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Fig. 1 · Structure
Cat. No.
A10387
CAS No.
98319-26-7
Formula
C23H36N2O2
Mol. Weight
372.5

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Finasteride

Cat. No. A10387 CAS 98319-26-7
Finasteride is a synthetic type II 5α-reductase inhibitor. This enzyme converts testosterone to dihydrotestosterone (DHT).

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Publications for Finasteride

2 publications citing this product

  1. Reilly Taylor, .et al. , Front. Biosci. (Elite Ed), 2026, 18(1): 44075 PMID: 41914162
  2. Chen CC, .et al. , Anticancer Res, 2017, Dec;37(12):6893-6898 PMID: 29187470
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Biological Activity

Bioactivity / Mechanism

Finasteride acts at human steroid 5α-reductase 2 through an inhibitor-derived NADP–dihydrofinasteride adduct. A 2.8 Å crystal structure places this adduct in an enclosed transmembrane binding cavity. The observed covalent linkage joins the cofactor and inhibitor-derived moiety. [1]

Finasteride also inhibits purified human AKR1D1, a steroid 5β-reductase, reversibly and competitively (Ki 2.1 μM with testosterone). No time-dependent inactivation was detected over 140 min in the preincubation/dilution experiment. [2]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
5-α reductase Ki 10.2 nM

Cellular Effect

Cell Line Activity Value Description Reference
DU-145 IC50 13.53 μM Cytotoxicity against human DU145 cells assessed as growth inhibition after 24 hrs by CCK8 assay [PMID: 29615343]
DU-145 IC50 14.53 μM Antiproliferative activity against human DU145 cells after 24 hrs by CCK-8 assay [PMID: 30482547]
DU-145 IC50 3.9 μM Cytotoxicity against Homo sapiens (human) DU145 cells after 48 hr by MTT assay 10.1007/s00044-010-9393-3
DU-145 IC50 3.9 μM Antiproliferative activity against human DU145 cells assessed as growth inhibition after 48 hrs by MTT assay [PMID: 20171759]
DU-145 IC50 548 μM Cytotoxicity against human DU145 cells by rapid colorimetric assay [PMID: 26780831]
HEK293 IC50 > 50 μM Cytotoxicity against HEK293 cells after 24 hrs by MTT assay [PMID: 28693914]
HEK293 IC50 218 nM In vitro inhibition of human Steroid 5-alpha-reductase type I in transfected 293 cells using [3H]- delta4-Androstenedione as substrate [PMID: 7739004]
HEK293 IC50 30.3 nM Inhibition of human type-2 5-alpha reductase expressed in HEK293 cells using [3H]-androstenedione as substrate after 30 mins by HPLC analysis [PMID: 22776417]
HEK293 IC50 40 nM Inhibition of human 5alpha-2 reductase expressed in HEK293 cells assessed as suppression of conversion of [3]androstenedione incubated for 30 mins by radioactivity-based HPLC analysis [PMID: 26780831]
HEK293 IC50 453 nM Inhibition of human type-1 5-alpha reductase expressed in HEK293 cells using [3H]-androstenedione as substrate after 30 mins by HPLC analysis [PMID: 22776417]
HEK293 IC50 453 nM Inhibition of human 5alpha-1 reductase expressed in HEK293 cells assessed as suppression of conversion of [3]androstenedione incubated for 30 mins by radioactivity-based HPLC analysis [PMID: 26780831]
LNCaP IC50 0.76 μM Inhibition of steroid 5-alpha-reductase in human LNCAP cells assessed as reduction in 5- dihydrotestosterone formation incubated for 60 mins by LC-MS analysis [PMID: 32040314]
LNCaP IC50 13.53 μM Antiproliferative activity against human LNCAP cells after 24 hrs by CCK-8 assay [PMID: 30482547]
LNCaP IC50 14.53 μM Cytotoxicity against human LNCAP cells assessed as growth inhibition after 24 hrs by CCK8 assay [PMID: 29615343]
LNCaP IC50 19.8 μg/mL Inhibitory activity against 5-alpha-reductase type 1 in cell culture system using LNCaP cells (androgen-sensitive human prostatic cancer cell line) [PMID: 11527731]
LNCaP IC50 53 μM Inhibitory activity against 5-alpha-reductase type 1 in cell culture system using LNCaP cells (androgen-sensitive human prostatic cancer cell line) [PMID: 11527731]
Macrophage IC50 28.2 μM Cytotoxicity against Balb/C mouse macrophages assessed as cell viability after 24 hrs by MTT assay [PMID: 20171759]
MCF7 IC50 44.14 μM Cytotoxicity against human MCF7 cells after 24 hrs by MTT assay [PMID: 28693914]
MDA-MB-231 IC50 > 50 μM Cytotoxicity against human MDA-MB-231 cells after 24 hrs by MTT assay [PMID: 28693914]
PC-3 IC50 > 80 μM Cytotoxicity against human PC3 cells after 48 hrs by MTT assay [PMID: 28757062]

