FINASTERIDE - finasteride tablet, coated 
Ascend Laboratories, LLC

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HIGHLIGHTS OF PRESCRIBING INFORMATION

These highlights do not include all the information needed to use FINASTERIDE TABLETS safely and effectively. See full prescribing information for FINASTERIDE TABLETS
FINASTERIDE tablets for oral use
Initial U.S. Approval: 1992

INDICATIONS AND USAGE

  • Finasteride tablets is  a  5α-reductase  inhibitor  indicated  for  the  treatment of  male  pattern  hair  loss  (androgenetic alopecia)  in  MEN  ONLY(1).
  • Finasteride tablets is  not  indicated  for  use  in women   (1,  4,  5.1).

DOSAGE AND ADMINISTRATION

  • Finasteride tablets, USP may  be  administered   w ith  or w ithout  meals   (2).
  • One   tablet  ( 1  mg )  taken   once   daily   (2).
  • In   general,   daily  use  for  three  months   or  more   is  necessary  before  benefit  is  observed  (2).

DOSAGE FORMS AND STRENGTHS

1  mg  tablets. (3)

CONTRAINDICATIONS


  • Pregnancy   (45.1,   8.1,   16).
  • H ypersensitivity   to   any   components   of   this   product   (4).

WARNINGS AND PRECAUTIONS


  • Finasteride tablets  is not  indicated  for  use  in women  or  pediatric  patients  ( 5.1 ,  5.4 ).
  • Women  should  not  handle  crushed  or  broken  finasteride tablets when  they  are  pregnant  or  may  potentially  be  pregnant  due  to potential  risk  to  a  male  fetus   (5.1 ,   8.1 ,  16 ).
  • Finasteride tablets causes a decrease in serum PSA levels. Any confirmed increase  in  PSA   while  on  finasteride tablets may  signal  the presence  of  prostate  cancer  and  should  be  evaluated, even  if those  values  are still w ithin  the normal  range  for men  not taking  a 5α-reductase  inhibitor   ( 5 . 2 ).
  • 5α-reductase   inhibitors  may  increase  the   risk   of  high - grade  prostate   cancer   ( 5 . 3 ,   6 . 1 ).

ADVERSE REACTIONS


The  most  common  adverse  reactions, reported  in  ≥1%  of  patients treated   w ith  finasteride tablets and  greater  than  in  patients  treated   w ith placebo  are:  decreased  libido,  ere ctile  d ysfunction and  ejaculation disorder   (6.1).

To report SUSPECTED ADVERSE REACTIONS, contact Ascend Laboratories, LLC at 1-877-ASC-RX01 (877-272-7901) or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

See 17 for PATIENT COUNSELING INFORMATION.

Revised: 1/2017

FULL PRESCRIBING INFORMATION: CONTENTS*

1 INDICATIONS & USAGE

2 DOSAGE & ADMINISTRATION

3 DOSAGE FORMS & STRENGTHS

4 CONTRAINDICATIONS

5 WARNINGS AND PRECAUTIONS

5.1 Exposure of Women-Risk to Male Fetus

5.2 Effects on Prostate Specific Antigen (PSA)

5.3 Increased Risk of High-Grade Prostate Cancer with 5a-Reductase Inhibitors

5.4 Pediatric Patients

6 ADVERSE REACTIONS

6.1 Clinical Trials Experience

6.2 Postmarketing Experience

7 DRUG INTERACTIONS

8 USE IN SPECIFIC POPULATIONS

8.1 Pregnancy

8.3 Nursing Mothers

8.4 Pediatric Use

8.5 Geriatric Use

8.6 Hepatic Impairment

8.7 Renal Impairment

10 OVERDOSAGE

11 DESCRIPTION

12 CLINICAL PHARMACOLOGY

12.1 Mechanism of Action

12.2 Pharmacodynamics

12.3 Pharmacokinetics

13 NONCLINICAL TOXICOLOGY

13.1 Carcinogenesis & Mutagenesis & Impairment Of Fertility

14 CLINICAL STUDIES

16 HOW SUPPLIED/STORAGE AND HANDLING

17 PATIENT COUNSELING INFORMATION

*
Sections or subsections omitted from the full prescribing information are not listed.

FULL PRESCRIBING INFORMATION

1 INDICATIONS & USAGE

Finasteride tablets  is  indicated  for  the  treatment  of  male  pattern  hair  loss  (androgenetic  alopecia)  in  MEN ONLY.


