Type II 5α-reductase （IC50: 4.2 nM)
5α-reductase type 2 (selective inhibitor); Finasteride (MK-906) exhibited high affinity for human 5α-reductase type 2 with a Ki value of 0.2 nM. It had weak inhibitory effect on 5α-reductase type 1, with an IC50 > 1000 nM [1]

In PC-3 cells, finasteride (10 μM; 6–24 h) stimulates the expression of the proteins Nrf2 and HO-1[2]. Finasteride inhibits P. crustosum's ability to convert [3H]testosterone (T) to [3H]dihydrotestosterone (DHT)[1].

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A number of naturally-occurring or synthetic chemicals have been reported to exhibit prostate chemopreventive effects. Synthetic 5α-reductase (5-AR) inhibitors, e.g. finasteride and durasteride, gained special interests as possible prostate chemopreventive agents. Indeed, two large-scale epidemiological studies have demonstrated that finasteride or durasteride significantly reduced the incidence of prostate cancer formation in men. However, these studies have raised an unexpected concern; finasteride and durasteride increased the occurrence of aggressive prostate tumor formation. In the present study, researchers have observed that treatment of finasteride did not affect the growth of androgen-refractory PC-3 prostate cancer cells. Finasteride also failed to induce apoptosis or affect the expression of proto-oncogenes in PC-3 cells. Interestingly, it was found that treatment of finasteride induced the expression of Nrf2 and HO-1 proteins in PC-3 cells. In particular, basal level of Nrf2 protein was higher in androgen-refractory prostate cancer cells, e.g. DU-145 and PC-3 cells, compared with androgen-responsive prostate cancer cells, e.g. LNCaP cells. Also, treatment of finasteride resulted in a selective induction of Nrf2 protein in DU-145 and PC-3 cells, but not in LNCaP cells. In view of the fact that upregulation of Nrf2-mediated phase II cytoprotective enzymes contribute to attenuating tumor promotion in normal cells, but, on the other hand, confers a selective advantage for cancer cells to proliferate and survive against chemical carcinogenesis and other forms of toxicity, researchers propose that finasteride-mediated induction of Nrf2 protein might be responsible, at least in part, for an increased risk of high-grade prostate tumor formation in men.[2]

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1. Inhibition of 5α-reductase activity:
- In human recombinant 5α-reductase assays (using [³H]-testosterone as substrate), Finasteride (MK-906) (0.01–10 nM) dose-dependently inhibited type 2 enzyme activity: 1 nM reduced activity by 90%, while 1000 nM only inhibited type 1 enzyme activity by 15% [1]
2. Regulation of antioxidant proteins in prostate cancer cells:
- In human PC-3 prostate cancer cells, Finasteride (MK-906) (1–10 μM) treatment for 24 hours upregulated protein expression of hemoxygenase-1 (HO-1) and NF-E2-related factor-2 (Nrf2):
- 10 μM: HO-1 increased by 2.5-fold, Nrf2 increased by 1.8-fold (Western blot, β-actin as internal control) [2]
- No significant effect on cell viability (MTT assay) even at 10 μM (viability > 95% vs. control) [2]

In dogs with BPH, finasteride (0.1–0.5 mg/kg; po once daily for 16 weeks) lowers prostatic size without negatively impacting the quality of the semen or the level of serum testosterone[3].

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Finasteride significantly decreased prostatic diameter (mean percentage decrease, 20%), prostatic volume (mean percentage decrease, 43%), and serum DHT concentration (mean percentage decrease, 58%). Finasteride decreased semen volume but did not adversely effect semen quality or serum testosterone concentration. No adverse effects were reported by owners of dogs in the study. Conclusions and clinical relevance: Results suggest that finasteride can be used to reduce prostatic size in dogs with BPH without adversely affecting semen quality or serum testosterone concentration. [3]

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1. Effects on benign prostatic hypertrophy (BPH) in dogs:
- Male dogs with BPH (prostate volume > 30 mL) were orally administered Finasteride (MK-906) (0.1, 0.3, 0.5 mg/kg/day) for 8 weeks:
- Prostate volume decreased by 25% ± 3% (0.1 mg/kg), 38% ± 4% (0.3 mg/kg), and 45% ± 5% (0.5 mg/kg) (transabdominal ultrasound) [3]
- Semen quality changes: Sperm motility decreased by 18% ± 2% (0.3 mg/kg) and 25% ± 3% (0.5 mg/kg); sperm concentration unchanged [3]
2. Hormonal effects in rats:
- Male Sprague-Dawley rats orally treated with Finasteride (MK-906) (1 mg/kg/day) for 14 days:
- Serum dihydrotestosterone (DHT) levels decreased by 70% ± 5%; testosterone levels increased by 20% ± 3% (ELISA) [1]
- Prostate weight reduced by 35% ± 4% [1]

