Active substance: FUROSEMIDE

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Furosemide 40 mg Tablets BP


Each tablet contains 40 mg of Furosemide

Each tablet contains 105mg lactose monohydrate

For the full list of excipients, see section 6.1


Round, white to off-white tablet embossed ‘F 40’ on one side (‘F’and ‘40’ seperated
by scoreline) and ‘’BL’’ on the other side.
The scoreline is only to facilitate breaking for ease of swallowing and not to divide
into equal doses.




Therapeutic indications
Furosemide is a potent diuretic with rapid action.
Furosemide tablets are indicated for:

1) The treatment of fluid retention associated with heart failure, including left
ventricular failure, cirrhosis of the liver and renal disease, including nephrotic

2) The treatment of mild to moderate hypertension (alone, or in combination with
other antihypertensive agents in the treatment of more severe cases).


Posology and method of administration

It is recommended that Furosemide tablets are taken on an empty stomach, and with
plenty of liquid.
Adults: The initial adult dose is 40mg daily, reduced to 20mg daily or 40mg on
alternative days. In some patients daily doses of 80mg or higher (given in divided
doses) may be required.
Children: Contra-indicated (see section 4.3)
Elderly: Caution is advised as furosemide is eliminated more slowly in elderly
patients.Treatment should be started with 20mg and titrated upwards as required (see
section 4.4).
Method of Administration:
For oral administration


• Hypersensitivity to furosemide or any of the excipients of this product.
• Hypersensitivity to amiloride, sulphonamides or sulphonamide derivatives
(because of cross-sensitivity between sulphonamides and furosemide).
• Hypovolaemia or dehydration (with or without accompanying hypotension)
(see section 4.4)
• Anuria, or renal failure with anuria not responding to furosemide.
• Renal failure as a result of poisoning by nephrotoxic or hepatotoxic agents or
renal failure associated with hepatic coma.
• Pre-comatose and comatose states associated with hepatic cirrhosis (see
section 4.4)
• Severe hypokalaemia, severe hyponatraemia. (see section 4.4)
• Breast feeding women (see section 4.6)
• Impaired renal function with a creatinine clearance below 30ml/min per 1.73
m2 body surface area (see section 4.4).
• Addison's disease (see section 4.4).
• Children and adolescents under 18 years of age (safety in this age group has
not yet been established).
• Digitalis intoxication (see section 4.5).

• Concomitant potassium supplements or potassium sparing diuretics (see
section 4.5).
• Porphyria

Special warnings and precautions for use:
Particularly careful monitoring or dose reduction is required in:

elderly patients (lower initial dose as particularly susceptible to side-effects see section 4.2)

difficulty with micturition including prostatic hypertrophy (increased risk of
urinary retention: consider lower dose). Closely monitor patients with partial
occlusion of the urinary tract

patients where latent diabetes may become manifest or the insulin
requirements of diabetic patients may increase. Stop furosemide before a
glucose tolerance test.

Pregnancy (see section 4.6)

patients with gout. Serum uric acid levels tend to rise during treatment with
Furosemide and an acute attack of gout may occasionally be precipitated.

impaired renal function (see section 4.3 and below-monitoring required)

impaired hepatic function (see section 4.3 and below-monitoring required)

Adrenal disease ( see section 4.3 and below-monitoring required.)

patients with hypoproteinaemia, e.g. associated with nephritic syndrome (the
effect of furosemide may be weakened and its ototoxicity potentiated).
Cautious dose titration is required.

acute hypercalcaemia (dehydration results from vomiting and diuresis - correct before
giving furosemide). Treatment of hypercalcaemia with a high dose of furosemide
results in fluid and electrolyte depletion - meticulous fluid replacement and correction
of electrolyte required.

Conditions requiring correction before furosemide is started (see also section 4.3)



Severe electrolyte disturbances - particularly hypokalaemia, hyponatraemia and acidbase disturbances.