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In Vitro Studies

In HepG2 cells exposed to cortisone, 2 μM finasteride for 8 h modestly reduced cortisone clearance. AKR1D1 mRNA was unchanged and the reduction in 5β-tetrahydrocortisone was not statistically significant, limiting attribution of the clearance effect to AKR1D1. [3]

Human SRD5A2 structure with an NADP–dihydrofinasteride adduct

Biochemical assay · Recombinant human SRD5A2 purified from insect cells and crystallized in lipidic mesophase [1]

The 2.8 Å crystal structure contains an NADP–dihydrofinasteride adduct in an enclosed intramembrane cavity. The covalent linkage is between cofactor and inhibitor-derived moiety; this does not establish a covalent bond to the enzyme protein.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Crystal diffraction resolutionresolution 2.8 Å[1]
Identity and placement of bound ligandstructural observation NADP–dihydrofinasteride adduct[1]

Literature-Reported Treatment Conditions

Treatment concentration
Finasteride in purification buffers: 0.5 μM at lysis and 1.0 μM in subsequent buffers
Method
Ligand-stabilized protein purification and X-ray crystallography
Reported limits
No binding IC50 or Ki was measured by this structural experiment; free ligand concentration in the final crystal is not stated.
Methods and source locations

Compound reported in the paper: Finasteride; Compound label in the paper: finasteride

Evidence applies to named finasteride under the reported experimental conditions; no supplier-lot equivalence is established.

Results: Structure determination and overall structure; Intermediate adduct formed between finasteride and NADPH; Binding pockets for NADP–DHF; Fig. 1b–e, Fig. 2a–d; Table 1; Methods: SRD5A2 expression and purification, Crystallization, X-ray data collection and structure determination

Crystal diffraction resolution: Molecular replacement and structural refinement; diffraction data from five crystals merged — Table 1 and footnote a; structure determination Results

Identity and placement of bound ligand: Ligand electron density and chemical modeling — Fig. 2a–b and Intermediate adduct Results

Reversible competitive inhibition of human AKR1D1

Biochemical assay · Purified recombinant human steroid 5β-reductase AKR1D1 with testosterone substrate [2]

Finasteride competitively inhibited AKR1D1 with Ki 2.1 μM. Preincubation with or without NADPH over 140 min gave no evidence of time-dependent inactivation after dilution. This endpoint concerns 5β-reductase, not SRD5A2.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Competitive inhibition of testosterone 5β-reductionKi 2.1 μM[2]
Residual activity after finasteride preincubation and dilutiontime dependence No evidence of time-dependent inactivation over 140 min[2]

Literature-Reported Treatment Conditions

Treatment concentration
0–20 μM finasteride in the Fig. 2 inhibition series; separate preincubation: 31.0 μM finasteride with 7.8 μM AKR1D1 ± 144 μM NADPH
Exposure duration
Preincubation monitored over 140 min
Method
Radiometric testosterone reduction at 37 °C, pH 6.0; preincubation aliquots diluted 100-fold into a fluorometric activity assay
Vehicle
Assay acetonitrile: 5% radiometric; 4% fluorometric
Reported limits
Ki uncertainty and replicate number are not stated in the relevant inhibition result. Finasteride stock solvent is not separately identified.
Methods and source locations

Compound reported in the paper: Finasteride; Compound label in the paper: finasteride

Evidence applies to named finasteride under the reported experimental conditions; no supplier-lot equivalence is established.

Experimental Procedures: Materials, Standard Radiometric Assay and Product Verification, Standard Spectrofluorometric Assay, Enzyme Inhibition Studies; Results: Inhibition Studies; Fig. 2

Competitive inhibition of testosterone 5β-reduction: Varied testosterone and finasteride; inhibition-pattern fitting — Results: Inhibition Studies; Fig. 2

Residual activity after finasteride preincubation and dilution: Preincubation with and without added NADPH, followed by 100-fold dilution into activity assay — Enzyme Inhibition Studies; Results: Inhibition Studies

Modest effects on cortisone clearance in HepG2 cells

Cell-based study · Human HepG2 hepatoma cells; vehicle and no-cell controls [3]