Efficacy in bitemporal recession has not been established.


Finasteride tablets is not indicated  for use in women.

2 DOSAGE & ADMINISTRATION

Finasteride tablets, USP may be administered  with or without meals.


The recommended  dose of finasteride tablets, USP is  one tablet (1 mg) taken once daily.


In  general,  daily  use  for  three months or more is  necessary before benefit is  observed. Continued use is recommended  to  sustain  benefit,  which  should  be  re-ev aluated  periodically.  Withdrawal  of  treatment leads to reversal of effect within 12 months.

3 DOSAGE FORMS & STRENGTHS

Finasteride tablets, USP are  reddish brown colored, 7 mm round, biconvex, film coated tablets, marked “F1” on one side and plain on other side.

4 CONTRAINDICATIONS


Finasteride tablets is contraindicated  in the following:


5 WARNINGS AND PRECAUTIONS

5.1 Exposure of Women-Risk to Male Fetus


Finasteride tablets  is  not  indicated  for use in women. Women should not handle crushed or broken finasteride tablets when  they  are  pregnant  or  may  potentially  be  pregnant  because  of  the possibility of absorption of finasteride  and  the  subsequent  potential  risk  to  a  male  fetus.  Finasteride Tablets are coated and will prevent  contact  with  the  active  ingredient  during  normal handling, provided that the tablets have not been broken  or  crushed .  [ See  Indications  and  Usage  (1)Contraindicat ions  (4),  Use  in  Specific  Populations  (8.1),  How  Supplied / Storage  and  Handling  ( 16 )   and  Patient  Counseling  Infor mation  (17.1).]

5.2 Effects on Prostate Specific Antigen (PSA)

In  clinical  studies  with  finasteride tablets 1 mg  (finasteride,  1 mg)  in  men  18 to 41  years  of  age,  the  mean  value  of serum  prostate  specific  antigen   (PSA)  decreased  from  0.7 ng/mL  at  ba seline  to  0.5 ng/mL  at  Month  12. Further,  in  clinical  studies with finasteride tablets 5 mg (fina steride, 5 mg) when used in older men who have benign prostatic  hyperplasia (BPH),  PSA  levels  are  decreased  by  approxi mately  50%.  Other  studies with finasteride tablets 5 mg showed it may al so cau se de crea ses in serum PSA in the pre sen ce of pro state can cer. The se findings  should  be  taken  into  account  for  proper  interpretation  of  serum  PSA  when  evaluating  men treated  with  fina steride. Any confirmed increa se f rom the lowest PSA value while on finasteride tablets may signal  the  presence  of  prostate  cancer  and  should  be  evaluated,  even  if  PSA  levels  are  still  within the normal  range  for  men  not  taking  a  5 α-reductase  inhibitor.  Non-compl iance  to  therapy  with  finasteride tablets may  also affe ct  PSA  te st  re sult s

5.3 Increased Risk of High-Grade Prostate Cancer with 5a-Reductase Inhibitors

Men  aged  55  and  over  with a normal digital rectal examination and PSA  ≤3.0 ng/mL at baseline taking finasteride  5  mg/day  (5  times  the  dose  of  finasteride tablets) in  the  7-year  Prostate  Cancer  Prevention  Trial (PCPT) had an increased risk of Gleason score 8 to 10 prost ate cancer (finasteride 1.8% vs placebo 1.1%). [See Adverse Reactions (6.1).] Similar results were observed in a 4-year placebo-controlled clinical trial with another 5α-reductase inhibitor (dutasteride, AVODART) (1% dutasteride vs 0.5% placebo). 5α- reductase inhibitors may increase the risk of development of high-grade prostate cancer. Whether the effect of 5α-reductase inhibitors to reduce prostate volume, or study-related factors, impacted the results of these studies has not been established.


5.4 Pediatric Patients


Finasteride Tablets is not indicated for use in pediatric patients  [see Use in Specific Populations (8.4) ] .

6 ADVERSE REACTIONS

6.1 Clinical Trials Experience

Because  clinical  trials  are  condu cted  under  widely  varying  conditions, adverse reaction rates observed in the  clinical  trials  of  a  drug  cannot  be  directly  compared  to  rates  in  the  clinical  trials  of another drug and may not reflect the rates obse rved in clinical practice.