Furosemide is not recommended

In patients at high risk for radiocontrast nephropathy - it should not be used for
diuresis as part of the preventative measures against radiocontrast-induced

Avoidance with other medicines (see also section 4.5 for other interactions

concurrent NSAIDs should be avoided - if not possible diuretic effect of furosemide
may be attenuated

ACE-inhibitors & Angiotensin II receptor antagonists - severe hypotension may occur
- dose of furosemide should be reduced/stopped (3 days) before starting or increasing
the dose of these

Laboratory monitoring requirements:

Serum sodium
Particularly in the elderly or in patients liable to electrolyte deficiency

Serum potassium
The possibility of hypokalaemia should be taken into account, in particular in patients
with cirrhosis of the liver, those receiving concomitant treatment with corticosteroids,
those with an unbalanced diet and those who abuse laxatives. Regular monitoring of
the potassium, and if necessary treatment with a potassium supplement, is
recommended in all cases, but is essential at higher doses and in patients with
impaired renal function. It is especially important in the event of concomitant
treatment with digoxin, as potassium deficiency can trigger or exacerbate the
symptoms of digitalis intoxication (see section 4.5). A potassium-rich diet is
recommended during long-term use.
Frequent checks of the serum potassium are necessary in patients with impaired renal
function and creatinine clearance below 60ml/min per 1.73m2 body surface area as
well as in cases where furosemide is taken in combination with certain other
drugswhich may lead to an increase in potassium levels (see section 4.5 & refer to
section 4.8 for details of electrolyte and metabolic abnormalities).

Renal function
Frequent BUN in first few months of treatment, periodically thereafter. Longterm/high-dose BUN should regularly be measured.Marked diuresis can cause
reversible impairment of kidney function in patients with renal dysfunction. Adequate
fluid intake isnecessary in such patients. Serum creatinine and urea levels tend to rise
during treatment.


Adverse effect on carbohydrate metabolism - exacerbation of existing carbohydrate
intolerance or diabetes mellitus. Regular monitoring of blood glucose levels is

Other electrolytes
Patients with hepatic failure/alcoholic cirrhosis are particularly at risk of
hypomagnesia (as well as hypokalaemia). During longterm therapy (especially at high
doses) magnesium, calcium, chloride, bicarbonate and uric acid should be regularly

Clinical monitoring requirements (see also section 4.8):
Regular monitoring for

blood dyscrasias. If these occur, stop furosemide immediately
liver damage
idiosyncratic reactions
Other alterations in lab values
Serum cholesterol and triglyceride levels may rise during Furosemide
treatment but will usually return to normal within six months.
Important information regarding the ingredients of this medicine
This medicinal product contains lactose. Patients with rare hereditary problems
of galactose intolerance, the LAPP lactase deficiency, orglucose-galactose
malabsorption should not take this medicine.


Interaction with other medicinal products and other forms of interaction
NSAIDS- Certain non-steroidal anti-inflammatory agents
(e.g.indometacin,ketorolac) may attenuate the action of furosemide (see
section 4.4)
Cardiac glycosides- In concurrent treatment with cardiac glycosides, it
should be taken into account that if hypokalaemia and/or electrolyte
disturbances (including hypomagnesaemia develop during therapy with
furosemide cardiotoxicity is increases.Drugs that prolong Q-T intervalThere is an increased risk toxicitywhen medicinal products that may cause
prolongation of the QT interval (e.g. terfenadine, some antiarrhythmics of
classes I and III) are used concomitantly, and in the presence of electrolyte

Anti-hypertensive agents- Enhanced hypotensive effect possible with all types.
Concurrent use with ACE inhibitors or Angiotensin II receptor antagonists can
result in marked falls in blood pressure, furosemide should be stopped or the dose
reduced before starting an ACE-inhibitor or Angiotensin II receptor

antagonists (see section 4.4)
Antipsychotics- Furosemide-induced hypokalaemia increases the risk of cardiac
toxicity. Avoid concurrent use with pimozide.Increased risk of ventricular
arrhythmias with amisulpride or sertindole. Enhanced hypotensive effect with

