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Finasteride | CAS No: 98319-26-7 | GMP-certified suppliers
A medication that treats benign prostatic hyperplasia and male pattern hair loss in men, helping alleviate urinary symptoms and support hair retention for dependable therapeutic use.
Therapeutic categories
5-alpha Reductase InhibitorsAdrenergic alpha-AntagonistsAdrenergic AntagonistsAgents that produce hypertensionAndrostanesAndrostenes
Generic name
Finasteride
Molecule type
small molecule
CAS number
98319-26-7
DrugBank ID
DB01216
Approval status
Approved drug
ATC code
D11AX10
Primary indications
- Finasteride is indicated for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to improve symptoms, reduce the risk of acute urinary retention, and reduce the risk of the need for surgery including transurethral resection of the prostate (TURP) and prostatectomy
- A combination product with [tadalafil] is also used for the symptomatic treatment of BPH for up to 26 weeks
- Finasteride is also indicated for the treatment of male pattern hair loss (androgenetic alopecia, hereditary alopecia, or common male baldness) in male patients
Product Snapshot
- Finasteride is supplied as an oral small‑molecule formulation with additional topical presentations for cutaneous use
- It is used for benign prostatic hyperplasia and for male pattern hair loss
- It is approved in major regulated markets including the US and Canada
Clinical Overview
Finasteride (CAS 98319-26-7) is a synthetic 4‑azasteroid and a selective inhibitor of Type II 5α‑reductase. It is indicated for the treatment of symptomatic benign prostatic hyperplasia in men with enlarged prostates to improve urinary symptoms and reduce the risk of acute urinary retention or surgical intervention. It is also indicated for male pattern hair loss. Finasteride is marketed in various regions under names such as Proscar for benign prostatic hyperplasia and Propecia for androgenetic alopecia, and it is sometimes used in combination with alpha‑blockers or a fixed‑dose combination with tadalafil for short‑term symptomatic management of benign prostatic hyperplasia.
Its pharmacologic effect is based on suppression of serum and intraprostatic dihydrotestosterone through competitive inhibition of Type II 5α‑reductase, the enzyme that converts testosterone to dihydrotestosterone. Serum dihydrotestosterone decreases rapidly, with maximal reduction occurring within hours of dosing. Chronic administration lowers serum dihydrotestosterone by about 70 percent and intraprostatic concentrations by more than 80 percent, while allowing a modest increase in circulating testosterone that remains within the physiologic range. In scalp tissue, finasteride reduces dihydrotestosterone levels by more than 60 percent, supporting its role in mitigating follicular miniaturization in androgenetic alopecia.
Finasteride is orally active and undergoes hepatic metabolism, with cytochrome P450 3A‑dependent pathways contributing to clearance. Systemic exposure is influenced by hepatic function. Dihydrotestosterone levels generally normalize within about two weeks after discontinuation.
Reported safety considerations include sexual dysfunction, decreased ejaculate volume, and breast‑related symptoms. Finasteride may reduce prostatic bleeding in some contexts. It is not intended for use in women or children, and exposure during pregnancy should be avoided.
For API procurement, manufacturers typically emphasize validated control of stereochemistry, impurity profiles, and robust management of residual solvents and particle‑size distribution to support consistent formulation performance and regulatory compliance.
Its pharmacologic effect is based on suppression of serum and intraprostatic dihydrotestosterone through competitive inhibition of Type II 5α‑reductase, the enzyme that converts testosterone to dihydrotestosterone. Serum dihydrotestosterone decreases rapidly, with maximal reduction occurring within hours of dosing. Chronic administration lowers serum dihydrotestosterone by about 70 percent and intraprostatic concentrations by more than 80 percent, while allowing a modest increase in circulating testosterone that remains within the physiologic range. In scalp tissue, finasteride reduces dihydrotestosterone levels by more than 60 percent, supporting its role in mitigating follicular miniaturization in androgenetic alopecia.