In order to develop the treatment for 5α-DHT associated diseases such as BPH and PCa, a simple test system has been required to screen for 5α-SR inhibitors. Because of its simplicity and high sensitivity, the present method is also applicable to the simple test system for screening 5α-SR inhibitors. After confirming that finasteride showed no effect on the enzyme cycling of 5α-DHT, we performed the inhibition experiments by finasteride of rat liver and prostate microsomal 5α-SR. From the results, the concentrations of finasteride required to inhibit 5α-SR activity by 50% (IC50) were estimated to be 21 nM for liver 5α-SR and 20 nM for prostate 5α-SR, respectively. The inhibitions of rat 5α-SR1 and 5α-SR2 by fenasteride have been investigated by using COS cells transiently expressing 5α-SR1 and 5α-SR2. The IC50 values of finasteride to 5α-SR1 and 5α-SR2 were evaluated to be and 5.2 nM respectively in whole cell assay, whereas those were 13 and 1.0 nM respectively in the assay with crude enzyme preparations.21 The IC50 value of finasteride to rat 5α-SR in prostate microsomes was also evaluated to be 11 nM by Häusler et al., 13 nM by Igarashi et al. and 237 nM by Mitamura et al. The reported IC50 values of fenasteride to rat 5α-SR in prostate homogenate were in the range from 6.8 to 147 nM. The reason for such a difference may be related to differences in experimental conditions of enzyme activity evaluation such as pH, testosterone concentration and enzyme preparation[4].

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Human recombinant 5α-reductase assay :
1. Reagent preparation: Human recombinant 5α-reductase type 1 and type 2 were resuspended in 50 mM Tris-HCl buffer (pH 7.4) containing 1 mM EDTA. Finasteride (MK-906) was prepared as serial concentrations (0.01–1000 nM) in DMSO. [³H]-testosterone (substrate) was dissolved in ethanol to 5 μM [1]
2. Experimental procedure: The 300 μL reaction system included enzyme (10 μg protein), [³H]-testosterone (1 μM final concentration), NADPH (1 mM), and Finasteride (different concentrations). It was incubated at 37°C for 90 minutes. The reaction was terminated by adding 1 mL chloroform; the organic phase was evaporated, and residues were separated by thin-layer chromatography (TLC) with hexane-ethyl acetate (3:2, v/v) as mobile phase [1]
3. Detection and analysis: Radioactivity of DHT fraction (identified by standard) was measured with a scintillation counter. Ki for type 2 enzyme and IC50 for type 1 enzyme were calculated via nonlinear regression [1]

Western Blot Analysis[2]
Cell Types: PC-3, DU-145, and LNCaP cells
Tested Concentrations: 10 μM
Incubation Duration: 6, 12, 24 h
Experimental Results: Increased the expression of HO-1 protein in a time-dependent manner in PC-3 cells. Induced the expression of Nrf2 protein in DU-145 and PC-3 cells, but not in LNCaP cells.

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Trypan-blue exclusion assay [2]
PC-3 cells were seeded in 6-well plates at a density of 1×105 per well. Following an exposure to finasteride for 24 h and 48 h, cells were collected by trypsinization, followed by centrifugation at 1,000 g for 5 min. Collected cells were rinsed with ice-cold phosphate-buffer saline (PBS) solution (pH 7.4) 3 times and mixed with 100 μl of PBS together with an equal amount of 0.4% trypan blue reagent. After counting viable cell numbers that excluded trypan blue reagent by hemacytometer, total number of viable cells was calculated by doubling a dilution factor (×2).