In risperidone placebo-controlled trials in elderly patients with dementia, a
higher incidence of mortality was observed in patients treated with
furosemide plus risperidone. No consistent pattern for cause of death was
observed but caution should be exercised and the risks and benefits of this
combination considered prior to the decision to use.
Anti-arrhythmics- (including amiodarone, disopyramide, flecanaide and
sotalol) - risk of cardiac toxicity (because of furosemideinduced
hypokalaemia). The effects of lidocaine, tocainide or mexiletine may be
antagonised by furosemide.
Vasodilators- enhanced hypotensive effect with moxisylyte (thymoxamine)
or hydralazine
Other diuretics - profound diuresis possible when furosemide given with
metolazone. Increased risk of hypokalaemia with thiazides. Contraindicated
with potassium sparing diuretics (eg Amiloride spironolactone) - increased
risk of hyperkalaemia (see section 4.3)
Renin inhibitors - aliskiren reduces plasma concentrations of furosemide
Nitrates - enhanced hypotensive effect
Antidepressants - enhanced hypotensive effect with MAOIs. Increased risk
of postural hypotension with TCAs (tricyclic antidepressants). Increased risk
of hypokalaemia with reboxetine
Antidiabetics - hypoglycaemic effects antagonised by furosemide
Antihistamines - hypokalaemia with increased risk of cardiac toxicity
Antifungals - increased risk of hypokalaemia and nephrotoxicity with

Anxiolytics and hypnotics - enhanced hypotensive effect. Chloral or
triclorfos may displace thyroid hormone from binding site.
CNS stimulants (drugs used for ADHD) - hypokalaemia increases the risk
of ventricular arrhythmias
Potassium salts - contraindicated - increased risk of hyperkalaemia (see
section 4.3)
Dopaminergics - enhanced hypotensive effect with levodopa.
Immunomodulators - enhanced hypotensive effect with aldesleukin.
Increased risk of hyperkalaemia with ciclosprin and tacrolimus. Increased
risk of gouty arthritis with ciclosporin
Muscle relaxants - enhanced hypotensive effect with baclofen or tizanidine.
Increased effect of curare-like muscle relaxants
Oestrogens - diuretic effect antagonised
Progestogens (drosperidone) - increased risk of hyperkalaemia
Prostaglandins - enhanced hypotensive effect with alprostadil
Theophylline - enhanced hypotensive effect
Anaesthetic agents - general anaesthetic agents may enhance the hypotensive
effects of furosemide. The effects of curare may be enhanced by furosemide.
Alcohol - enhanced hypotensive effect
Lithium- In common with other diuretics, serum lithium levels may be
increased when lithium is given concomitantly with furosemide, resulting in
increased lithium toxicity. Therefore, it is recommended that lithium levels
are carefully monitored and where necessary the lithium dosage is adjusted in
patients receiving this combination.
Salicylates- effects may be potentiated by furosemide. Patients receiving
high doses of salicylates concomitantly with furosemide, may experience
salicylate toxicity.
Chelating-agents- Oral furosemide and sucralfate must not be taken within 2
hours of each other because sucralfate decreases the absorption of
furosemide from the intestine and so reduced its effect.

Antihypertensives- The effects of other antihypertensives can be potentiated
by concomitant administration of furosemide. Severe fall in blood pressure
have been observed in combination with ACE inhibitors, furosemide therapy
should be temporarily discontinued (or at least the dose reduced) for three
days before therapy with an ACE inhibitor is initiated or the dose of an ACE
inhibitor is increased.
Antibiotics- The toxic effects of nephrotoxic antibiotics (e.g.
aminoglycosides, cephalosporins, ) may be increased by concomitant
administration of potent diuretics such as furosemide.
Furosemide may potentiate the ototoxicity of aminoglycosides,polymyxins or
vancomycin and other ototoxic medicinal products. Since this may lead to
irreversible damage, these medicinal products must only be used with
furosemide if there are compelling medical reasons. . Furosemide can
decrease vancomycin serum levels after cardiac surgery. Increased risk of
hypokalaemia with trimethoprim.
Cytotoxics -There is a risk of ototoxic effects if platinum
compounds/cisplatin and furosemide are given concomitantly. In addition,
nephrotoxicity of cisplatin may be enhanced
Anti-epileptics- Attenuation of the effect of furosemide may occur following
concurrent administration of phenytoin. Concomitant administration of
carbamazepine may increase the risk of hyponatraemia.

Corticosteroids - diuretic effect anatgonised (sodium retention) and increased
risk of hypokalaemia
Glychyrrizin -(contained in liquorice) may and increase the risk of
developing hypokalaemia
Sympathomimetics - increased risk of hypokalaemia with high doses of
beta2 sympathomimetics
Laxative abuse - increases the risk of potassium loss
Probenecid and anti-metabolites- Probenecid, methotrexate and other
products which, like furosemide, undergo significant renal tubular secretion
may reduce the effect of furosemide.


