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Old 02-13-2021, 03:36 PM   #1
liftsiron
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Finasteride/Propecia/Proscar

5-alpha reductase inhibitor
Used for symptomatic treatment of BPH and male pattern baldness (i.e., androgenetic alopecia)
May decrease risk of low-grade prostate cancer; but, may increase risk of more serious high-grade prostate cancer
COMMON BRAND NAMES

Propecia, Proscar
HOW SUPPLIED

Finasteride/Propecia/Proscar Oral Tab: 1mg, 5mg
DOSAGE & INDICATIONS
For the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to improve symptoms, to reduce the risk of acute urinary retention, and to reduce the risk of the need for surgery including transurethral resection of the prostate (TURP) and prostatectomy.
Oral dosage (Proscar)
Adult males

5 mg PO once daily. A minimum of 6 months therapy may be necessary to assess response, with up to 12 months necessary in some patients. In a double-blind, randomized, placebo-controlled study, 3040 men with moderate to severe urinary symptoms and enlarged prostate were treated with finasteride 5 mg PO once daily or placebo for 4 years. Finasteride reduced BPH symptoms and prostate volume, increased the urinary flow rate, and reduced the probability of surgery and acute urinary retention. In a long-term, double-blind clinical trial of 3047 men with BPH, combination therapy of doxazosin (4—8 mg PO once daily) and finasteride (5 mg PO once daily) was shown to significantly reduce the risk of overall clinical progression of BPH than either drug alone. However, further study is required.
For the treatment of male pattern hair loss (i.e., androgenetic alopecia), in patients with mild to moderate hair loss of the vertex and anterior mid-scalp area.
Oral dosage(Propecia)
Adult males, including Geriatric males

1 mg PO once daily. Daily use for >= 3 months is necessary before benefit is observed. Continued use is recommended to sustain benefit. Withdrawal of treatment leads to reversal of effect within 12 months.
For the second-line treatment of hirsutism†.
Oral dosage
Adult, non-pregnant women

5 mg PO once daily either alone or in combination with oral contraceptives was shown to reduce hirsutism in women with mild hirsutism. Women with moderate to severe hirsutism either do not respond or only respond initially. Adverse effects from finasteride were minimal compared to other antiandrogens such as cyproterone, flutamide, and spironolactone.
For prostate cancer prophylaxis†.
Oral dosage
Adults

The risks of finasteride for prostate cancer prevention outweigh the benefits. In a 7-year placebo-controlled study, finasteride 5 mg PO once daily was shown to prevent or delay the development of prostate cancer in healthy men (>= 55 years of age) with a low risk of prostate cancer (PSA <= 3 ng/mL). Prostate specific antigen (PSA) levels, digital rectal exams, and biopsies were used to aid in the diagnosis of prostate cancer. Results showed that men receiving finasteride had a 26% decreased risk of being diagnosed with prostate cancer compared to placebo (p < 0.0001); however, the risk reduction was limited to Gleason score (GS) <= 6 cancers. There was an increased incidence of high-grade prostate cancer (GS 7—10) with finasteride compared to placebo (6.4% vs. 5.2%, respectively, p = 0.005). Finasteride was also associated with a higher incidence of sexual side effects versus placebo.

†Indicates off-label use
MAXIMUM DOSAGE
Adults

Males: 5 mg/day PO for benign prostatic hyperplasia (BPH); the manufacturer literature states that patients have received up to 80 mg/day PO for three months without adverse effects; however, it is not clear if the dose was used therapeutically or provided additional benefit over the usual dose range. Maximum dose-response is 1 mg/day PO for alopecia.
Elderly

Males: 5 mg/day PO for benign prostatic hyperplasia (BPH); the manufacturer literature states that patients have received up to 80 mg/day PO for three months without adverse effects; however, it is not clear if the dose was used therapeutically or provided additional benefit over the usual dose range. Maximum dose-response is 1 mg/day PO for alopecia.
Adolescents

Not indicated.
Children

Not indicated.
DOSING CONSIDERATIONS
Hepatic Impairment

Finasteride should be initiated with caution in patients with hepatic disease. Since finasteride is metabolized extensively in the liver, reduced metabolism is possible. The effect of hepatic impairment on finasteride pharmacokinetics has not been studied.
Renal Impairment

Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.
ADMINISTRATION
Oral Administration