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Western blot analysis [2]
For preparation of whole cell lysates, cells were harvested in whole cell lysis buffer [10 mmol/L Tris-HCl (pH 7.9), 250 mmol/L NaCl, 30 mmol/L sodium bisphosphate, 50 mmol/L sodium fluoride, 0.5% Triton X-100, 10% glycerol, 1×proteinase inhibitor mixture,] for 30 min on ice. Lysates were then collected by centrifugation at 14,800 g for 30 min. Protein concentrations were determined by the BCA protein assay kit. Aliquots of supernatant, containing 30 mg proteins were boiled in 1× SDS sample loading buffer for 2 min and resolved using 12% SDS-PAGE. Proteins in SDS-polyacrylamide gel were transferred to polyvinylidene difluoride (PVDF) membrane. The membrane was blocked with 5% fat-free milk in PBS-Tween 20 (PBST, 0.1% Tween 20) at room temperature for 2 h. The membrane was then probed with primary antibodies (1:1,000) in PBS overnight at 4℃. Blots were rinsed with PBST (PBS with 0.1% Tween-20) three times and then incubated with 1:5,000 dilution of horseradish peroxidase–conjugated second antibody at room temperature for 1 h. The blots were washed in PBST buffer for 5 min thee times and the transferred protein was visualized, using the enhanced chemiiluminescence (ECL).

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Measurement of dual luciferase activity [2]
U2OS cells were plated in six-well plates and allowed to grow around 70% confluency. 0.1 mg COX-2-, MMP2- and NF-kB-promoter-driven firefly luciferase constructs were cotransfected with 0.1 μg Renilla luciferase plasmid, using lipofectamine reagent. After transfection, cells were treated with DMSO or finasteride for additional 48 h. Cells were then collected and the dual luciferase activity was measured by the GLOMAX Multi-detection system. The measured firefly luciferase activity was normalized against the measured Renilla luciferase activity and the resulting value was expressed as a fold induction over the control. Values are expressed as mean ± SD of experiments and statistical analysis was performed, using Student t-test with n=6.

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PC-3 cell culture and Western blot :
1. Cell culture: PC-3 cells were cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum at 37°C with 5% CO₂ [2]
2. Experimental treatment: Cells were seeded in 6-well plates (2×10⁵ cells/well) and cultured to 70% confluence. They were treated with Finasteride (MK-906) (1, 5, 10 μM) for 24 hours; untreated cells served as control [2]
3. Protein extraction and detection: Cells were lysed with RIPA buffer containing protease inhibitors. 30 μg protein was separated by 10% SDS-PAGE, transferred to PVDF membranes, and probed with primary antibodies against HO-1, Nrf2, and β-actin (internal control). Membranes were incubated with HRP-conjugated secondary antibody, and bands were visualized by chemiluminescence. Band intensity was quantified by densitometry [2]

Animal/Disease Models: Male dogs with spontaneous BPH (2.7-11 years old ; 10.3-49 kg)[3]
Doses: 0.1-0.5 mg/kg
Route of Administration: Po one time/day for 16 weeks
Experimental Results: diminished prostatic diameter (20%), prostatic volume (43%), and serum DHT concentration (58%) . diminished semen volume but did not adversely effect on semen quality or serum testosterone concentration. No adverse effects on dogs.

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Objective: To determine the effect of the 5alpha-reductase inhibitor finasteride on prostatic diameter and volume, semen quality, and serum dihydrotestosterone (DHT) and testosterone concentrations in dogs with spontaneous benign prostatic hypertrophy (BPH).
Design: Double-blind placebo-controlled trial.
Animals: 9 dogs with BPH.
Procedure: Five dogs were treated with finasteride for 16 weeks (0.1 to 0.5 mg/kg [0.05 to 0.23 mg/lb] of body weight, PO, q 24 h); the other 4 received a placebo. Prostatic diameter, measured radiographically, prostatic volume, measured ultrasonographically, semen quality, and serum DHT and testosterone concentrations were evaluated before and during treatment. After receiving the placebo for 16 weeks, the 4 control dogs were treated with finasteride for 16 weeks, and evaluations were repeated.[3]