Fertility, pregnancy and lactation
It should only be used for the pathological causes of oedema which are not
directly or indirectly linked to the pregnancy. Treatment of oedema and
hypertension caused by pregnancy with diuretics is not advisable in general as
the placental perfusion may be lowered. Treatment during pregnancy requires
monitoring of foetal growth. However, furosemide has been given after the first
trimester of pregnancy for oedema, hypertension and toxaemia of pregnancy
without causing fetal or newborn adverse effects.
If use of furosemide is essential for the treatment of cardiac or renal
insufficiency during pregnancy, careful monitoring of electrolytes, haematocrit
and foetal growth is essential. Possible displacement of bilirubin from the
albumin binding and thus elevated risk of nuclear icterus in hyperbilirubinaemia
is discussed for furosemide.
Furosemide passes the placenta and reaches 100% of the maternal serum
concentration in cord blood. No malformations in humans which might be
associated with exposure to furosemide have been reported to date. However, there
is insufficient experience to allow a concluding evaluation of a potential damaging
effect in the embryo/foetus. In utero urinary production can be stimulated in the
foetus. Urolithiasis has been observed after treatment of premature infants with

Furosemide passes into breast milk and may inhibit lactation. Women must not
breast feed if they are treated with Furosemide (see section 4.3)


Effects on ability to drive and use machines
Reduced mental alertness, dizziness and blurred vision have been reported,
particularly at the start of treatment, with dose changes and in combination with
alcohol. Patients should be advised that if affected, they should not drive, operate
machinery or take part in activities where these effects could put themselves or others
at risk.


Undesirable effects

The evaluation of adverse reactions is based on the following definition of

Very common:
> 1/10
> 1/100, < 1/10
> 1/1000, < 1/100
> 1/10000, < 1/1000
Very rare: < 1/10000, including isolated reports
Blood and lymphatic system disorders
Uncommon: thrombocytopenia
Rare: eosinophilia, leukopenia, bone marrow depression (necessitates withdrawal of

Very rare: haemolytic anaemia oraplastic anaemia, agranulocytosis,. The
haemopoietic status should be therefore be regularly monitored.
Endocrine disorders
Glucose tolerance may decrease during treatment with furosemide. In patients with
diabetes mellitus this may lead to a deterioration of the metabolic status in patients
with manifest diabetes mellitus. Latent diabetes mellitus may become manifest.
Insulin requirements of diabetic patients may increase.
Eye disorders
Uncommon: visual disturbance

Metabolism and nutrition disorders
Impairment of electrolyte and fluid balance as a consequence of increased
electrolyte excretion are commonly observed during prolonged therapy with
furosemide. Regular monitoring of serum electrolytes (especially potassium, sodium
and calcium) is therefore indicated.
Metabolic acidosis can also occur. Possible development of electrolyte disorders is
influenced by underlying disorders (e.g. hepatocirrhosis, heart failure), concomitant
medication (see section 4.5 and nutrition).
Symptomatic electrolyte disturbances and metabolic alkalosis may develop in the
form of a gradually increasing electrolyte deficit or e.g. where higher furosemide
doses are administered to patients with normal renal function, acute severe
electrolyte losses,

Symptoms of electrolyte imbalance depend on the type of disturbance
As a result of increased renal sodium losses, hyponatraemia with corresponding
symptoms may occur, particularly if the supply of sodium chloride is restricted.
Commonly observed symptoms of sodium deficiency are, confusion, muscle cramps
and weakness, inappetence, dizziness, drowsiness vomiting
Particularly when the supply of potassium is concomitantly reduced and/or
extrarenal potassium losses are increased (e.g. in vomiting or chronic diarrhoea),
hypokalaemia may occur as a result of increased renal potassium losses. This is
manifested as neuromuscular (myasthenia, , pareses), intestinal (vomiting,
constipation, meteorism), renal (polyuria,) and cardiac (impaired paced setting and
conduction disorders) symptoms. Severe potassium losses may lead to paralytic ileus
or confusion with coma in extreme cases.
Increased serum renal calcium losses can lead to hypocalcaemia, which may induce
tetania in rare cases.
Magnesium and calcium deficiency, results tetania or cardiac arrhythmia in rare
Nephrocalcinosis/Nephrolithiasis has been reported in premature infants
As with other diuretics treatment with furosemide may lead to transitory increase in
blood creatinine and urea levels. Serum levels of uric acid may increase and attacks
of gout may occur.
Serum levels of cholesterol (reduction of serum HDL-cholesterol, elevation of serum
LDL-cholesterol) and triglycerides may be elevated during furosemide treatment.
During long-term therapy they will usually return to normal within six months.
The diuretic action of furosemide may lead to or contribute to hypovolaemia and
dehydration, especially in elderly patients. Severe fluid depletion may lead to
haemoconcentration with a tendency for thromboses to develop.
Increased production of urine may provoke or aggravate complaints in patients with
an obstruction of urinary outflow. Thus, acute retention of urine with possible
secondary complications may occur. For example, in patients with bladder-emptying
disorders, prostatic hyperplasia or narrowing of the urethra.

