FINASID are indicated for the treatment and control of benign prostatic hyperplasia
(BPH) to:
- cause regression of the enlarged prostate, improve urinary flow and improve the
symptoms associated with BPH,
- reduce the incidence of acute urinary retention and reduce need for surgery
including transurethral resection of the prostate (TURP) and prostatectomy.
FINASID should be administered in patients with an enlarged prostate (prostate
volume above ca. 40 ml).
5α reductase inhibitors is not approved for prevention of prostate cancer
 

For oral use only.
The recommended dosage is one 5 mg tablet daily with or without food. The tablet
should be swallowed whole and must not be divided or crushed (See section 6.6).
Even though improvement can be seen within a short time, treatment for at least 6
months may be necessary in order to determine objectively whether a satisfactory
response to treatment has been achieved.
Dosage in the elderly
Dosage adjustments are not necessary although pharmacokinetic studies have
shown that the elimination rate of finasteride is slightly decreased in patients over
the age of 70.
Dosage in hepatic insufficiency
There are no data available in patients with hepatic insufficiency (See section 4.4).
Dosage in renal insufficiency
Dosage adjustments are not necessary in patients with varying degrees of renal
insufficiency (starting from creatinine clearance as low as 9 ml/min) as in
pharmacokinetic studies renal insufficiency was not found to affect the elimination
of finasteride. Finasteride has not been studied in patients on hemodialysis.
 

Hypersensitivity to finasteride or to any of the excipients. Contra-indicated in women and children (see sections 4.4, 4.6 and 6.6) Pregnancy - Use in women when they are or may potentially be pregnant (see 4.6 Pregnancy and lactation, Exposure to finasteride - risk to male fetus).

General:
• Patients with large residual urine volume and/or severely diminished urinary flow
should be carefully monitored for obstructive uropathy.
• Consultation of an urologist should be considered in patients treated with
finasteride.
• Obstruction due to trilobular growth pattern of the prostate should be excluded
before starting treatment with finasteride.
• There is no experience in patients with liver insufficiency. Since finasteride is
metabolised in the liver (see section 5.2). Caution is advised in patients with
decreased hepatic function as the plasma-levels of finasteride may be increased in
such patients.
• This medicinal product contains lactose-monohydrate. Patients with rare
hereditary problems of galactose intolerance, Lapp lactase deficiency or
glucosegalactose malabsorption should not take this medicine.
• To avoid obstructive complications it is important that patients with large residual
urine and/or heavily decreased urinary flow are carefully controlled. The possibility
of surgery should be an option.
Effects on prostate-specific antigen (PSA) and prostate cancer detection:
No clinical benefit has yet been demonstrated in patients with prostate cancer
treated with finasteride. Patients with BPH and elevated serum prostate specific
antigen (PSA) were monitored in controlled clinical studies with serial PSAs and
prostate biopsies. In these BPH studies, finasteride did not appear to alter the rate of
prostate cancer detection, and the overall incidence of prostate cancer was not
significantly different in patients treated with finasteride or placebo.
Digital rectal examination, and, if necessary, determination of prostate-specificantigen (PSA) in serum should be carried out on patients prior to initiating therapy
with finasteride and periodically during treatment to rule out prostate Cancer.
Serum PSA is also used for prostate cancer detection. Generally a baseline PSA >10
ng/mL (Hybritech) prompts further evaluation and consideration of biopsy; for PSA
levels between 4 and 10 ng/mL, further evaluation is advisable. There is considerable
overlap in PSA levels among men with and without prostate Cancer. Therefore, in
men with BPH, PSA values within the normal reference range do not rule out
prostate Cancer regardless of treatment with finasteride. A baseline PSA <4 ng/mL
does not exclude prostate cancer.
Finasteride causes a decrease in Serum PSA concentrations by approximately 50% in
patients with BPH even in the presence of prostate Cancer. This decrease in Serum
PSA levels in patients with BPH treated with finasteride should be considered when
evaluating PSA data and does not rule out concomitant prostate Cancer. This
decrease is predictable over the entire range of PSA values, although it may vary in
individual patients. In patients treated with finasteride for six months or more, PSA
values should be doubled for comparison with normal ranges in untreated men. This
adjustment preserves the sensitivity or specificity of the PSA assay and maintains its
ability to detect prostate Cancer.
Any sustained increase in PSA levels of patients treated with finasteride should be
carefully evaluated, including consideration of non-compliance to finasteride
therapy.
Percent free PSA (free to total PSA ratio) is not significantly decreased by finasteride
and remains constant even under the influence of finasteride.
When percent free PSA is used as an aid in the detection of prostate Cancer, no
adjustment is necessary.
- 5 α reductase inhibitors may increase the risk of development of high grade
prostate cancer
Women who are pregnant or may become pregnant should not handle crushed or
broken finasteride tablets because of the possibility of absorption of finasteride and
the subsequent potential risk to a male foetus. Finasteride tablets have a film
coating which prevents contact with the active ingredient provided that the tablets
have not been broken or crushed (see sections 4.6 and 6.6).
Evaluation for other urological disease:
Prior to initiating therapy with finasteride, perform appropriate evaluation to rule
out other urological conditions, including prostate cancer that might mimic benin
prostatic hyperplasia (BPH)
Drug/laboratory test interactions
Effect on levels of PSA
Serum PSA concentration is correlated with patient age and prostatic volume, and
prostatic volume is correlated with patient age. When PSA laboratory
determinations are evaluated, consideration should be given to the fact that PSA
levels decrease in patients treated with finasteride. In most patients, a rapid
decrease in PSA is seen within the first months of therapy, after which time PSA
levels stabilize to a new baseline. The post-treatment baseline approximates half of
the pre-treatment value. Therefore, in typical patients treated with finasteride for six
months or more, PSA values should be doubled for comparison to normal ranges in
untreated men. For clinical interpretation, see 4.4 Special warnings and precautions
for use, Effects on PSA and prostate cancer detection.
Breast cancer in men
Breast cancer has been reported in men taking FINASID 5 mg during clinical trials and
the post-marketing period. Physicians should instruct their patients to promptly
report any changes in their breast tissue such as lumps, pain, gynaecomastia or
nipple discharge.
Pediatric use
FINASID is not indicated for use in children.
Safety and effectiveness in children have not been established.
Lactose
The tablet contains lactose monohydrate. Patients with any of the following genetic
deficiencies should not take this drug: galactose intolerance, total lactase deficiency
or glucose-galactose malabsorption.
 