Finasteride is orally active and undergoes hepatic metabolism, with cytochrome P450 3A‑dependent pathways contributing to clearance. Systemic exposure is influenced by hepatic function. Dihydrotestosterone levels generally normalize within about two weeks after discontinuation.
Reported safety considerations include sexual dysfunction, decreased ejaculate volume, and breast‑related symptoms. Finasteride may reduce prostatic bleeding in some contexts. It is not intended for use in women or children, and exposure during pregnancy should be avoided.
For API procurement, manufacturers typically emphasize validated control of stereochemistry, impurity profiles, and robust management of residual solvents and particle‑size distribution to support consistent formulation performance and regulatory compliance.
Identification & chemistry
| Generic name | Finasteride |
|---|---|
| Molecule type | Small molecule |
| CAS | 98319-26-7 |
| UNII | 57GNO57U7G |
| DrugBank ID | DB01216 |
Pharmacology
| Summary | Finasteride is a selective inhibitor of type II 5α‑reductase, blocking the conversion of testosterone to dihydrotestosterone (DHT) in prostate tissue, hair follicles, and other androgen‑responsive sites. This inhibition lowers serum and intratissue DHT levels, reducing DHT‑driven prostatic growth and modifying androgen signaling relevant to male pattern hair loss. Chronic exposure may also partially affect type I 5α‑reductase, contributing to broader reductions in DHT production. |
|---|---|
| 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 testosteroneand 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. |
Targets
| Target | Organism | Actions |
|---|---|---|
| 3-oxo-5-alpha-steroid 4-dehydrogenase 2 | Humans | inhibitor |
| 3-oxo-5-alpha-steroid 4-dehydrogenase 1 | Humans | inhibitor |
| 3-oxo-5-beta-steroid 4-dehydrogenase | Humans | inhibitor |
ADME / PK
| Absorption | Finasteride is well absorbed following oral administration and displays a slow accumulation phase after multiple dosing.[lablel] In healthy male subjects receiving oral finasteride, the mean oral bioavailability was 65% for 1 mg finasteride and 63% for 5 mg finasteride, and the values ranged from 26 to 170% for 1 mg dose and from 34 to 108% for 5 mg dose, respectively.It is reported that food intake does not affect the oral bioavailability of the drug.The peak plasma concentrations (Cmax) averaged 37 ng/mL (range, 27-49 ng/mL) and was reached 1-2 hours post administration.The AUC(0-24 hr) was 53 ngxhr/mL (range, 20-154 ngxhr/mL).The plasma concentrations and AUC are reported to be higher in elderly male patients aged 70 years or older. |
|---|---|
| Half-life | In healthy young subjects receiving finasteride, the mean elimination half-life in plasma was 6 hours ranging from 3 to 16 hours. In elderly patients over the age of 70 years, the half-life is prolonged to 8 hours. |
| Protein binding | Approximately 90% of circulating finasteride is bound to plasma proteins. |
| Metabolism | Finasteride undergoes extensive hepatic metabolism predominantly mediated by the cytochrome P450 3A4 (CYP3A4) enzyme to form the t-butyl side chain monohydroxylated and monocarboxylic acid metabolites.Theses metabolites retain less than 20% of the pharmacological activity of the parent compound. |
| Route of elimination | In healthy subjects, about 32-46% of total oral dose of finasteride was excreted in the urine in the form of metabolites while about 51-64% of the dose was excreted in the feces. In patients with renal impairment, the extent of urinary excretion of finasteride is expected to be decreased while the fecal excretion is increased. |
| Volume of distribution | The volume of distribution is 76 L at steady state, ranging from 44 to 96 L. Finasteride has been shown to cross the blood brain barrier but does not appear to distribute preferentially to the CSF.It is not known whether finasteride is excreted in human milk. |
| Clearance | In healthy young subjects (n=15), the mean plasma clearance of finasteride was 165 mL/min with the range between 70 and 279 mL/min. |
Formulation & handling
- Finasteride is a small‑molecule, highly lipophilic solid suitable for oral solid‑dose formulations, though its very low aqueous solubility may require solubility‑enhancing approaches.