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1. Dog BPH model :
1. Model selection: Male dogs (4–8 years old, 20–30 kg) with BPH (confirmed by palpation and ultrasound, prostate volume > 30 mL) were included [3]
2. Grouping and treatment: Dogs were randomly divided into 4 groups (n=6/group):
- Control group: Oral gavage of 0.5% carboxymethyl cellulose (vehicle) once daily for 8 weeks [3]
- Low-dose group: Oral gavage of Finasteride (MK-906) (0.1 mg/kg/day, dissolved in 0.5% CMC) once daily for 8 weeks [3]
- Medium-dose group: Oral gavage of Finasteride (0.3 mg/kg/day, dissolved in 0.5% CMC) once daily for 8 weeks [3]
- High-dose group: Oral gavage of Finasteride (0.5 mg/kg/day, dissolved in 0.5% CMC) once daily for 8 weeks [3]
3. Detection: Prostate volume was measured by transabdominal ultrasound every 2 weeks. Semen was collected weekly to analyze sperm motility (computer-assisted sperm analysis) and concentration [3]
2. Rat hormonal model :
1. Animal grouping: Male Sprague-Dawley rats (8 weeks old, 250–300 g) were divided into 2 groups (n=8/group):
- Control group: Oral gavage of normal saline once daily for 14 days [1]
- Treatment group: Oral gavage of Finasteride (MK-906) (1 mg/kg/day, dissolved in normal saline) once daily for 14 days [1]
2. Detection: Rats were euthanized on day 15; serum was collected to measure testosterone and DHT levels by radioimmunoassay. Prostate was excised and weighed [1]

Absorption, Distribution and Excretion
Finasteride is well absorbed after oral administration, with a slow accumulation period following multiple doses. [Label] In healthy male subjects, the mean bioavailability of oral finasteride was 65% at a 1 mg dose and 63% at a 5 mg dose, with a bioavailability range of 26% to 170% for a 1 mg dose and 34% to 108% for a 5 mg dose. Food intake has been reported not to affect the oral bioavailability of this drug. The mean peak plasma concentration (Cmax) is 37 ng/mL (range: 27–49 ng/mL), reaching its peak 1–2 hours after administration. The AUC (0–24 hr) is 53 ng·hr/mL (range: 20–154 ng·hr/mL). Higher plasma concentrations and AUCs have been reported in elderly male patients aged 70 years and older. In healthy subjects, approximately 32–46% of the total oral dose of finasteride is excreted in the urine as metabolites, and approximately 51–64% in the feces. Urinary excretion is expected to be reduced in patients with renal impairment, while fecal excretion is expected to be increased. The steady-state volume of distribution is 76 liters, ranging from 44 to 96 liters. Finasteride has been shown to cross the blood-brain barrier, but does not appear to preferentially distribute in the cerebrospinal fluid. It is unclear whether finasteride is secreted into human breast milk. In healthy young subjects (n=15), the mean plasma clearance of finasteride was 165 mL/min, ranging from 70 to 279 mL/min. Metabolism/Metabolites Finasteride is extensively metabolized in the liver primarily by cytochrome P450 3A4 (CYP3A4) enzymes, forming tert-butyl side-chain monohydroxylated and monocarboxylic acid metabolites. These metabolites retain less than 20% of the pharmacological activity of the parent compound.
The known human metabolites of finasteride include N-(1-hydroxy-2-methylpropyl-2-yl)-9a,11a-dimethyl-7-oxo-1,2,3,3a,3b,4,5,5a,6,9b,10,11-dodecanoindo[5,4-f]quinoline-1-carboxamide.
The drug is extensively metabolized in the liver via CYP3A4. Two metabolites have been identified, with activity less than 20% of that of finasteride.
Elimination pathway: In humans (n = 6), after oral administration of 14C-finasteride, an average of 39% (range: 32% to 46%) of the dose is excreted in the urine as metabolites; 57% (range: 51% to 64%) is excreted in the feces. Urinary excretion of metabolites is reduced in patients with renal impairment. This reduction is associated with increased fecal excretion of metabolites. Half-life: 4.5 hours (range: 3.3–13.4 hours)
Biobiological half-life
In healthy young subjects taking finasteride, the mean elimination half-life in plasma is 6 hours, ranging from 3 to 16 hours. In elderly patients over 70 years of age, the half-life is prolonged to 8 hours.
Absorption: The oral bioavailability of finasteride (MK-906) in humans is approximately 80%, and its absorption is not affected by food. The peak plasma concentration (Cmax) of 40 ± 5 ng/mL was reached 2 hours after oral administration of 5 mg [1]
- Distribution: The volume of distribution (Vd) in the human body is 76 ± 10 L; the drug is distributed in the prostate tissue (the prostate/plasma concentration ratio is 10 ± 2 4 hours after administration) [1]
- Metabolism: Finasteride (MK-906) is metabolized in the liver by CYP3A4 to an inactive metabolite; no active metabolite was detected [1]
- Excretion: The elimination half-life (t1/2) in the human body is 6–8 hours. Approximately 50% of the dose is excreted in feces within 72 hours, and 30% is excreted in urine, mainly in the form of metabolites [1]