No clinically significant drug interactions have been identified. Finasteride does not
appear to significantly affect the cytochrome P450-Iinked drug metabolizing enzyme
system. The following medicinal products have been investigated in man, and no
clinically meaningful interactions have been found: propanolol, digoxin,
glibenclamide, warfarin, theophylline and antipyrine and no clinically meaningful
interactions were found.
 

Pregnancy: FINASID is contra indicated in women when they are or may potentially
be pregnant (see section 4.3).
Because of the ability of 5α-Reductase-inhibitors to inhibit conversion of
testosterone to dihydrotestosterone, these drugs, including FINASID, might cause
abnormalities of the external genitalia of a male foetus when administered to a
pregnant woman (See section 5.3 and section 6.6).
Exposure to FINASID - risk to male foetus.
Women who are pregnant or may become pregnant should not handle FINASID
tablets especially if crushed or broken because of the possibility of absorption of
FINASID and the subsequent potential risk to a male foetus (see section 6.6).
FINASID tablets are coated and will prevent contact with the active ingredient during
normal handling, provided that the tablets have not been broken or crushed.
Small amounts of FINASID have been recovered from the semen in subjects receiving
FINASID 5 mg/day. It is not known whether a male foetus may be adversely affected
if his mother is exposed to the semen of a patient being treated with FINASID. When
the patient's sexual partner is or may potentially be pregnant, the patient is
recommended to minimise exposure of his partner to semen.
Lactation: FINASID are not indicated for use in women. It is not known whether
FINASID is excreted in breast milk.
 

There is no available information indicating that FINASID would have an influence on
the ability to drive or use machines.
 

Within each frequency grouping, undesirable effects are presented in order of
decreasing seriousness.

Other Long-Term Data
In a 7-year placebo-controlled trial that enrolled 18,882 healthy men, of whom 9060
had prostate needle biopsy data available for analysis, prostate cancer was detected
in 803 (18.4%) men receiving FINASID and 1147 (24.4%) men receiving placebo. In
the FINASID group, 280 (6.4%) men had prostate cancer with Gleason scores of 7-10
detected on needle biopsy vs. 237 (5.1%) men in the placebo group. Additional
analyses suggest that the increase in the prevalence of high-grade prostate cancer
observed in the FINASID group may be explained by a detection bias due to the
effect of FINASID on prostate volume. Of the total cases of prostate cancer
diagnosed in this study, approximately 98% were classified as intracapsular (clinical
stage T1 or T2) at diagnosis. The clinical significance of the Gleason 7-10 data is
unknown.
Laboratory test findings: Serum PSA concentration is correlated with patient age and
prostatic volume, and prostatic volume is correlated with patient age. When PSA
laboratory determinations are evaluated, consideration should be given to the fact
that PSA levels generally decrease in patients treated with FINASID. In most patients,
a rapid decrease in PSA is seen within the first months of therapy, after which time
PSA levels stabilize to a new baseline. The post-treatment baseline approximates half
of the pre-treatment value. Therefore, in typical patients treated with FINASID for six
months or more, PSA values should be doubled for comparison to normal ranges in
untreated men. For details and clinical interpretation See section 4.4 (Paragraph
Effects on prostate specific antigen (PSA) and prostate Cancer detection).
 