- Food has minimal impact on absorption, allowing flexible administration without food‑dependent formulation constraints.
- Topical and cutaneous products benefit from its lipophilicity, supporting incorporation into lipidic or solvent‑based vehicles for dermal delivery.
Regulatory status
| Lifecycle | Patent protections for this API in the United States and Canada expired between 2011 and 2018, indicating no remaining primary exclusivities. With established marketing in both countries, the product is in a mature stage of its lifecycle. |
|---|
| Markets | Canada, US |
|---|
Supply Chain
| Supply chain summary | Finasteride was originally developed by a single originator company, with subsequent manufacturing now dominated by a large number of generic producers and repackagers supplying the US and Canadian markets. Branded and generic products are widely available in both regions, supported by extensive distribution through numerous pharmaceutical packaging and supply firms. All listed patent protections have expired, indicating that generic competition is already well established. |
|---|
Safety
| Toxicity | **LD50** Oral LD50 is about 418 mg/kg in rats[MSDS] and there have been cases of lethality in rats receiving a single oral dose of 400 mg/kg in males and 1000 mg/kg in females. **Nonclinical toxicology** In a 24-month rat study, there were no signs of the tumorigenic potential of finasteride.In a 19-month carcinogenicity study in CD-1 mice, high doses of finasteride, at 1824 times the human exposure (250 mg/kg/day), resulted in an increase in the incidence of testicular Leydig cell adenomas and an increase in serum LH levels._In vitro_ mutagenesis assays demonstrated no evidence of mutagenicity. In an in vitro chromosome aberration assay, using Chinese hamster ovary cells, there was a slight increase in chromosome aberrations with much higher doses of finasteride. **Overdose** There were no reported significant adverse events in clinical trials of male patients receiving single oral doses of finasteride up to 400 mg and multiple doses of finasteride up to 80 mg/day for three months.As there have been no cases of overdose or clinically significant toxicity with finasteride, there are no specific recommendations in case of an overdose. **Significant adverse events** Common reproductive adverse events seen with finasteride therapy include erectile dysfunction, ejaculatory dysfunction, and loss of libido.These adverse events tend to disappear after discontinuation or chronic use of the drug. Only causal adverse event occurring at the male reproductive system that is caused by finasteride is decreased ejaculatory volume because of the predominant action of DHT on the prostate. **Special populations** Finasteride can be safely used in elderly patients or those with renal impairment with no specific dosing adjustment recommendations.Finasteride is indicated for male patients only, and it is advised that exposure to finasteride is avoided in pregnant women carrying male fetuses as it may lead to abnormal development of external genitalia in male fetuses. |
|---|
High Level Warnings:
- Oral toxicity is moderate, with an LD50 of approximately 418 mg/kg in rats
- High‑dose rodent studies identified testicular Leydig cell adenomas at exposure levels far exceeding human therapeutic exposure
- In vitro genotoxicity assays showed no mutagenicity, with only slight chromosome aberrations at supraphysiologic concentrations
Good Manufacturing Practices
Active pharmaceutical ingredients are made in GMP-certified manufacturing facilities. GMP stands for Good Manufacturing Practices and is the main standard in the pharmaceutical industry. cGMP or Current GMP means that the company complies with the most recent requirements/version of GMP. The WHO has its own guideline for GMP, the World Health Organization or WHO GMP. The authority that has audited the company can also be from a country like China (Chinese GMP) or from the EU (EU GMP), every authority has different GMP requirements.
Finasteride is a type of 5-alfa-reductase Inhibitors
5-alfa-reductase inhibitors belong to a subcategory of pharmaceutical active ingredients known for their effectiveness in treating conditions related to hormonal imbalances. These inhibitors specifically target and block the activity of the enzyme 5-alfa-reductase, which plays a crucial role in converting testosterone into dihydrotestosterone (DHT) in the body. By inhibiting this enzyme, 5-alfa-reductase inhibitors effectively reduce the levels of DHT, thereby providing therapeutic benefits.
