
patients has not been conducted. Caution should be exercised when initiating Ezetrol in the setting of
ciclosporin. Ciclosporin concentrations should be monitored in patients receiving Ezetrol and ciclosporin
(see section 4.4).
Warfarin: Concomitant administration of ezetimibe (10 mg once daily) had no significant effect on
bioavailability of warfarin and prothrombin time in a study of twelve healthy adult males. There have been
post-marketing reports of increased International Normalised Ratio in patients who had Ezetrol added to
warfarin (see section 4.4).
4.6
Use during pregnancy and lactation

Ezetrol co-administered with a statin is contraindicated during pregnancy and lactation (see section 4.3),
please refer to the SPC for that particular statin.
Pregnancy:
Ezetrol should be given to pregnant women only if clearly necessary. No clinical data are available on
the use of Ezetrol during pregnancy. Animal studies on the use of ezetimibe in monotherapy have shown
no evidence of direct or indirect harmful effects on pregnancy, embryofoetal development, birth or
postnatal development (see section 5.3).
Lactation:
Ezetrol should not be used during lactation. Studies on rats have shown that ezetimibe is secreted into
breast milk. It is not known if ezetimibe is secreted into human breast milk.
4.7
Effects on ability to drive and use machines

No studies of the effects on the ability to drive and use of machines have been performed. However,
Ezetrol is not expected to affect the ability to drive and use machines.
4.8 Undesirable

Clinical Studies
In clinical studies of 8 to 14 weeks duration, Ezetrol 10 mg daily was administered alone or with a statin in
3366 patients. Adverse reactions were usually mild and transient. The overall incidence of side effects
reported with Ezetrol was similar between Ezetrol and placebo. Similarly, the discontinuation rate due to
adverse experiences was comparable between Ezetrol and placebo.

The following common (≥1/100, <1/10) drug-related adverse experiences were reported in patients taking
Ezetrol alone (n = 1691) or co-administered with a statin (n = 1675):
Ezetrol administered alone:
Nervous system disorders: headache
Gastrointestinal disorders: abdominal pain and diarrhoea
Ezetrol co-administered with a statin:
Nervous system disorders: headache and fatigue
Gastrointestinal disorders: abdominal pain, constipation, diarrhoea, flatulence and nausea Musculoskeletal and connective tissue disorders: myalgia Laboratory Values:
In controlled clinical monotherapy trials, the incidence of clinically important elevations in serum
transaminases (ALT and/or AST ≥ 3 X ULN, consecutive) was similar between Ezetrol (0.5 %) and
placebo (0.3 %). In co-administration trials, the incidence was 1.3 % for patients treated with Ezetrol co-
administered with a statin and 0.4% for patients treated with a statin alone. These elevations were
generally asymptomatic, not associated with cholestasis, and returned to baseline after discontinuation of
therapy or with continued treatment. (See section 4.4.)

In clinical trials, CPK >10 X ULN was reported for 4 of 1674 (0.2 %) patients administered Ezetrol alone
vs 1 of 786 (0.1 %) patients administered placebo, and for 1 of 917 (0.1 %) patients co-administered
Ezetrol and a statin vs 4 of 929 (0.4 %) patients administered a statin alone. There was no excess of
myopathy or rhabdomyolysis associated with Ezetrol compared with the relevant control arm (placebo or
statin alone). (See section 4.4.)

Post-marketing Experience
The following additional rare (≥1/10000, < 1/1000) or very rare (<1/10000) adverse reactions have been
reported in post-marketing experience:
Blood and lymphatic system disorders: thrombocytopaenia (very rare)
Immune system disorders: hypersensitivity, including rash (rare) and angio-oedema (very rare)
Gastrointestinal disorders: nausea (rare); pancreatitis (very rare)
Hepatobiliary disorders: hepatitis (rare), cholelithiasis (very rare), cholecystitis (very rare)
Musculoskeletal and connective tissue disorders: myalgia (rare); myopathy/rhabdomyolysis (very rare;
see section 4.4)
Laboratory values: increased transaminases (rare); increased CPK (rare)


4.9 Overdose
In clinical studies administration of ezetimibe, 50 mg/day to 15 healthy subjects for up to 14 days, or
40 mg/day to 18 patients with primary hypercholesterolaemia for up to 56 days, was generally well
tolerated. In animals, no toxicity was observed after single oral doses of 5000 mg/kg of ezetimibe in rats
and mice and 3000 mg/kg in dogs.
A few cases of overdosage with Ezetrol have been reported; most have not been associated with adverse
experiences. Reported adverse experiences have not been serious. In the event of an overdose,
symptomatic and supportive measures should be employed.