At 2 μM, finasteride modestly reduced cortisone clearance during an 8-h exposure to 200 nM cortisone. AKR1D1 mRNA was unchanged, and the decrease in 5β-tetrahydrocortisone did not reach statistical significance. The clearance effect cannot be attributed specifically to AKR1D1.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cortisone remaining in medium / cortisone clearancedirection and significance Modest decrease in clearance; p < 0.05 versus vehicle (Fig. 5e asterisk)[3]
5β-tetrahydrocortisone generationsignificance Reduction did not reach statistical significance[3]
AKR1D1 mRNA expressiondirection No detectable treatment effect[3]

Literature-Reported Treatment Conditions

Treatment concentration
2 μM finasteride; 200 nM cortisone
Exposure duration
8 h
Method
Cells treated in serum-free, phenol red-free medium
Vehicle
Vehicle control shown; chemical identity and final solvent concentration not stated in the relevant treatment description
Co-treatment
Cortisone substrate; dutasteride is a separate comparator, not a co-treatment
Reported limits
No exact numerical clearance/metabolite means are transcribed from bars. Finasteride stock solvent and lot are not stated.
Methods and source locations

Compound reported in the paper: Finasteride; Compound label in the paper: finasteride

Evidence applies to named finasteride under the reported experimental conditions; no supplier-lot equivalence is established.

Methods 2.1, 2.6–2.8 and qPCR normalization; Results inhibitor subsection immediately preceding Fig. 5; Fig. 5d–f and caption; Discussion on cortisone metabolism by 5α-reductases

Cortisone remaining in medium / cortisone clearance: GC–MS; n = 3 experiments, mean ± SE — Fig. 5e and caption; inhibitor Results; Methods 2.7

5β-tetrahydrocortisone generation: GC–MS; n = 3 experiments, mean ± SE — Fig. 5f and caption; inhibitor Results

AKR1D1 mRNA expression: qPCR normalized to 18SrRNA; n = 3 experiments, mean ± SE — Fig. 5d and caption; inhibitor Results

In Vivo Studies

During testosterone-driven prostate regrowth in castrated rats, finasteride reduced intraprostatic DHT and day-7 ventral prostate weight. The day-2 weight difference was not significant, and prostate regrowth persisted above the castrated baseline. These findings describe finasteride with testosterone replacement. [4]

Finasteride during testosterone-driven rat prostate regrowth

Animal study · Adult male Sprague-Dawley rats; testosterone replacement after 7 days of castration [4]

Finasteride reduced day-7 prostate regrowth and lowered DHT during testosterone replacement. The early weight reduction was nonsignificant, and residual prostate regrowth remained despite treatment. Tissue androgen assays used pooled samples.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Ventral prostate wet weight with testosterone, vehicle versus finasteridemean ± SEM Day 2: 90 ± 5 versus 80 ± 3 mg (not significant); day 7: 240 ± 16 versus 168 ± 10 mg (p = 0.04)[4]
Intraprostatic DHT with testosterone, vehicle versus finasteridemean ± SEM Day 2: 14.55 ± 0.72 versus 1.35 ± 0.09 ng/g; day 7: 13.95 ± 2.33 versus 1.58 ± 0.09 ng/g[4]
Prostate regrowth during finasteride plus testosterone versus castrated baselineresidual effect Regrowth persisted above baseline; ventral and lateral p = 0.001, dorsal p = 0.01[4]

Conditions shared by the study groups

Frequency
Daily injection; testosterone delivered by implant
Treatment course
Finasteride/vehicle started 1 day before testosterone implantation; endpoints 2 and 7 days after implantation
Vehicle
1 ml of 10% ethanol in sesame oil
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Testosterone plus vehicle
0.75-cm testosterone-filled silastic implant; finasteride absent		Matched finasteride group; C7 castrated baseline also shownVentral prostate wet weight: 90 ± 5 mg at day 2 and 240 ± 16 mg at day 7; mean ± SEM[4]
Testosterone plus finasteride
Finasteride reported as 40 mg/kg or 12 mg/rat; 0.75-cm testosterone-filled silastic implant		Testosterone plus matched vehicle; C7 castrated baseline also shownVentral prostate wet weight: 80 ± 3 mg at day 2 and 168 ± 10 mg at day 7; mean ± SEM. Day-2 reduction nonsignificant; day-7 p = 0.04. Regrowth persisted above castrated baseline.[4]
Testosterone plus vehicle
Model: Adult male Sprague-Dawley rats, 250–300 g; castrated 7 days before androgen replacement
Route: Subcutaneous vehicle injection; testosterone delivered by silastic implant (anatomical placement not specified).
Reported limits: Methods describe dose as 40 mg/kg or 12 mg/rat without allocating these alternatives to groups. Animal numbers for this time-course design are not stated in the relevant text/captions. The anatomical placement of the testosterone-filled silastic implant is not specified in the retained Experimental Animals paragraph or Figure 2 caption.
Testosterone plus finasteride
Model: Adult male Sprague-Dawley rats, 250–300 g; castrated 7 days before androgen replacement
Route: Subcutaneous finasteride injection; testosterone delivered by silastic implant (anatomical placement not specified).
Reported limits: Methods describe dose as 40 mg/kg or 12 mg/rat without allocating these alternatives to groups. Animal numbers for this time-course design are not stated in the relevant text/captions. The anatomical placement of the testosterone-filled silastic implant is not specified in the retained Experimental Animals paragraph or Figure 2 caption.
Methods and source locations

