Finstal-5

Each film-coated tablet contains: Finasteride 5 mg.
Blue coloured, round shaped, biconvex, film-coated tablet plain on both sides.

Pharmacology: Pharmacodynamics: Finasteride is a competitive inhibitor of human 5 α-reductase, an intracellular enzyme which metabolises testosterone into the more potent androgen, dihydrotestosterone (DHT). In benign prostatic hyperplasia (BPH), enlargement of the prostate gland is dependent upon the conversion of testosterone to DHT within the prostate. Finasteride is highly effective in reducing circulating and intraprostatic DHT. Finasteride has no affinity for the androgen receptor.
In clinical studies of patients with moderate to severe symptoms of BPH, an enlarged prostate on digital rectal examination and low residual urinary volumes, Finasteride reduced the incidence of acute retention of urine from 7/100 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 QUASI-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 Finasteride 5 mg/day, Doxazosin 4 or 8 mg/day*, the combination of Finasteride 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 Finasteride, 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 Finasteride, 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 Finasteride, Doxazosin, and combination groups, respectively, compared to placebo. Only the Finasteride 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.
Pharmacokinetics: After an oral dose of 14C-Finasteride in man, 39% of the dose was excreted in the urine in the form of metabolites (virtually no unchanged drug was excreted in the urine), and 57% of total dose was excreted in the faeces. Two metabolites have been identified which possess only a small fraction of the Type II 5 α-reductase activity of Finasteride.
The oral bioavailability of Finasteride is approximately 80%, relative to an intravenous reference dose, and is unaffected by food. Maximum plasma concentrations are reached approximately two hours after dosing and the absorption is complete within 6-8 hours. Protein binding is approximately 93%. Plasma clearance and the volume of distribution are approximately 165 mL/min and 76 L, respectively.
In the elderly, the elimination rate of Finasteride is somewhat decreased. Half-life is prolonged from a mean half-life of approximately six hours in men aged 18-60 years to eight hours in men aged more than 70 years. This is of no clinical significance and does not warrant a reduction in dosage.
In patients with chronic renal impairment, whose creatinine clearance ranged from 9-55 mL/min, the disposition of a single dose of 14C-Finasteride was not different from that in healthy volunteers. 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.
There are no data available in patients with hepatic insufficiency.
Finasteride has been found to cross the blood-brain barrier. Small amounts of Finasteride have been recovered in the seminal fluid of treated patients.

Finasteride is indicated for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to: Improve urinary flow and improve the symptoms associated with BPH causing regression of the enlarge prostate.
Decrease the incidence of acute urinary retention.
Decrease the incidence of surgery including transurethral reaction of the prostate (TURP) and prostatectomy.

Finasteride is an Azasteroid that inhibits the type-2 isoform of 5±-reductase, the enzyme responsible for conversion of testosterone to the more active dihydrotestosterone, and therefore has anti-androgenic properties. It is given orally in a dose of 5 mg daily in the management of benign prostatic hyperplasia to cause regression of the enlarged prostate and to improve symptoms; it may reduce the incidence of acute urinary retention and the need for surgery. Response may be delayed and treatment may be required for 6 months or more to assess whether benefit has been achieved. In the treatment of male-pattern baldness (alopecia androgenetica) in men, Finasteride is given orally in a dose of 1 mg daily. In general, use for 3 months or more is required before benefit is seen, and effects are reversed within 12 months of ceasing therapy.
Or as prescribed by the physician.

No specific treatment of overdosage with Finasteride is recommended. Treatment is symptomatic and supportive.

Hypersensitivity to any components of Finasteride.
Pregnancy-Use in women when they are or may potentially be pregnant.
Finasteride is not indicated for use in women.
Finasteride is not indicated for paediatric use.

In pregnant women, it may cause abnormalities of the external genitalia of a male fetus when administered to a pregnant woman.
It is not known whether Finasteride is excreted in breast milk. Serum Prostate Specific Antigens (S-PSA) levels decrease in patients treated with Finasteride.

General: The beneficial response of Finasteride may not be manifested immediately and thus patients with large residual urine volume and/or severely diminished urinary flow should be monitored carefully for obstructive neuropathy. Since serum markers of prostate cancer may be reduced in patients taking Finasteride, such malignancies should be excluded before treatment of benign prostatic hyperplasia is initiated.
Effects of PSA and prostate cancer detection: No clinical benefit has been demonstrated in patients with prostate cancer treated with Finasteride. Digital rectal examinations as well as other evaluations for prostate cancer are recommended prior to initiating therapy with Finasteride and periodically thereafter. Serum prostate-specific antigen (S-PSA) is also used for prostate cancer detection.
Generally, a baseline S-PSA greater than 10 ng/mL prompts further evaluation and consideration of biopsy; for S-PSA levels between 4 and 10 ng/mL, further evaluation and consideration of biopsy; for S-PSA <4 ng/mL does not exclude prostate cancer.
Finasteride causes a decrease in S-PSA concentrations even in the presence of prostate cancer. The reduction of levels in patients with BPH treated with Finasteride should be considered when evaluating S-PSA data and does not rule out concomitant prostate cancer. Patients treated with Finasteride who have a sustained increase in S-PSA levels should be carefully evaluated.

Use in pregnancy: Finasteride is contraindicated in pregnancy because of the ability of Type II 5-alpha reductase inhibitors to inhibit conversion of testosterone to dihydrotestosterone. These drugs, including Finasteride, may cause abnormalities of the external genitalia of a male foetus when administered to a pregnant woman.
Use in Lactation: It is not known if Finasteride is excreted in human milk.
Exposure to Finasteride (by pregnant women) - Risk to Male fetus: Finasteride tablets are film-coated and will prevent contamination with the active ingredient during normal handling, provided that the tablets have not been broken or crushed. Pregnant women should not handle crushed or broken Finasteride tablets because of the possibility of absorption of Finasteride and the subsequent potential risk to male fetus. In addition, since Finasteride is present in semen, male patients should wear condom or otherwise avoid exposure of female sexual partners at risk of becoming pregnant.

Reproductive system and breast disorders: Less frequent: Impotence, decreased libido, decreased volume of ejaculate, ejaculation disorders, gynecomastia (breast tenderness and enlargement).
Incidence unknown: Testicular Pain.
Skin and subcutaneous tissue disorders: Less frequent: skin rash.
Other: Less frequent: Hypersensitivity reactions including pruritus, urticaria and swelling of the lips and the face.

No interactions of clinical importance have been identified.
Finasteride does not appear to significantly affect the cytochrome P450-linked drug metabolising enzyme system. Compounds tested in men included digoxin, propranolol, warfarin, glibenclamide and theophylline and no clinically meaningful interactions were found.
Finasteride has been used concomitantly with ACE-inhibitors, paracetamol, acetyl salicylic acid, alpha-blockers, beta blocker, calcium channel blocker, cardiac nitrates, diuretics, H2 antagonists, HMG-CoA reductase inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), quinolones and benzodiazepines without evidence of clinically significant adverse interactions.

Store at temperatures not exceeding 30°C.

Drugs for Bladder & Prostate Disorders

G04CB01 - finasteride ; Belongs to the class of testosterone-5-alpha reductase inhibitors. Used in the treatment of benign prostatic hypertrophy.

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