Finasteride may be administered without regard to meals.
Women who are pregnant or may get pregnant must not handle/administer broken or crushed finasteride tablets; the active ingredient could harm the unborn baby. Exposure to whole tablets is not expected to cause harm as long as they are not swallowed.
STORAGE

Propecia:
- Protect from moisture
- Store at controlled room temperature (between 68 and 77 degrees F)
Proscar:
- Protect from light
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
CONTRAINDICATIONS / PRECAUTIONS
Females, pregnancy

Finasteride is not FDA-approved for use in females of childbearing potential and is contraindicated during pregnancy. Finasteride may cause fetal harm. Finasteride and other 5-alpha-reductase inhibitors, by inhibiting the conversion of testosterone to DHT, have the ability to cause abnormalities in the external genitalia of the male fetus. Pregnant women or females trying to conceive should not handle crushed or broken finasteride tablets. The distribution of finasteride into human semen has been assessed and appears to be well below the threshold concentration associated with fetal anomalies in animals.
Breast-feeding

Finasteride is not FDA-approved for use in females of childbearing potential and is recommended to be avoided during breast-feeding. It is not known whether finasteride is excreted in human milk. Therefore, the effects of finasteride on breast-feeding or a nursing infant cannot be determined.
Children, infants

Finasteride is not indicated for use in adolescents, children, or infants. Safety and effectiveness have not been established in pediatric patients under 18 years of age.
Hepatic disease

Finasteride should be used with caution in patients with hepatic disease, since finasteride is metabolized extensively in the liver. Data are lacking regarding the incidence of adverse effects or drug accumulation in patients with hepatic impairment.
Prostate cancer, urinary tract obstruction

Finasteride reduces total serum prostate specific antigen (PSA). In a typical patient undergoing treatment for BPH with finasteride (>= 6 months), a 50% decrease in serum PSA concentrations can be expected; however, individual patients may experience varying decreases in PSA values. During treatment, serum PSA concentrations may decrease even in the presence of prostate cancer. If clinicians use serum PSA concentrations as an aid in the detection of prostate cancer in men receiving finasteride, values should be doubled for comparison with normal ranges in untreated men. Any increase from baseline, even if the value is within the normal range for untreated men, may signal the presence of prostate cancer. If clinicians elect to use percent free PSA (free to total PSA ratio) as a marker, no adjustment in PSA values appear to be necessary as the value is not significantly decreased by finasteride. In June 2011, a review of two large, randomized controlled trials, the Prostate Cancer Prevention Trial (PCPT) and the Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial prompted the FDA to alert healthcare professionals of the potential risk of an increased incidence of high-grade prostate cancer in patients receiving finasteride or dutasteride treatment. Results from the PCPT trial showed that men receiving finasteride had a 26% decreased risk of being diagnosed with prostate cancer when compared to placebo (p < 0.0001); however, the risk reduction was limited to Gleason score (GS) <= 6 cancers. There was an increased incidence of GS 8—10 prostate cancers with finasteride compared to placebo (1.8% vs. 1.1%, respectively). Therefore, in initiating or continuing treatment with finasteride, clinicians should weigh the known benefits of treatment against the potential risk and be aware that finasteride may increase the risk of high-grade prostate cancer. Further, lower urinary tract symptoms of BPH can be indicative of other urological diseases, including prostate cancer. Patients should be assessed to rule out other urological diseases prior to treatment with finasteride. Patients with a large residual urinary volume and/or severely diminished urinary flow may not be good candidates for 5-alpha-reductase inhibitor therapy and should be carefully monitored for urinary tract obstruction.
Blood donation

Men treated with finasteride should refrain from blood donation while taking finasteride. The purpose of this is to prevent administration of finasteride to a pregnant female transfusion recipient.
Geriatric

Clinical efficacy studies of finasteride for hair loss did not include subjects aged 65 and over. Based on the pharmacokinetics of finasteride 5 mg, no dosage adjustment is necessary in the geriatric patient. However, the efficacy of finasteride for hair loss in the elderly has not been established.
Infertility