Nervous system disorders
Rare: paraesthesia, hyperosmolar coma

Ear and labyrinth disorders
Rare: dysacusis (hearing disorder) and/or syrigmus (tinnitus aurium) can occur,
This undesirable effect is particularly associated with too rapid i.v. injection,

predominantly in patients with coexisting renal insufficiency or hypoproteinaemia
(e.g. in nephrotic syndrome).

Hepato-biliary disorders
Very rare: acute pancreatitis, intrahepatic cholestasis, increase in hepatic
transaminases may develop
Hepatic encephalopathy in patients with hepatocellular insufficiency may occur (see
Section 4.3).
Vascular Disorder
Rare: vasculitis
Skin and subcutaneous tissue disorders
Uncommon photosensitivity
Rare: Skin and mucous membrane reactions may occasionally occur, e.g. itching,
urticaria, other rashes or bullous lesions, fever, hypersensitivity to light, exsudative
erythema multiforme (Lyell's syndrome and Stevens-Johnson syndrome), bullous
exanthema, exfoliative dermatitis, purpura

Cardiac disorders
Uncommon: Cardiac arrhythmias
Furosemide may cause reduction in blood pressure .These are predominantly
manifested as impairment of concentration and reactions, light headedness,
sensations of pressure in the head, headache, vertigo, drowsiness, dysopia,
xerostomia and thirst, and orthostatic dysregulation. Dehydration and - as a
consequence of hypovolaemia - circulatory collapse and haemoconcentration may
occur as a result of excessive diuresis. As a result of haemoconcentration, there may
be an increased risk of thromboses, particularly in elderly patients.

Congenital, familial and genetic disorders
If furosemide is administered to premature infants during the first weeks of life, it
may increase the risk of persistence of patent ductus arteriosus. The product is
contraindicated in children and adolescents under 18 years of age.
General disorders and administration site conditions
Uncommon: Fatigue
Rare: Severe anaphylactic or anaphylactoid reactions (e.g. with shock) occur rarely,
fever, Malaise

Gastrointestinal disorders
Uncommon: dry mouth, thirst, nausea, bowel motility disturbances, vomiting,
diarrhea, constipation.
Rare: Acute Pancreatitis, gastrointestinal complaints (e.g. nausea, vomiting,
diarrhoea), malaise may occur but not usually severe enough to necessitate
withdrawal of treatment.
Renal and urinary disorders
Uncommon: serum creatinine and urea levels can be temporarily elevated during
treatment with furosemide.
Rare: interstitial nephritis, acute renal failure.
Increased urine production, urinary incontinence, can be caused or symptoms can be
exacerbated in patients with urinary tract obstruction. Acute urine retention, possibly
accompanied by complications, can occur for example in patients with bladder
disorders, prostatic hyperplasia or narrowing of the urethra.
Pregnancy, puerperium and perinatal conditions
In premature infants with respiratory distress syndrome, administration of
Furosemide Accord Tablets in the initial weeks after birth entails an increased risk
of a persistent patent ductus arteriosus.
In premature infants, furosemide can be precipitated as nephrocalcinosis/kidney
Rare complications may include minor psychiatric disturbances.


Overdose can cause massive diuresis resulting in dehydration, volume depletion and
electrolyte disturbances with consequent hypotension and cardiac toxicity. High doses
have the potential to cause transient deafness and may precipitate gout (disturbed uric
acid secretion).