Compound reported in the paper: Finasteride; Compound label in the paper: finasteride

Evidence applies to named finasteride under the reported experimental conditions; no supplier-lot equivalence is established.

Materials and Methods: Materials, Experimental Animals, sample preparation, androgen assays and statistics; Results: Finasteride Inhibits the Regrowth of the Prostate in the 7-Day Castrated Rats; Finasteride Inhibits the Conversion of Exogenous Testosterone to DHT in Rats; Figs. 2–3 and captions

Ventral prostate wet weight with testosterone, vehicle versus finasteride: Tissue wet weight; Kruskal–Wallis followed by Mann–Whitney tests when significant; group n not stated for this design — Fig. 2; first Results subsection, paragraph beginning We further tested

Intraprostatic DHT with testosterone, vehicle versus finasteride: Radioimmunoassay of left ventral prostate samples pooled from two to three rats; assay duplicates; independent pool count not stated — Fig. 3B; Results: Finasteride Inhibits the Conversion of Exogenous Testosterone to DHT in Rats

Prostate regrowth during finasteride plus testosterone versus castrated baseline: Prostate wet weight — Fig. 2 and final paragraph of first Results subsection

Testosterone plus vehicle · Materials and Methods: Materials, Experimental Animals, sample preparation, androgen assays and statistics; Results: Finasteride Inhibits the Regrowth of the Prostate in the 7-Day Castrated Rats; Finasteride Inhibits the Conversion of Exogenous Testosterone to DHT in Rats; Figs. 2–3 and captions

Testosterone plus finasteride · Materials and Methods: Materials, Experimental Animals, sample preparation, androgen assays and statistics; Results: Finasteride Inhibits the Regrowth of the Prostate in the 7-Day Castrated Rats; Finasteride Inhibits the Conversion of Exogenous Testosterone to DHT in Rats; Figs. 2–3 and captions

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 98319-26-7
Formula C23H36N2O2
Molecular Weight 372.5
Synonyms Proscar; Propecia
SMILES
C[C@]12CC[C@H]3[C@H]([C@@H]1CC[C@@H]2C(=O)NC(C)(C)C)CC[C@@H]4[C@@]3(C=CC(=O)N4)C

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 67 mg/mL (179.85 mM)
Water Insoluble
Ethanol 67 mg/mL (179.85 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Xiao Q, Wang L, Supekar S, et al. Structure of human steroid 5α-reductase 2 with the anti-androgen drug finasteride Nature communications (2020). PMID: 33110062 DOI: 10.1038/s41467-020-19249-z Source material
  2. [2] Drury JE, Di Costanzo L, Penning TM, et al. Inhibition of human steroid 5beta-reductase (AKR1D1) by finasteride and structure of the enzyme-inhibitor complex The Journal of biological chemistry (2009). PMID: 19515843 DOI: 10.1074/jbc.c109.016931 Source material
  3. [3] Nikolaou N, Gathercole LL, Kirkwood L, et al. AKR1D1 regulates glucocorticoid availability and glucocorticoid receptor activation in human hepatoma cells The Journal of steroid biochemistry and molecular biology (2019). PMID: 30769091 DOI: 10.1016/j.jsbmb.2019.02.002 Source material
  4. [4] Dadras SS, Cai X, Abasolo I, et al. Inhibition of 5alpha-reductase in rat prostate reveals differential regulation of androgen-response gene expression by testosterone and dihydrotestosterone Gene expression (2001). PMID: 11444528 DOI: 10.3727/000000001783992551 Source material

Publications

2 publications citing this product

  1. Reilly Taylor, .et al. , Front. Biosci. (Elite Ed), 2026, 18(1): 44075 PMID: 41914162
  2. Chen CC, .et al. , Anticancer Res, 2017, Dec;37(12):6893-6898 PMID: 29187470

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