The clinical significance of finasteride’s effect on semen characteristics for an individual male patient’s fertility is not known; consider the potential effects on semen when assessing a male with infertility. Finasteride may cause spermatogenesis inhibition or oligospermia, decreased sperm motility, or decreased semen volume. In a 52-week, randomized, double-blind, placebo-controlled study in healthy men, finasteride (5 mg PO once daily) significantly decreased total sperm count (-34.3%) compared to baseline at 26 weeks but not at 52 weeks or at the 24-week follow-up. Semen volume was decreased at 52 weeks for finasteride (-14.5%), but the effect was not statistically significant. Sperm concentration was decreased by finasteride (-7.4%) but was not significant for either drug. Significant reductions of 6 to 12% in sperm motility were observed during treatment. Sperm morphology was not affected. One subject taking finasteride had decreases in sperm count of more than 90% of baseline values at 52 weeks; partial recovery was noted at the 24-week follow-up. During post marketing surveillance, male infertility and/or poor seminal quality following treatment discontinuation have been reported. It should be noted that normalization or improvement of seminal quality has also been reported after discontinuation of finasteride.
ADVERSE REACTIONS
Severe

angioedema / Rapid / Incidence not known
new primary malignancy / Delayed / Incidence not known
teratogenesis / Delayed / Incidence not known
Moderate

impotence (erectile dysfunction) / Delayed / Incidence not known
ejaculation dysfunction / Delayed / Incidence not known
depression / Delayed / Incidence not known
infertility / Delayed / Incidence not known
Mild

libido decrease / Delayed / 1.8-1.8
gynecomastia / Delayed / 10.0
breast enlargement / Delayed / 10.0
testicular pain / Early / Incidence not known
decreased ejaculate volume / Delayed / Incidence not known
pruritus / Rapid / Incidence not known
orgasm dysfunction / Delayed / Incidence not known
mastalgia / Delayed / Incidence not known
rash / Early / Incidence not known
urticaria / Rapid / Incidence not known
oligospermia / Delayed / Incidence not known
spermatogenesis inhibition / Delayed / Incidence not known
DRUG INTERACTIONS

Saw Palmetto, Serenoa repens: (Moderate) Saw palmetto may inhibit 5 alpha-reductase, preventing the conversion of testosterone to dihydrotestosterone. This action is similar to the action of 5-alpha reductase inhibitors, such as dutasteride and finasteride. Co-use is likely to be common by patients, but the effects of co-use are not known. In theory, the effects could be additive, but it is not known if the added effects would be beneficial or harmful. Clinicians should be alert for any unusual effects if patients ingest saw palmetto supplements while taking 5-alpha reductase inhibitors.
Terazosin: (Minor) Terazosin has been reported to increase peak concentrations of finasteride by 16% and AUC by 31% when the two agents are coadministered. The interaction is of minor importance.
PREGNANCY AND LACTATION
Pregnancy

Finasteride is not FDA-approved for use in females of childbearing potential and is contraindicated during pregnancy. Finasteride may cause fetal harm. Finasteride and other 5-alpha-reductase inhibitors, by inhibiting the conversion of testosterone to DHT, have the ability to cause abnormalities in the external genitalia of the male fetus. Pregnant women or females trying to conceive should not handle crushed or broken finasteride tablets. The distribution of finasteride into human semen has been assessed and appears to be well below the threshold concentration associated with fetal anomalies in animals.
MECHANISM OF ACTION

Finasteride is a synthetic 4-aza analog of testosterone that acts as a competitive, specific inhibitor of type II 5-alpha-reductase, an intracellular enzyme that converts testosterone to the potent androgen 5-alpha-dihydrotestosterone (DHT). The type II 5alpha-reductase isozyme is primarily found in prostate, seminal vesicles, epididymides, and hair follicles, as well as liver. The type II isozyme is responsible for two-thirds of circulating DHT. DHT is the primary androgen that stimulates the development of prostate tissue. When used for the treatment of benign prostatic hyperplasia, as the enzymatic conversion from testosterone to DHT is inhibited, a desirable reduction in prostate hypertrophy is achieved, and urine flow should be improved. In male pattern hair loss, the balding scalp contains miniaturized hair follicles and increased amounts of DHT compared with hairy scalp. Finasteride decreases scalp and serum DHT concentrations, thus interrupting a key factor in the development of androgenetic alopecia in those patients genetically predisposed. Finasteride does not appear to affect circulating concentrations of cortisol, estradiol, prolactin, thyroid-stimulating hormone, thyroxine or cholesterol. Research to date also suggests that finasteride does not affect the hypothalamic-pituitary-testicular-axis.
PHARMACOKINETICS