Patients have received Single doses of FINASID up to 400 mg and multiple doses up
to 80 mg/day without adverse effects. There is no specific recommended treatment
of overdose of FINASID.
 

Pharmacotherapeutic group: Testosteron-5α-reductase-inhibitors
ATC-Code: G 04 CB 01
Finasteride is a synthetic 4-azasteroid, a specific competitive inhibitor of the
intracellular enzyme Type-II-5a-reductase. The enzyme converts testosterone into
the more potent androgen dihydrotestosterone (DHT). The prostate gland and,
consequently, also the hyperplasic prostate tissue are dependent on the conversion,
of testosterone to DHT for their normal function and growth. Finasteride has no
affinity for the androgen receptor.
Clinical studies show a rapid reduction of the Serum DHT levels of 70%, which leads
to a reduction on prostate volume. After 3 months, a reduction of approx. 20% in the
volume of the gland occurs, and the shrinking continues and reaches approx. 27%
after 3 years. Marked reduction takes place in the periurethral Zone immediately
surrounding the Urethra. Urodynamic measurements have also confirmed a
significant reduction of detrusor pressure as a result of the reduced obstruction.
Significant improvements in maximum urinary flow rate and symptoms have been
obtained after a few weeks, compared with the start of treatment. Differences from
Placebo have been documented at 4 and 7 months, respectively.
All efficacy parameters have been maintained over a 3-year follow-up period.
Effects of four years treatment with FINASID on incidence of acute urine retention,
need for surgery, symptom-Score and prostate volume:
In clinical studies of patients with moderate to severe symptoms of BPH, an enlarged
prostate on digital rectal examination and low residual urinary volumes, FINASID
reduced the incidence of acute retention of urine from 7/1 00 to 3/100 over four
years and the need for surgery (TURP or prostatectomy) from 10/100 to 5/100.
These reductions were associated with a 2-point improvement in QUASJ-AUA
Symptom Score (range 0-34), a sustained regression in prostate volume of
approximately 20% and a sustained increase in urinary flow rate.
Medical therapy of prostatic symptoms
The Medical Therapy of Prostatic Symptoms (MTOPS) Trial was a 4- to 6-year study
in 3047 men with symptomatic BPH who were randomised to receive FINASID 5
mg/day, doxazosin 4 or 8 mg/day*, the combination of FINASID 5 mg/day and
doxazosin 4 or 8 mg/day*, or placebo. The primary endpoint was time to clinical
progression of BPH, defined as a 4 point confirmed increase from baseline in
symptom score, acute urinary retention, BPH-related renal insufficiency, recurrent
urinary tract infections or urosepsis, or incontinence. Compared to placebo,
treatment with FINASID, doxazosin, or combination therapy resulted in a significant
reduction in the risk of clinical progression of BPH by 34 (p=0.002), 39 (p<0.001), and
67% (p<0.001), respectively.
The majority of the events (274 out of 351) that constituted BPH progression were
confirmed 4 point increases in symptom score; the risk of symptom score
progression was reduced by 30 (95% CI 6 to 48%), 46 (95% CI 25 to 60%), and 64%
(95% CI 48 to 75%) in the FINASID, doxazosin, and combination groups, respectively,
compared to placebo. Acute urinary retention accounted for 41 of the 351 events of
BPH progression; the risk of developing acute urinary retention was reduced by 67
(p=0.011), 31 (p=0.296), and 79% (p=0.001) in the FINASID, doxazosin, and
combination groups, respectively, compared to placebo. Only the FINASID and
combination therapy groups were significantly different from placebo.
* Titrated from 1 mg to 4 or 8 mg as tolerated over a 3-week period
In this study the safety and tolerability profile of combined treatment was broadly
similar to the profile of each of the drugs taken separately. However, undesirable
effects concerning the "nervous system" and "uro-genital system" organ classes
were observed more frequently when the two drugs were used in combination (see
section 4.8).
 