5. PHARMACOLOGICAL

PROPERTIES
5.1 Pharmacodynamic
properties

Pharmacotherapeutic group: Other cholesterol and triglyceride reducers, ATC code: C10A X09

Ezetrol is in a new class of lipid-lowering compounds that selectively inhibit the intestinal absorption of
cholesterol and related plant sterols. Ezetrol is orally active, and has a mechanism of action that differs
from other classes of cholesterol-reducing compounds (e.g., statins, bile acid sequestrants [resins], fibric
acid derivatives, and plant stanols).
Ezetimibe localises at the brush border of the small intestine and inhibits the absorption of cholesterol,
leading to a decrease in the delivery of intestinal cholesterol to the liver; statins reduce cholesterol
synthesis in the liver and together these distinct mechanisms provide complementary cholesterol
reduction. The molecular mechanism of action is not fully understood. In a 2-week clinical study in
18 hypercholesterolaemic patients, Ezetrol inhibited intestinal cholesterol absorption by 54 %, compared
with placebo.
A series of preclinical studies was performed to determine the selectivity of ezetimibe for inhibiting
cholesterol absorption. Ezetimibe inhibited the absorption of [14C]-cholesterol with no effect on the
absorption of triglycerides, fatty acids, bile acids, progesterone, ethinyl estradiol, or fat soluble vitamins A
and D.)
Epidemiologic studies have established that cardiovascular morbidity and mortality vary directly with the
level of total-C and LDL-C and inversely with the level of HDL-C. Studies to demonstrate the efficacy of
Ezetrol in the prevention of complications of atherosclerosis have not yet been completed.
CLINICAL TRIALS
In controlled clinical studies, Ezetrol either as monotherapy or co-administered with a statin significantly
reduced total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B),
and triglycerides (TG) and increased high-density lipoprotein cholesterol (HDL-C) in patients with
hypercholesterolaemia.
Primary Hypercholesterolaemia
In a double-blind, placebo-controlled, 8-week study, 769 patients with hypercholesterolaemia already
receiving statin monotherapy and not at National Cholesterol Education Program (NCEP) LDL-C goal (2.6
to 4.1 mmol/l [100 to 160 mg/dl]), depending on baseline characteristics) were randomised to receive
either Ezetrol 10 mg or placebo in addition to their on-going statin therapy.
Among statin-treated patients not at LDL-C goal at baseline (~82 %), significantly more patients
randomised to Ezetrol achieved their LDL-C goal at study endpoint compared to patients randomised to
placebo, 72 % and 19 %, respectively. The corresponding LDL-C reductions were significantly different
(25% and 4% for ezetrol versus placebo, respectively). In addition, Ezetrol, added to on-going statin
therapy, significantly decreased total-C, Apo B, TG and increased HDL-C, compared with placebo.
Ezetrol or placebo added to statin therapy reduced median C-reactive protein by 10 % or 0 % from
baseline, respectively.
In two, double-blind, randomised placebo-controlled, 12-week studies in 1719 patients with primary
hypercholesterolaemia, ezetrol 10 mg significantly lowered total-C (13%), LDL-C (19%), Apo B (14%),
and TG (8%) and increased HDL-C (3%) compared to placebo. In addition, Ezetrol had no effect on the
plasma concentrations of fat-soluble vitamins A, D, and E, no effect on prothrombin time, and, like other
lipid lowering agents, did not impair adrenocortical steroid hormone production.
Homozygous Familial Hypercholesterolaemia (HoFH)

A double-blind, randomised, 12-week study enrolled 50 patients with a clinical and/or genotypic diagnosis
of HoFH, who were receiving atorvastatin or simvastatin (40mg) with or without concomitant LDL
apheresis. Ezetrol co-administered with atorvastatin (40 or 80 mg) or simvastatin (40 or 80 mg),
significantly reduced LDL-C by 15% compared with increasing the dose of simvastatin or atorvastatin
monotherapy from 40 to 80 mg.
Homozygous Sitosterolaemia (Phytosterolaemia)