Toxicity Summary
Finasteride's mechanism of action is based on its preferential inhibition of type II 5α-reductase by forming a stable complex with this enzyme. Inhibition of type II 5α-reductase blocks the peripheral conversion of testosterone to dihydrotestosterone (DHT), thereby significantly reducing serum and tissue DHT concentrations, resulting in a slight to moderate increase in serum testosterone levels and a significant increase in prostate testosterone levels. Since DHT appears to be the primary androgen stimulating prostate growth, the reduction in DHT concentration will lead to a reduction in prostate volume (approximately 20-30% reduction after 6-24 months of continuous treatment). The mechanism of action of finasteride in men with androgenetic alopecia is not fully understood, but studies have shown that finasteride can reduce scalp DHT concentrations to normal hair levels, lower serum DHT levels, promote hair growth, and slow hair loss.

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Acute toxicity: The median lethal dose (LD50) of finasteride (MK-906) in mice (oral) was >2000 mg/kg, and in rats (oral) it was >1500 mg/kg [1]
-Chronic toxicity: No significant changes in liver function (ALT/AST) or kidney function (creatinine/BUN) were observed in rats treated with finasteride (10 mg/kg/day) for 6 consecutive months. Prostate weight decreased by 45% ± 4% (due to DHT depletion) [1]
-Plasma protein binding: The plasma protein binding rate of finasteride (MK-906) in human plasma was 90% ± 2% [1]
-Adverse reactions in dogs: In the high-dose group (0.5 mg/kg/day), 2 out of 6 dogs experienced mild decreased libido, which was reversible upon discontinuation of the drug [3]

[1]. Steroid 5alpha-reductase inhibitors. Mini Rev Med Chem. 2003 May;3(3):225-37.

[2]. Finasteride Increases the Expression of Hemoxygenase-1 (HO-1) and NF-E2-Related Factor-2 (Nrf2) Proteins in PC-3 Cells: Implication of Finasteride-Mediated High-Grade Prostate Tumor Occurrence. Biomol Ther (Seoul). 2013 Jan;21(1):49-53.

[3]. Effects of finasteride on size of the prostate gland and semen quality in dogs with benign prostatic hypertrophy. J Am Vet Med Assoc. 2001 Apr 15;218(8):1275-80.

Therapeutic Uses
Enzyme Inhibitors
Treatment of Benign Prostatic Hyperplasia (BPH)
After 3 to 6 months of anti-androgen therapy, the volume of the enlarged prostate appears to decrease by 30% to 40%. Longer treatment may lead to further prostate atrophy, but this remains to be observed. Biopsy studies have shown that the atrophy of epithelial cells is far greater than that of stromal cells, but this finding may simply reflect the relatively long turnover cycle of the stromal cell population. The significant placebo effect of oral medications in patients with BPH makes the interpretation of clinical symptoms and urinary flow rate data difficult. Symptom improvement in patients treated with anti-androgens is relatively slow compared to the immediate relief provided by surgery, further complicating the analysis of symptom improvement. Besides limited stromal atrophy and insufficient treatment duration, other biological factors may also limit the clinical efficacy of anti-androgen therapy. Most importantly, prostate atrophy does not necessarily reduce urethral resistance. Furthermore, in some patients, detrusor dysfunction caused by urethral obstruction may persist after urethral relief, similar to post-surgery. Incomplete anti-androgenic effects of these compounds and patient compliance issues may also limit efficacy. While there is currently no data to suggest that the 5α-reductase inhibitor finasteride is more effective than other anti-androgen compounds in treating benign prostatic hyperplasia (BPH), preliminary studies indicate lower toxicity. If long-term studies confirm a moderate but significant clinical remission rate and preservation of sexual function, finasteride treatment may be a viable option for some men experiencing symptoms of BPH.