Clinical Studies for finasteride tablets 1 mg in the Treatment of Male Pattern Hair Loss 

In  three  controlled  clinical  trials  for  finasteride tablets of  12-month  duration, 1.4%  of  patients  taking  finasteride tablets (n=945)  were  discontinued  due  to  adverse  experiences  that  were considered to  be possibly, probably or definitely drug-related  (1.6% for placebo; n=934).


Clinical  adverse  experiences  that  were  reported  as  possibly,  probably or  definitely  drug-related in  >1% of patients treated with finasteride tablets or placebo are presented in Table 1.


T ABLE  1:  Drug-Related   Ad verse  Experiences  for  Finasteride tablets 1 mg  (finasteride  1  mg)  inYear  1  ( %)
M ALE  P ATTERN  H AIR  LOSS 
 
Finasteride
N=945 
Placebo 
N=934 
Decreased  Libido
1.8 
1.3 
Erectile  D ysfunction
1.3 
0.7 
Ejaculation  Disorder
(Decreased  Volu me  of 
Ejaculate) 
1.2 
(0.8) 
0.7 
(0.4) 
Discontinuation  due  to
drug-related  sexual adverse  experiences
1.2 
0.9 

Integrated  analysis  of  clinical  adverse  experiences  showed that  during treatment  with  finasteride tablets,  36 (3.8%)  of  945  men  had  reported  one  or  more  of  these  adverse  experiences  as  compared  to  20  (2.1%)  of 934  men  treated  with  placebo (p=0.04). Resolution  occurred in men who discontinued therapy with finasteride tablets due  to  these  side  effects  and  in  most  of  those  who continued therapy. The  incidence of  each of the above adverse experiences decreased to <0.3%  by  the  fifth year  of treatment  with  finasteride tablets.


In  a  study  of  finasteride  1 mg  daily  in  healthy  men,  a  median  decrease  in  ejaculate  volume  of  0.3 mL  (-11%)  compared  with  0.2 mL  (-8%)  for  placebo  was  observed  after  48  weeks  of  treatment.  Two  other studies  showed  that  finasteride  at  5  times  the  dosage  of  finasteride tablets  (5 mg  daily)  produced  significant median  decreases  of  approximately 0 .5 mL (-25%) compared to placebo in ejaculate volume, but this was reversible  after discontinuation  of treatment.


In  the  clinical  studies  with  finasteride tablets,  the  incidences  for  breast  tenderness  and enlargement, hypersensitivity  reactions,  and  testicu lar  pain  in  finasteride-treated  patients  were  not  different  from  those in patients treated with placebo.


Controlled  Clinical  Trials  and  Long-Term  Open  Extension  Studies  for  finasteride tablets    5 mg (finasteride 5 mg) and AVODART (dutasteride) in the Treat ment of Benign Prostatic H yperplasia 


In  the  finasteride tablets 5 mg Long-Term  Efficacy  and  Safety  Study (PLESS),  a  4-year  controlled clinical study,  3040 patients  between  the  ages  of  45  and  78  with  symptomatic  BPH  and  an  enlarged  prostate were evaluated for  safety  over  a  period  of  4 years (1524 on finasteride tablets, 5 mg /day and 1516 on placebo). 3.7% (57 patients)  treated  with  finasteride tablets 5  mg  and  2.1%  (32 patients) treated with placebo discontinued therapy as  a  result  of  adverse  reactions  related  to  se xual  function,  which  are  the  most  frequently  reported adverse reactions.


Table  2  presents  the  only  clinical  adverse  react ions  considered  possibly,  probably  or  definitely  drug related  by  the  investigator,  for  which  the  incidence  on  finasteride tablets 5 mg  was  >1%  and  greater  than  placebo over  the  4  years  of  the  study.  In  years  2 to 4  of  the  study,  there was no significant difference between treatment groups in the incidences  of impoten ce, decreased libido and ejaculation disorder.