Finasteride is administered orally in the treatment of either BPH or male pattern baldness. Approximately 90% is bound to plasma proteins; yet the drug has been found to cross the blood-brain barrier. This is not problematic, since finasteride generally does not affect other hormones. Daily dosing causes accumulation to occur, with plasma concentrations increasing by 50% over those observed from a single dose. The mean plasma elimination half-life of finasteride is 4.8 to 6 hours (range, 3 to 16 hours); however, the turnover rate for the type II 5-alpha-reductase enzyme complex is slow, with a turnover half-life of approximately 30 days. After oral dosing, about half of the unchanged drug is excreted in the feces, and one-third is metabolized in the liver to the 17-carboxylic acid, which is then excreted in the urine (39%) and the feces (57%).

A single 5 mg oral dose rapidly reduces serum DHT concentrations by as much as 70%, with the maximum reduction occurring at about 8 hours. The effect lasts for at least 24 hours, so once daily dosing is appropriate. Actual clinical effects, however, are not realized for 3 to 6 months after beginning therapy.

Affected cytochrome P450(CYP450) isoenzymes and drug transporters: CYP3A4, UGT1A4
While finasteride is metabolized by hepatic CYP3A4 isoenzymes, no drug interactions of clinical importance have been identified, likely due to the hormonal mechanisms of action and relatively large therapeutic window of effect. Finasteride does not appear to affect the CYP450-linked drug metabolizing enzyme system. Compounds that have been tested in man have included antipyrine, digoxin, propranolol, theophylline, and warfarin and no clinically meaningful interactions were found. Finasteride has not been associated with clinically important drug interactions during clinical trials, including a 4-year safety trial of 3,040 males aged 45 to 78 years. while finasteride markedly inhibited UGT1A4 activity in vitro in a drug transporter study; the data strongly suggested that finasteride is unlikely to cause clinically significant drug-drug interactions mediated via inhibition of the hepatic UGT enzymes involved in drug metabolism in vivo.
Oral Route

The mean bioavailability following a single dose of finasteride is about 63—65%; however, bioavailability is highly variable.
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Old 02-15-2021, 09:41 AM   #2
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What's the latest finasteride FUD?
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Old 02-15-2021, 03:49 PM   #3
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Quote:
Originally Posted by 956Vette View Post
What's the latest finasteride FUD?
Here is an interesting post on that exact topic.
Posted byu/rancorfood
2 months ago
My thoughts on the FUD surrounding Finasteride
Finasteride/Dutasteride

Finasteride can raise endogenous testosterone levels by as much as 10%. This is documented and can increase mood as elevated test tends to do that for men, because biology. As far as I know, outside of some speculation of 5ar possibly preventing progesterone conversion to allopregnanolone in amounts significant enough for it to matter in regards to brain health, the mechanism for the rare side effect of brain fog from finasteride is still not definitively known and is only temporary. The other issue with this theory is that reduced allopregnanolone is inhibited by type II 5ar and fin only affects type I, so the jury is out on that. People who quit treatment prematurely (ie, a few months into a drug that requires at least 1 whole year to see desired results) never find that out though. People complain about "their dick falling off" and yet here I am 6 months in, still getting raging boners, no hair fall in the shower anymore, and complete mental clarity. I got noticeable, yet mild cognitive issues (mostly word recall and short term memory loss..caffeine and making sure I hit dietary macros and achieved overall balanced nutrition combat this) 2 months in and it subsided by the 5th month as my body acclimated to reduced DHT levels. This medication has been on the market for 20 years, with millions of men taking it. If the side effects were as disastrous as the vocal minority claim it to be, it would have been pulled years ago. Hell, Japan approved dutasteride for hair loss and that affects type I and II with 90% serum reduction. If the brain fog was really that bad duta would be chemically lobotomizing people left and right. Perhaps the brain fog from fin exaggerates preexisting malnutrition and that correlation has yet to be studied.
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Old 02-16-2021, 10:16 AM   #4
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Good stuff, thank you liftsiron!! Been using finasteride for mpb for 20 years without much drama. Dr. Crisler is the last doctor who sparked fear, uncertainty and doubt re: finasteride, unsure what his issue was.
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