In a double-blind, placebo-controlled, 8-week trial, 37 patients with homozygous sitosterolaemia were
randomised to receive Ezetrol 10 mg (n=30) or placebo (n=7). Some patients were receiving other
treatments (e.g., statins, resins). Ezetrol significantly lowered the two major plant sterols, sitosterol and
campesterol, by 21 % and 24 % from baseline, respectively. The effects of decreasing sitosterol on
morbidity and mortality in this population are not known.
5.2 Pharmacokinetic
properties

Absorption:
After oral administration, ezetimibe is rapidly absorbed and extensively conjugated to a
pharmacologically active phenolic glucuronide (ezetimibe-glucuronide). Mean maximum plasma
concentrations (Cmax) occur within 1 to 2 hours for ezetimibe-glucuronide and 4 to 12 hours for
ezetimibe. The absolute bioavailability of ezetimibe cannot be determined as the compound is virtually
insoluble in aqueous media suitable for injection.
Concomitant food administration (high fat or non-fat meals) had no effect on the oral bioavailability of
ezetimibe when administered as Ezetrol 10-mg tablets. Ezetrol can be administered with or without food.
Distribution: Ezetimibe and ezetimibe-glucuronide are bound 99.7% and 88 to 92% to human plasma
proteins, respectively.
Biotransformation: Ezetimibe is metabolised primarily in the small intestine and liver via glucuronide
conjugation (a phase II reaction) with subsequent biliary excretion. Minimal oxidative metabolism (a
phase I reaction) has been observed in all species evaluated. Ezetimibe and ezetimibe-glucuronide are
the major drug-derived compounds detected in plasma, constituting approximately 10 to 20 % and 80 to
90 % of the total drug in plasma, respectively. Both ezetimibe and ezetimibe-glucuronide are slowly
eliminated from plasma with evidence of significant enterohepatic recycling. The half-life for ezetimibe
and ezetimibe-glucuronide is approximately 22 hours.
Elimination: Following oral administration of 14C-ezetimibe (20 mg) to human subjects, total ezetimibe
accounted for approximately 93 % of the total radioactivity in plasma. Approximately 78 % and 11 % of
the administered radioactivity were recovered in the faeces and urine, respectively, over a 10-day
collection period. After 48 hours, there were no detectable levels of radioactivity in the plasma.
Special Populations:
Paediatric Patients
The absorption and metabolism of ezetimibe are similar between children and adolescents (10 to 18
years) and adults. Based on total ezetimibe, there are no pharmacokinetic differences between
adolescents and adults. Pharmacokinetic data in the paediatric population <10 years of age are not
available. Clinical experience in paediatric and adolescent patients (ages 9 to 17) has been limited to
patients with HoFH or sitosterolaemia.
Geriatric Patients
Plasma concentrations for total ezetimibe are about 2-fold higher in the elderly (≥ 65 years) than in the
young (18 to 45 years). LDL-C reduction and safety profile are comparable between elderly and young
subjects treated with Ezetrol. Therefore, no dosage adjustment is necessary in the elderly.
Hepatic Insufficiency
After a single 10-mg dose of ezetimibe, the mean AUC for total ezetimibe was increased approximately
1.7-fold in patients with mild hepatic insufficiency (Child Pugh score 5 or 6), compared to healthy
subjects. In a 14-day, multiple-dose study (10 mg daily) in patients with moderate hepatic insufficiency
(Child Pugh score 7 to 9), the mean AUC for total ezetimibe was increased approximately 4-fold on Day 1
and Day 14 compared to healthy subjects. No dosage adjustment is necessary for patients with mild
hepatic insufficiency. Due to the unknown effects of the increased exposure to ezetimibe in patients with
moderate or severe (Child Pugh score > 9) hepatic insufficiency, ezetrol is not recommended in these
patients (see section 4.4).
Renal Insufficiency
After a single 10-mg dose of ezetimibe in patients with severe renal disease (n=8; mean CrCl
≤ 30 ml/min/1.73 m2), the mean AUC for total ezetimibe was increased approximately 1.5-fold, compared
to healthy subjects (n=9). This result is not considered clinically significant. No dosage adjustment is
necessary for renally impaired patients.