The primary medical application of 5-alfa-reductase inhibitors lies in the treatment of benign prostatic hyperplasia (BPH), a condition characterized by the enlargement of the prostate gland. By inhibiting the conversion of testosterone to DHT, these inhibitors effectively shrink the prostate gland, relieving symptoms such as urinary hesitancy, frequent urination, and weak urine flow.
Furthermore, 5-alfa-reductase inhibitors have demonstrated efficacy in the treatment of male pattern baldness, also known as androgenic alopecia. By reducing the levels of DHT, these inhibitors help slow down hair loss and stimulate hair regrowth in individuals experiencing this condition.
Some commonly prescribed 5-alfa-reductase inhibitors include finasteride and dutasteride. These medications are typically administered orally and are well-tolerated by most individuals. However, it's worth noting that 5-alfa-reductase inhibitors may have potential side effects, including sexual dysfunction and breast tenderness.
In conclusion, 5-alfa-reductase inhibitors are a valuable class of pharmaceutical active ingredients used to treat conditions such as benign prostatic hyperplasia and androgenic alopecia. By blocking the activity of the enzyme 5-alfa-reductase, these inhibitors effectively reduce the levels of dihydrotestosterone, providing therapeutic benefits to patients.
Finasteride (5-alfa-reductase Inhibitors), classified under Hormonal Agents
Hormonal agents are a prominent category of pharmaceutical active pharmaceutical ingredients (APIs) widely used in the medical field. These substances play a crucial role in regulating and modulating hormonal functions within the body. Hormonal agents are designed to mimic or manipulate the effects of naturally occurring hormones, allowing healthcare professionals to treat various endocrine disorders and hormonal imbalances.
Hormonal agents are commonly employed in the treatment of conditions such as hypothyroidism, hyperthyroidism, diabetes, and hormonal cancers. These APIs work by interacting with specific hormone receptors, either by stimulating or inhibiting their activity, to restore the balance of hormones in the body. They can be administered orally, intravenously, or through other routes depending on the specific medication and patient needs.
Pharmaceutical companies employ rigorous manufacturing processes and quality control measures to ensure the purity, potency, and safety of hormonal agent APIs. These APIs are synthesized using chemical or biotechnological methods, often starting from natural hormone sources or through recombinant DNA technology. Stringent regulatory guidelines are in place to guarantee the efficacy and safety of hormonal agent APIs, ensuring that patients receive high-quality medications.
As the demand for hormone-related therapies continues to grow, ongoing research and development efforts focus on enhancing the effectiveness and reducing the side effects of hormonal agent APIs. This includes the exploration of novel delivery systems, advanced formulations, and targeted drug delivery methods. By continuously advancing our understanding and capabilities in hormonal agents, the medical community can improve patient outcomes and quality of life for individuals with hormonal disorders.