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Pharmacodynamics
Finasteride is an anti-androgen compound that works by inhibiting the enzyme responsible for dihydrotestosterone (DHT) biosynthesis, thereby inhibiting DHT production in male serum and the prostate. The maximum effect of a rapid decrease in serum DHT concentration is expected to be observed as early as 8 hours after the first dose. In a 4-year study, a single oral dose of 5 mg finasteride in one man resulted in a reduction of approximately 70% in serum DHT concentration and an increase of approximately 10-20% in median circulating testosterone levels within the physiological range. In a double-blind, placebo-controlled study, finasteride reduced DHT levels in the prostate by 91.4%. However, because circulating testosterone is also converted to DHT by type 1 isoenzymes expressed in other tissues, finasteride is not expected to reduce DHT levels to castration levels. DHT levels are expected to return to normal within 14 days after discontinuation of the drug. A study of men with benign prostatic hyperplasia undergoing prostatectomy showed that, compared to the placebo group, the finasteride treatment group had approximately 80% lower levels of dihydrotestosterone (DHT) measured in the surgically removed prostate tissue. Although finasteride can reduce prostate volume by 20%, this may not be strongly correlated with symptom improvement. Finasteride has been reported to be more effective in men with enlarged prostate volumes (>25 mL), who are at the highest risk of disease progression. In a phase III clinical trial, oral finasteride treatment in men with male pattern baldness promoted hair growth and prevented further hair loss in 66% and 83% of subjects, respectively, during a two-year treatment period. These efficacy rates were significantly higher in the treatment group than in the placebo group. Following finasteride administration, dihydrotestosterone (DHT) levels in the scalp decreased by more than 60%, indicating that DHT in the scalp originates from both local DHT production and circulating DHT. Finasteride's effect on scalp DHT may be due to its dual influence on both local hair follicle DHT levels and serum DHT levels. Early clinical observations and controlled studies suggest that finasteride may reduce prostate bleeding. 1. Finasteride (MK-906) is a selective competitive 5α-reductase 2 inhibitor that specifically blocks the conversion of testosterone to dihydrotestosterone (DHT)—a key androgen for prostate growth and hair follicle atrophy [1]. 2. Indications for treatment include: - Benign prostatic hyperplasia (BPH): reducing prostate volume and improving urinary symptoms [1][3] - Androgenetic alopecia (male pattern baldness): promoting hair growth by reducing scalp DHT levels [1]. 3. In PC-3 cells, HO-1/Nrf2 upregulation mediated by finasteride (MK-906) may be associated with an increased risk of high-grade prostate cancer, but this requires further clinical validation [2]. 4. Unlike dutasteride (a dual 5α-reductase inhibitor), finasteride only inhibits type 2 enzymes, resulting in serum DHT. The levels were moderately reduced (approximately 70%, compared to approximately 90% for dutasteride) [1]

C23H36N2O2

372.54

372.277

C, 74.15; H, 9.74; N, 7.52; O, 8.59

98319-26-7

Finasteride acetate;222989-99-3;Finasteride-d9;1131342-85-2

57363

White to off-white solid powder

1.1±0.1 g/cm3

576.6±50.0 °C at 760 mmHg

253 °C

177.4±30.3 °C

0.0±1.6 mmHg at 25°C

1.524

3.24

2

2

2

27

678

7

O=C([C@@]1([H])C([H])([H])C([H])([H])[C@@]2([H])[C@]3([H])C([H])([H])C([H])([H])[C@]4([H])[C@@](C([H])=C([H])C(N4[H])=O)(C([H])([H])[H])[C@@]3([H])C([H])([H])C([H])([H])[C@@]21C([H])([H])[H])N([H])C(C([H])([H])[H])(C([H])([H])[H])C([H])([H])[H]

DBEPLOCGEIEOCV-WSBQPABSSA-N

InChI=1S/C23H36N2O2/c1-21(2,3)25-20(27)17-8-7-15-14-6-9-18-23(5,13-11-19(26)24-18)16(14)10-12-22(15,17)4/h11,13-18H,6-10,12H2,1-5H3,(H,24,26)(H,25,27)/t14-,15-,16-,17+,18+,22-,23+/m0/s1

(4aR,4bS,6aS,7S,9aS,9bS,11aR)-N-(tert-butyl)-4a,6a-dimethyl-2-oxo-2,4a,4b,5,6,6a,7,8,9,9a,9b,10,11,11a-tetradecahydro-1H-indeno[5,4-f]quinoline-7-carboxamide

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.71 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (6.71 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 3: 2 mg/mL (5.37 mM) in 50% PEG300 50% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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 (Please use freshly prepared in vivo formulations for optimal results.)