Benefits of gastric decontamination are uncertain. In patients presenting within 1
hour of ingestion, consider activated charcoal (50g for adults) Observe for a minimum
of 4 hours - monitor pulse and blood pressure.
Treat hypotension and dehydration with appropriate IV fluids

Monitor urinary output and serum electrolytes (including chloride and bicarbonate).
Correct electrolyte imbalances. Monitor 12
lead ECG in patients with significant electrolyte disturbances




Pharmacodynamic properties
Pharmacotherapeutic Group: - High-ceiling diuretic sulfonamides, loop diuretics;

ATC code: CO3C A01
The evidence from many experimental studies suggests that furosemide acts along the
entire nephron with the exception of the distal exchange site. The main effect is on
the ascending limb of the loop of Henley with a complex effect on renal circulation.
Blood-flow is diverted from the juxta-medullary region to the outer cortex.
The principle renal action of furosemide is to inhibit active chloride transport in the
thick ascending limb. Re-absorption of sodium, chloride from the nephron is reduced
hypotonic or isotonic urine produced.
It has been established that prostaglandin (PG) biosynthesis the renin-angiotensin
system are affected by furosemide administration and that furosemide alters the renal
permeability of the glomerulus to serum proteins.


Pharmacokinetic properties
Approximately 65% of the dose is absorbed after oral administration. The plasma
half-life is biphasic with a terminal elimination phase of about 1½ hours. Furosemide
is up to 99% bound to plasma proteins and is mainly excreted in the urine, largely
unchanged, but also excreted in the bile, non-renal elimination being considerably
increased in renal failure. Furosemide crosses the placental barrier and is excreted in
the milk.
Furosemide is a weak carboxylic acid which exists mainly in the dissociated form in
the gastro-intestinal tract. Furosemide is rapidly but incompletely absorbed (60-70%)
on oral administration and its effect is largely over within four hours. The optimal
absorption site is the upper duodenum at pH 5.0. Regardless of route of
administration, 69-97% of activity from a radio-labelled dose is excreted in the first 4
hours after the furosemide is given. Furosemide is bound to plasma albumin and little

biotransformation takes place. Furosemide is mainly eliminated via the kidneys (8090%); a small fraction of the dose undergoes biliary elimination and 10-15% of the
activity can be recovered from the faeces.
a) In renal/hepatic impairment
Where liver disease is present, biliary elimination is reduced. Up to 50% renal
impairment has little effect on the elimination rate of furosemide Tablets, but less
than 20% residual renal function increases the elimination time.

b) The Elderly
The elimination of furosemide is delayed in the elderly where a certain degree of
renal impairment is present.

c) New-born
A sustained diuretic effect is seen, possibly due to immature tubular function.


Preclinical safety data
Acute oral toxicity was low in all species tested. Chronic toxicity studies in
the rat and dog led to renal alterations (among others fibrous degeneration
and renal calcification).

In vitro and in vivo tests of genetic toxicology did not reveal any clinically
relevant evidence of a genotoxic potential of furosemide.

Long-term studies in mice and rats did not yield any relevant evidence of a
tumorigenic potential.

In studies of reproductive toxicology in foetal rats, a reduced number of
differentiated glomeruli, skeletal anomalies of the scapulae, humerus and
ribs (induced by hypokalaemia), as well as hydronephrosis occurred in
foetal mice and rabbits after administration of high doses.




List of excipients
Lactose monohydrate
Maize starch
Pregelatinised maize starch

Sodium starch glycollate (Type A)
Magnesium stearate


Not applicable.


Shelf life
Blisters: 4 years
HDPE containers: 3 years


Special precautions for storage
Blisters: Do not store above 25°C. Store in the original package.
Tablet Containers: Do not store above 25°C. Keep the container tightly closed.


Nature and contents of container
Al/ PVC/PVdC blister, pack sizes of 28, 30, 50, 56, 84, 98, 100 tablets.
HDPE tablet containers, pack sizes of 100, 250, 500 and 1000 tablets
Not all pack sizes may be marketed.


Special precautions for disposal
No special requirement..


Bristol Laboratories Ltd
Unit 3, Canalside,
Northbridge Road,
Hertfordshire HP4 1EG
United Kingdom


PL 17907/0019





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Source: Medicines and Healthcare Products Regulatory Agency

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