Finasteride API manufacturers & distributors
Compare qualified Finasteride API suppliers worldwide. We currently have 18 companies offering Finasteride API, with manufacturing taking place in 5 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| Apollo Healthcare Resourc... | Distributor | Singapore | Singapore | BSE/TSE, CEP, CoA, EDMF/ASMF, FDA, GMP, ISO9001, JDMF, KDMF, MSDS, USDMF, WC | 200 products |
| Aquatic Remedies Pvt Ltd | Producer | India | India | CoA | 35 products |
| Aurora Industry Co., Ltd | Distributor | China | China | BSE/TSE, CEP, CoA, FDA, GMP, ISO9001, MSDS, USDMF, WC | 250 products |
| Cerata Pharmaceuticals LL... | Producer | India | India | CoA, FDA, GMP | 34 products |
| Chongqing Waycome | Producer | China | China | CoA, WC | 1 products |
| Chr. Olesen Group | Distributor | Denmark | China | USDMF | 252 products |
| Cipla | Producer | India | India | CEP, CoA, FDA, GMP, KDMF, USDMF, WC | 164 products |
| Curia | Producer | United States | Spain | CEP, CoA, GMP, KDMF, MSDS | 106 products |
| Dr. Reddy's | Producer | India | India | BSE/TSE, CEP, CoA, FDA, GMP, JDMF, KDMF, MSDS, USDMF, WC | 170 products |
| Gedeon Richter | Producer | Hungary | Hungary | CoA, GMP, USDMF | 48 products |
| Hari Ganesh Pharma Privat... | Distributor | India | India | CoA, FDA, GMP | 35 products |
| Hetero Labs | Producer | India | India | CEP, CoA, FDA, GMP, JDMF, KDMF, USDMF, WC | 90 products |
| HuNan Kerey | Producer | China | China | CoA | 2 products |
| Hunan Yuxin Pharmaceutica... | Producer | China | China | CoA, GMP, USDMF, WC | 14 products |
| Metapharmaceutical Indust... | Producer | Spain | China | BSE/TSE, CoA, GDP, GMP, ISO14001, MSDS, WC | 21 products |
| MSN Labs. | Producer | India | India | CEP, CoA, FDA, GMP, USDMF, WC | 119 products |
| SETV Global | Producer | India | India | CoA, FDA, GMP | 515 products |
| Sun Pharma | Producer | India | India | CoA, GMP, USDMF, WC | 219 products |
When sending a request, specify which Finasteride API quality you need: for example EP (Ph. Eur.), USP, JP, BP, or another pharmacopoeial standard, as well as the required grade (base, salt, micronised, specific purity, etc.).
Use the list above to find high-quality Finasteride API suppliers. For example, you can select GMP, FDA or ISO certified suppliers. Visit our help page to learn more about sourcing APIs via Pharmaoffer.
Frequently asked questions about Finasteride API
Sourcing
What matters most when sourcing GMP-grade Finasteride?
Key considerations include verifying that the manufacturer complies with GMP standards recognized in the US and Canada and ensuring the material is supported by appropriate regulatory documentation. Because Finasteride is supplied by many generic producers, confirming traceability, change‑control practices, and consistent quality across batches is essential. It is also important to work with suppliers that maintain reliable distribution and repackaging practices suitable for these markets.
Which documents are typically required when sourcing Finasteride API?
Request the core API documentation set: CoA (16 companies), GMP (13 companies), USDMF (10 companies), WC (9 companies), FDA (9 companies). Confirm versions and validity dates match the destination market to avoid delays in qualification.
Which manufacturers are known to produce Finasteride API?
Known or reported manufacturers for Finasteride: Aurora Industry Co., Ltd, Chr. Olesen Group, SETV Global, Apollo Healthcare Resources (Singapore), Cerata Pharmaceuticals LLP, Hari Ganesh Pharma Private Limited. Evaluate their GMP history, scale, and regional coverage before requesting dossiers or allocating demand.
How can I request quotes for Finasteride API from GMP suppliers?
Submit quote requests through the supplier listings with your specs and required documents (specifications, target volume, delivery timeline, and destination). Providing consistent details upfront speeds comparable offers and clarifies technical feasibility.
Is a GMP audit report available for Finasteride manufacturers?
Audit reports may be requested for Finasteride: 8 GMP audit reports available. Confirm the scope and recency of any audit before relying on it for qualification decisions.
How many suppliers offer Finasteride API on Pharmaoffer?
Reported supplier count for Finasteride: 17 verified suppliers. Filter listings by certifications, regions, and delivery options to match your qualification plan.
Which countries are known to manufacture Finasteride API?
Production countries reported for Finasteride: India (9 producers), China (5 producers), Singapore (1 producer). Knowing the manufacturing geography helps anticipate logistics lead times and import compliance needs.
Which certifications do suppliers of Finasteride usually hold?