TABLE 2: Drug-Related Adverse Experiences for Finasteride tablets 5 mg BENIGN PROSTATIC HYPERPLASIA
 
Year 1 (%)
Years 2, 3 and 4* (%)
Finasteride 5 mg
Placebo
Finasteride 5 mg
Placebo
Impotence
8.1
3.7
5.1
5.1
Decreased Libido
6.4
3.4
2.6
2.6
Decreased Volume of Ejaculate
3.7
0.8
1.5
0.5
Ejaculation Disorder
0.8
0.1
0.2
0.1
Breast Enlargement
0.5
0.1
1.8
1.1
Breast Tenderness
0.4
0.1
0.7
0.3
Rash
0.5
0.2
0.5
0.1

*Combined   Years  2 to 4

N  =  1524  and  1516,  finasteride  vs  placebo,  respectively


The  adverse  experience  profiles  in  the  1-year,  pla cebo-controlled,  Phase  III  BPH  studies and the 5-year open extensions with finasteride tablets 5 mg and PLESS were similar.


There  is  no  evidence  of  increased sexual adverse experiences with i ncreased duration of  treatment with finasteride tablets 5 mg.  New  reports  of  drug-related  sexual  adverse  experiences  decreased  with  duration  of therapy.


During  the  4-  to  6-year  placebo- and  comparator- controlled Medical Therapy of Prostatic Symptoms (MTOPS)  study  that  enrolled 3047  men,  there  were 4  cases  of  breast  cancer  in  men  treated  with finasteride tablets  but  no  cases  in  men  not  treated  with  finasteride tablets.  During  the  4-year  placebo-controlled PLESS  study  that  enrolled 3040 men, there were 2 cases of breast cancer in placebo-treated men, but no cases were reported in men treated with finasteride tablets.


During  the 7-year placebo-controlled Prostate Cancer  Prevention Trial (PCPT) that enrolled 18,882 men, there  was  1  case  of  breast  cancer  in  men  treated  w ith  finasteride tablets,  and  1  case of breast cancer in men treated  with  placebo.  The  relationship  between long-t erm use of finasteride and male breast neoplasia is currently unknown.


The  PCPT  trial  was  a 7-year randomized, double- blind, placebo-controlled trial that enrolled 18,882 healthy  men  ≥55  years  of  age  with  a  normal  digital  rectal  examination  and  a PSA  ≤3.0 ng/mL. Men received  either  finasteride tablets 5 mg  (finasteride  5  mg)  or p lacebo daily. Patients were evaluated  annually  with PSA and  digital  rectal  exams.  Biopsies  were  performed  f or  elevated PSA,  an  abnormal digital rectal  exam,  or the  end  of  study.  The  incidence  of  Gleason score 8 to 10  prostate cancer was higher in men treated with finasteride  (1.8%)  than  in  those  treated  with placebo (1.1%). In a 4-year placebo -controlled clinical trial with  another 5 α-reductase inhibitor [AVODART (dutaster ide)], similar results for Gleason score 8 to 10 prostate  cancer  were  observed  (1%  dutasteride vs 0.5% placebo). The  clinical significance of these findings with respect to use of  finasteride tablets by men is unknown.


No  clinical  benefit  has  been  demonstrated  in patients with prostate cancer treated with finasteride tablets. Finasteride tablets is not approved to reduce the  risk of developing  prostate cancer.

6.2 Postmarketing Experience

The  following  adverse  reactions have been identified  during post approval use  of finasteride tablets. Because these  reactions  are  reported voluntarily from a population of uncertain size, it is not always possible to reliably  estimate their frequency or establi sh a causal relationship to drug exposure:


Hypersensitivity Reaction: hypersensitivity reactions such as rash, pruritus, urticaria, and angioedema (including swelling of the lips, tongue, throat, and face);


Reproductive System: sexual dysfunction that continued after discontinuation of treatment, including erectile dysfunction, libido disorders, ejaculation disorders, and orgasm disorders; male infertility and/or poor seminal quality (normalization or improvement of seminal quality has been reported after discontinuation of finasteride); testicular pain. [See Adverse Reactions (6.1).]


Neoplasms: male breast cancer;


Breast disorders: breast tenderness and enlargement;

Nervous System/Psychiatric: depression

7 DRUG INTERACTIONS

7.1 Cytochrome P450-Linked Drug Metabolizing Enzyme System

No drug interactions of clinical importance have been identified. Finasteride does not appear to affect the cytochrome P450-linked drug-metabolizing enzyme system. Compounds that have been tested in man include antipyrine, digoxin, propranolol, theophylline, and warfarinand no clinically meaningful interactions were found.


