PROPECIA
(finasteride)
Tablets, 1 mg
DESCRIPTION
Buy PROPECIA
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(Finasteride), a synthetic 4-azasteroid compound, is a specific inhibitor of steroid Type II
5α-reductase, an intracellular
enzyme that converts
the androgen testosterone into
5α-dihydrotestosterone (DHT).
Finasteride
is
4-azaandrost-1-ene-17-carboxamide,N-(1,1-dimethylethyl)-3-oxo-,(5α,17β)-.
The
empirical formula of finasteride is C23H34N2O3
and its molecular weight is 372.55. Its structural formula is:
Finasteride is a white crystalline powder with a melting point near 250°C. It is freely soluble in
chloroform and in lower alcohol solvents but is practically insoluble in water.
PROPECIA tablets for oral administration are film-coated tablets that contain 1 mg of finasteride and
the following inactive ingredients: lactose monohydrate, microcrystalline cellulose, pregelatinized starch,
sodium starch glycolate, hydroxypropyl methylcellulose, hydroxypropyl cellulose LF, titanium dioxide,
magnesium stearate, talc, docusate sodium, yellow ferric oxide, and red ferric oxide.
CLINICAL PHARMACOLOGY(BUY PROPECIA)
Finasteride is a competitive and specific inhibitor of Type II 5α-reductase, an intracellular enzyme that
converts the androgen testosterone into DHT. Two distinct isozymes are found in mice, rats, monkeys,
and humans: Type I and II. Each of these isozymes is differentially expressed in tissues and
developmental stages. In humans, Type I 5α-reductase is predominant in the sebaceous glands of most
regions of skin, including scalp, and liver. Type I 5α-reductase is responsible for approximately one-third
of circulating DHT. The Type II 5α-reductase isozyme is primarily found in prostate, seminal vesicles,
epididymides, and hair follicles as well as liver, and is responsible for two-thirds of circulating DHT.
In humans, the mechanism of action of finasteride is based on its preferential inhibition of the Type II
isozyme. Using native tissues (scalp and prostate), in vitro binding studies examining the potential of
finasteride to inhibit either isozyme revealed a 100-fold selectivity for the human Type II 5α-reductase over
Type I isozyme (IC
50
=500 and 4.2 nM for Type I and II, respectively). For both isozymes, the inhibition by
finasteride is accompanied by reduction of the inhibitor to dihydrofinasteride and adduct formation with
NADP+. The turnover for the enzyme complex is slow (t
1/2
approximately 30 days for the Type II enzyme
complex and 14 days for the Type I complex).
Finasteride has no affinity for the androgen receptor and has no androgenic, antiandrogenic,
estrogenic, antiestrogenic, or progestational effects. Inhibition of Type II 5α-reductase blocks the
peripheral conversion of testosterone to DHT, resulting in significant decreases in serum and tissue DHT
concentrations. Finasteride produces a rapid reduction in serum DHT concentration, reaching 65%.