Absorption:
The bioavailability of FINASID is approx. 80%. Peak plasma concentrations are
reached approx. 2 hours after drug intake, and absorption is complete after 6-8
hours.
Distribution:
Binding to plasma proteins is approx. 93%.
Clearance and volume of distribution are approx. 165 ml/min (70-279 ml/min) and
76 l (44-96 l), respectively. Accumulation of small amounts of FINASID is seen on
repeated administration. After a daily dose of 5 mg the lowest steady-state
concentration of FINASID has been calculated to be 8-1 0 ng/ml, which remains
stable over time.
Biotransformation:
FINASID is metabolised in the liver. FINASID does not significantly affect the
cytochrome P 450 enzyme system. Two metabolites with low 5α-reductase-inhibiting
effects have been identified.
Elimination:
The plasma half-life averages 6 hours (4-12 hours) (in men >70 years of age, 8 hours,
range 6-15 hours). After administration of radioactively labelled FINASID, approx.
39% (32-46%) of the given dose is excreted in the urine in the form of metabolites.
Virtually no unchanged FINASID is recovered in the urine. Approximately 57% (51-
64%) of the total dose is excreted in the faeces.
FINASID has been found to cross the blood-brain barrier. Small amounts of FINASID
have been recovered in the seminal fluid of treated. In 2 studies of healthy subjects
(n=69) receiving FINASID 5 mg/day for 6-24 weeks, FINASID concentrations in semen
ranged from undetectable (<0.1 ng/ml) to 10.54 ng/ml. In an earlier study using a
less sensitive assay, FINASID concentrations in the semen of 16 subjects receiving
FINASID 5 mg/day ranged from undetectable (<1.0 ng/ml) to 21 ng/ml. Thus, based
on a 5-ml ejaculate volume, the amount of FINASID in semen was estimated to be
50- to 100-fold less than the dose of FINASID (5 μg) that had no effect on circulating
DHT levels in men (see also section 5.3.).
In patients with chronic renal impairment, whose creatinine clearance ranged from
9-55 ml/min, the disposition of a single dose of 14C-FINASID was not different from
that in healthy volunteers (see section 4.2). Protein binding also did not differ in
patients with renal impairment. A portion of the metabolites, which normally is
excreted renally, was excreted in the faeces. It therefore appears that faecal
excretion increases commensurate to the decrease in urinary excretion of
metabolites. Dosage adjustment in non-dialysed patients with renal impairment is
not necessary.
 

Non-clinical data reveal no special hazard for humans based on conventional studies
of repeated dose toxicity, genotoxicity, and carcinogenic potential.
Reproduction toxicology studies in male rats have demonstrated reduced prostate
and seminal vesicular weights, reduced secretion from accessory genital glands and
reduced fertility index (caused by the primary pharmacological effect of FINASID).
The clinical relevance of these findings is unclear.
As with other 5-alpha-reductase inhibitors, femininisation of male rat foetuses has
been seen with administration of FINASID in the gestation period. Intravenous
administration of FINASID to pregnant rhesus monkeys at doses up to 800 ng/day
during the entire period of embryonic and fetal development resulted in no
abnormalities in male fetuses. This does is about 60 to120 times higher than the
estimated amount in semen of a man who have taken 5 mg FINASID, and to which a
woman could be exposed via semen. In confirmation of the relevance of the Rhesus
model for human foetal development, oral administration of FINASID 2 mg/kg/day
(the systemic exposure (AUC) of monkeys was slightly higher (3x) than that of men
who have taken 5 mg FINASID, or approximately 1 to 2 million times the estimated
amount of FINASID in semen) to pregnant monkeys resulted in external genital
abnormalities in male foetuses. No other abnormalities were observed in male
foetuses and no FINASID-related abnormalities were observed in female foetuses at
any dose.
 

Lactose monohydrate,
Hydroxypropylcellulose
Docusate Sodium,
Magnesium stearate (E572)
Opadry blue
 

Not applicable.
 

4 years.

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

An opaque white (PVC –PVDC /Aluminium) Blister
The FINASID 5mg tablets are packed in blister packs of 30 tablets
 

Women who are pregnant or may become pregnant should not handle FINASID
tablets especially if crushed or broken because of the possibility of absorption of
FINASID and the subsequent potential risk to a male foetus (see section 4.6).
Any unused product or waste material should be disposed of in accordance with
local requirements.