An additional patient in this study (post-renal transplant and receiving multiple medications, including
ciclosporin) had a 12-fold greater exposure to total ezetimibe.
Gender
Plasma concentrations for total ezetimibe are slightly higher (approximately 20 %) in women than in men.
LDL-C reduction and safety profile are comparable between men and women treated with Ezetrol.
Therefore, no dosage adjustment is necessary on the basis of gender.
5.3
Preclinical safety data

Animal studies on the chronic toxicity of ezetimibe identified no target organs for toxic effects. In dogs
treated for four weeks with ezetimibe (≥ 0.03 mg/kg/day) the cholesterol concentration in the cystic bile
was increased by a factor of 2.5 to 3.5. However, in a one-year study on dogs given doses of up to 300
mg/kg/day no increased incidence of cholelithiasis or other hepatobiliary effects were observed. The
significance of these data for humans is not known. A lithogenic risk associated with the therapeutic use
of Ezetrol cannot be ruled out.
In co-administration studies with ezetimibe and statins the toxic effects observed were essentially those
typically associated with statins. Some of the toxic effects were more pronounced than observed during
treatment with statins alone. This is attributed to pharmacokinetic and pharmacodynamic interactions in
co-administration therapy. No such interactions occurred in the clinical studies. Myopathies occurred in
rats only after exposure to doses that were several times higher than the human therapeutic dose (ap-
proximately 20 times the AUC level for statins and 500 to 2000 times the AUC level for the active
metabolites).
In a series of in vivo and in vitro assays ezetimibe, given alone or in co-administered with statins,
exhibited no genotoxic potential. Long-term carcinogenicity tests on ezetimibe were negative.
Ezetimibe had no effect on the fertility of male or female rats, nor was it found to be teratogenic in rats or
rabbits, nor did it affect prenatal or postnatal development. Ezetimibe crossed the placental barrier in
pregnant rats and rabbits given multiple doses of 1000 mg/kg/day. The co-administration of ezetimibe
and statins was not teratogenic in rats. In pregnant rabbits a small number of skeletal deformities (fused
thoracic and caudal vertebrae, reduced number of caudal vertebrae) were observed. The co-
administration of ezetimibe with lovastatin resulted in embryolethal effects.
6. PHARMACEUTICAL
PARTICULARS
excipients

Croscarmellose sodium
Lactose monohydrate
Magnesium stearate
Microcrystalline cellulose
Povidone (K29-32)
Sodium laurilsulfate

6.2 Incompatibilities

Not applicable.
6.3 Shelf-life

2 years.
6.4
Special precautions for storage

Do not store above 30°C.
Blisters: Store in the original package.
6.5

Nature and contents of container

Unit Dose peelable blisters of clear polychlorotrifluoroethylene/PVC sealed to vinyl coated aluminium
backed with paper and polyester in packs of 7, 10, 14, 20, 28, 30, 50, 98, 100, or 300 tablets.
Push through blisters of clear polychlorotrifluoroethylene/PVC sealed to vinyl coated aluminium in packs
of 7, 10, 14, 20, 28, 30, 50, 98, 100, or 300 tablets.
Unit dose push through blisters of clear polycholortrifluoroethylene/PVC coated aluminium in packs of 50,
100 or 300 tablets.
Not all pack sizes may be marketed.
6.6 Instructions
use/handling

No special requirements.
7. MARKETING
AUTHORISATION

License Holder: Merck Sharp & Dohme (Israel-1996) Company Ltd., PO Box 7121, Petah-Tiqva 49170.

8. MARKETING

AUTHORISATION

Registration No.: 128 41 30721 00/ 128 41 30721 05


COPYRIGHT MSD Israel, 2003 All rights reserved.
The format of this leaflet was determined by the Ministry of Health and its content was checked and
approved in August 2005.

Source: http://ezetrol.co.il/secure/resources/pi/pi.pdf

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Secretariat of the Pacific Community Style Guide October 2001 This style guide was prepared by Kim Des Rochers and Alison Southby with input from previous SPC editors. 1. INTRODUCTION .1 Preparing publications .1 SPC’s copyright .2 ISBN, ISSN, Agdex and CIP .3 SPC’s address .4 2. SPELLING .4 Conventions .4 Capital letters .5 Geographical names .6 Hyphen

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