Common certifications for Finasteride suppliers: CoA (16 companies), GMP (13 companies), USDMF (10 companies), WC (9 companies), FDA (9 companies). Always verify issuing authorities and expiry dates when reviewing audit packages.
Technical
What is Finasteride (CAS 98319-26-7) used for?
Finasteride is used to treat symptomatic benign prostatic hyperplasia in men with enlarged prostates and to manage male pattern hair loss. It works by selectively inhibiting Type II 5α‑reductase, which lowers dihydrotestosterone levels in serum, prostate, and scalp. This reduction helps improve urinary symptoms, decrease prostate volume, and slow hair follicle miniaturization.
Which therapeutic class does Finasteride fall into?
Finasteride belongs to the following therapeutic categories: 5-alpha Reductase Inhibitors, Adrenergic alpha-Antagonists, Adrenergic Antagonists, Agents that produce hypertension, Androstanes. This positioning helps teams compare alternative APIs, anticipate pharmacology expectations, and align early research priorities.
What conditions is Finasteride mainly prescribed for?
The primary indications for Finasteride: Finasteride is indicated for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to improve symptoms, reduce the risk of acute urinary retention, and reduce the risk of the need for surgery including transurethral resection of the prostate (TURP) and prostatectomy, A combination product with [tadalafil] is also used for the symptomatic treatment of BPH for up to 26 weeks, Finasteride is also indicated for the treatment of male pattern hair loss (androgenetic alopecia, hereditary alopecia, or common male baldness) in male patients. These use cases frame the target patient populations and help prioritize formulation and safety evaluations.
How does Finasteride work?
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 testosteroneand 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.
What should someone know about the safety or toxicity profile of Finasteride?
Finasteride shows moderate acute oral toxicity, with an LD50 of about 418 mg/kg in rats. High‑dose rodent studies identified Leydig cell adenomas only at exposures far above those reached with therapeutic use. It was not mutagenic in standard in vitro assays, aside from slight chromosome aberrations at supraphysiologic concentrations. Reported safety considerations include sexual dysfunction, decreased ejaculate volume, breast‑related symptoms, and the need to avoid exposure during pregnancy.
What are important formulation and handling considerations for Finasteride as an API?
Finasteride’s very low aqueous solubility often necessitates solubility‑enhancing strategies for oral solid‑dose formulations. Its high lipophilicity supports use in lipid‑based systems and facilitates incorporation into topical vehicles. Handling considerations include controlling for its solid‑state properties and ensuring suitable dispersion or dissolution within the chosen dosage form. Food has minimal effect on absorption, so formulations do not require food‑specific design.
Is Finasteride a small molecule?
Finasteride is classified as a small molecule. That classification shapes process design, impurity profiling, and analytical control strategies.
Are there special stability concerns for oral Finasteride?
Finasteride is a lipophilic, poorly water‑soluble solid that is generally suitable for oral solid‑dose formulations, and its low aqueous solubility mainly affects solubility‑enhancing formulation needs rather than chemical stability. No food‑related stability constraints are noted, as food has minimal impact on absorption. No other special stability considerations are described in the provided information.
Regulatory
Where is Finasteride approved or in use globally?
Finasteride is reported as approved in the following major regions: Canada, US. Understanding geographic coverage informs regulatory filings, supply planning, and risk assessments before escalating procurement.
Pharmaoffer
How does Pharmaoffer’s Smart Sourcing Service help with Finasteride procurement?
Pharmaoffer's Smart Sourcing Service coordinates compliant suppliers, documentation, and competitive quotes for Finasteride. It centralizes outreach, follow-ups, and document validation to shorten procurement timelines.
Is Finasteride included in the PRO Data Insights coverage?
PRO Data Insights coverage for Finasteride: 1472 verified transactions across 407 suppliers and 212 buyers worldwide. Use the dataset to benchmark suppliers and monitor regulatory activity where available.
Where can I access the API market report for Finasteride?
Market report availability for Finasteride: Report Available. The report highlights demand trends, pricing drivers, and supplier landscape insights for procurement planning.
