Binfin 5 Tablets

Indications

• Benign prostatic hyperplasia
• Androgenetic alopecia in men

Dosage

Adults: For benign prostatic hyperplasia, the recommended dose is 5 mg orally once daily, with treatment review at 3-6 months

Mechanism of action

Finasteride acts as a competitive and specific inhibitor of Type II 5α-reductase, an intracellular enzyme primarily located in prostatic stromal cells. This enzyme converts testosterone into the more active metabolite, dihydrotestosterone (DHT). By inhibiting this conversion, finasteride reduces DHT levels in serum and prostate tissue, thereby decreasing the androgenic stimulation that contributes to prostatic hyperplasia and hair loss.

Pharmacodynamics

Finasteride is characterized as an antiandrogenic compound that effectively suppresses serum and intraprostatic DHT production. The maximum reduction in serum DHT levels occurs approximately 8 hours post-administration of a single dose. In clinical studies, finasteride has shown to reduce serum DHT concentrations by about 70% and increase testosterone levels by 10-20%. It significantly lowers DHT content in the prostate, with an approximate reduction of 91.4% observed in treated individuals, although it does not reduce DHT to castrate levels.

Pharmacokinetics

Finasteride is well absorbed after oral administration, with peak concentrations occurring about 1-2 hours post-dose. It has a half-life of approximately 5-6 hours in healthy individuals and is primarily metabolized in the liver via the cytochrome P450 system. The drug's elimination is primarily through urine, with about 39% of the dose excreted unchanged. DHT levels return to baseline within approximately 14 days after discontinuation of finasteride.

Contra-indications

• Hypersensitivity to finasteride or any component of the formulation
• Pregnancy or potential for pregnancy in women

Adverse effects

• Decreased libido
• Erectile dysfunction
• Ejaculation disorders
• Gynecomastia
• Depression
• Suicidal thoughts

Interactions

• May interact with other medications that are metabolized by the liver
• Caution is advised when used with other antiandrogens

Precautions

• Patients should be monitored for signs of depression
• Caution in patients with hepatic impairment
• Not recommended for use in women of childbearing potential

Pregnancy

Finasteride is contraindicated in pregnancy due to potential teratogenic effects on a male fetus.

Breast-feeding

It is not recommended for use in breastfeeding women due to potential risks to the infant.

Storage

Store below 30°C in a dry place, protect from light.

Formulations

• Finasteride 1 mg tablets
• Finasteride 5 mg tablets
• Finasteride oral suspension (special order)

Mechanism of action

Finasteride acts as a competitive and specific inhibitor of Type II 5α-reductase, a nuclear-bound steroid intracellular enzyme primarily located in the prostatic stromal cell that converts the androgen testosterone into the more active metabolite, 5α-dihydrotestosterone (DHT). DHT is considered to be the primary androgen playing a role in the development and enlargement of the prostate gland. It serves as the hormonal mediator for the hyperplasia upon accumulation within the prostate gland. DHT displays a higher affinity towards androgen receptors in the prostate gland compared to testosterone and by acting on the androgen receptors, DHT modulates genes that are responsible for cell proliferation. Responsible for the production of DHT together with type I 5α-reductase, the type II 5α-reductase isozyme is primarily found in the prostate, seminal vesicles, epididymides, and hair follicles as well as liver. Although finasteride is 100-fold more selective for type II 5α-reductase than for the type I isoenzyme, chronic treatment with this drug may have some effect on type I 5α-reductase, which is predominantly expressed in sebaceous glands of most regions of skin, including the scalp, and liver. It is proposed that the type I 5α-reductase and type II 5α-reductase is responsible for the production of one-third and two-thirds of circulating DHT, respectively. The mechanism of action of Finasteride is based on its preferential inhibition of Type II 5α-reductase through the formation of a stable complex with the enzyme _in vitro_ and _in vivo_. Finasteride works selectively, where it preferentially displays a 100-fold selectivity for the human Type II 5α-reductase over type I enzyme. Inhibition of Type II 5α-reductase blocks the peripheral conversion of testosterone to DHT, resulting in significant decreases in serum and tissue DHT concentrations, minimal to moderate increase in serum testosterone concentrations, and substantial increases in prostatic testosterone concentrations. As DHT appears to be the principal androgen responsible for stimulation of prostatic growth, a decrease in DHT concentrations will result in a decrease in prostatic volume (approximately 20-30% after 6-24 months of continued therapy). It is suggested that increased levels of DHT can lead to potentiated transcription of prostaglandin D2, which promotes the proliferation of prostate cancer cells. In men with androgenic alopecia, the mechanism of action has not been fully determined, but finasteride has shown to decrease scalp DHT concentration to the levels found in the hairy scalp, reduce serum DHT, increase hair regrowth, and slow hair loss. Another study suggests that finasteride may work to reduce bleeding of prostatic origin by inhibiting vascular endothelial growth factor (VEGF) in the prostate, leading to atrophy and programmed cell death. This may bestow the drug therapeutic benefits in patients idiopathic prostatic bleeding, bleeding during anticoagulation, or bleeding after instrumentation.

Pharmacodynamics

Finasteride is an antiandrogenic compound that works by suppressing the production of serum and intraprostatic dihydrotestosterone (DHT) in men via inhibiting the enzyme responsible for the biosynthesis of DHT. The maximum effect of a rapid reduction in serum DHT concentration is expected to be observed 8 hours following administration of the first dose. In a single man receiving a single oral dose of 5 mg finasteride for up to 4 years, there was a reduction in the serum DHT concentrations by approximately 70% and the median circulating level of testosterone increased by approximately 10-20% within the physiologic range. In a double-blind, placebo-controlled study, finasteride reduced intraprostatic DHT level by 91.4% but finasteride is not expected to decrease the DHT levels to castrate levels since circulating testosterone is also converted to DHT by the type 1 isoenzyme expressed in other tissues. It is expected that DHT levels return to normal within 14 days upon discontinuation of the drug. In a study of male patients with benign prostatic hyperplasia prior to prostatectomy, the treatment with finasteride resulted in an approximate 80% lower DHT content was measured in prostatic tissue removed at surgery compared to placebo. While finasteride reduces the size of the prostate gland by 20%, this may not correlate well with improvement in symptoms. The effects of finasteride are reported to be more pronounced in male patients with enlarged prostates (>25 mL) who are at the greatest risk of disease progression. In phase III clinical studies, oral administration of finasteride in male patients with male pattern hair loss promoted hair growth and prevented further hair loss by 66% and 83% of the subjects, respectively, which lasted during two years' treatment. The incidences of these effects in treatment groups were significantly higher than that of the group receiving a placebo. Following finasteride administration, the levels of DHT in the scalp skin was shown to be reduced by more than 60%, indicating that the DHT found in scalp is derived from both local DHT production and circulating DHT. The effect of finasteride on scalp DHT is likely seen because of its effect on both local follicular DHT levels as well as serum DHT levels.. There is evidence from early clinical observations and controlled studies that finasteride may reduce bleeding of prostatic origin.