7.2 Other Concomitant Therapy

Although specific interaction studies were not performed, finasteride doses of 1 mg or more were concomitantly used in clinical studies with acetaminophen, acetylsalicylic acid, α-blockers, analgesics, angiotensin-converting enzyme (ACE) inhibitors, anticonvulsants, benzodiazepines, beta blockers, calcium-channel blockers, cardiac nitrates, diuretics, H2 antagonists, HMG-CoA reductase inhibitors, prostaglandin synthetase inhibitors (also referred to as NSAIDs), and quinolone anti-infectives without evidence of clinically significant adverse interactions.

8 USE IN SPECIFIC POPULATIONS

8.1 Pregnancy

Pregnancy Category X [see Contraindications (4)].


Finasteride tablets is  contraindicated  for  use  in  women  who  are  or  may  become  pregnant.  Finasteride tablets is  a  Type II  5 α-reductase  inhibitor  that  prevents  conversion of testosterone to 5 α-dihydrotestosterone (DHT), a hormone  necessary  for  normal  development  of  male  genitalia.  In animal studies, finasteride caused abnormal  development  of  external  genitalia  in  male fet uses. If this drug is used  during pregnancy, or if the patient  becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the male  fetu s.


Abnormal  male  genital  development  is an expected  consequence when conversion of testosterone to 5α- dihydrotestosterone  (DHT)  is  inhibited  by  5 α-reductase  inhibitors. These outcomes are similar to those reported  in  male  infants  with  genetic  5 α-reductase  deficiency.  Women  could  be  exposed  to finasteride through  contact  with  crushed  or  b roken  finasteride tablets or  semen  from  a  male partner taking finasteride tablets.  With  regard  to  finasteride  exposure  th rough  the  skin,  finasteride tablets are coated and will prevent  skin  contact  with  finasteride  during  norm al  handling  if  the  tablets  have  not  been  crushed  or broken.  Women  who  are  pregnant  or  may  beco me  pregnant should not handle crushed or broken finasteride tablets  because  of  possib le  exposure  of  a  male fetus. If a pregnant woman comes in contact with  crushed  or  broken  finasteride tablets,  the  contact  area  should  be  washed  immediately  with  soap and  water.  With  regard  to  potential  finasteride  e xposure  through  semen,  a  study  has  been conducted in men receiving finasteride tablets 1 mg/day that measured finasteride concentrations in  semen

[see Clinical Pharmacology (12.3)].


In an embryo-fetal development study, pregnant rats received finasteride during the period of major organogenesis (gestation days 6 to 17). At maternal doses of oral finasteride approximately 1 to 684 times the recommended human dose (RHD) of 1 mg/day (based on AUC at animal doses of 0.1 to 100 mg/kg/day) there was a dose-dependent increase in hypospadias that occurred in 3.6 to 100% of male offspring.  Exposure multiples were estimated using data from nonpregnant rats. Days 16 to 17 of gestation is a critical period in male fetal rats for differentiation of the external genitalia. At oral maternal doses approximately 0.2 times the RHD (based on AUC at animal dose of 0.03 mg/kg/day), male offspring had decreased prostatic and seminal vesicular weights, delayed preputial separation and transient nipple development. Decreased anogenital distance occurred in male offspring of pregnant rats that received approximately 0.02 times the RHD (based on AUC at animal dose of 0.003 mg/kg/day). No abnormalities were observed in female offspring exposed to any dose of finasteride in utero.


No developmental abnormalities were observed in the offspring of untreated females mated with finasteride-treated male rats that received approximately 488 times the RHD (based on AUC at animal dose of 80 mg/kg/day). Slightly decreased fertility was observed in male offspring after administration of about 20 times the RHD (based on AUC at animal dose of 3 mg/kg/day) to female rats during late gestation and lactation. No effects on fertility were seen in female offspring under these conditions.


No evidence of male external genital malformations or other abnormalities were observed in rabbit fetuses exposed to finasteride during the period of major organogenesis (gestation days 6 to 18) at maternal doses up to 100 mg/kg/day (finasteride exposure levels were not measured in rabbits). However, this study may not have included the critical period for finasteride effects on development of male external genitalia in the rabbit.


The fetal effects of maternal finasteride exposure during the period of embryonic and fetal development were evaluated in the rhesus monkey (gestation days 20 to 100), in a species and development period more predictive of specific effects in humans than the studies in rats and rabbits. Intravenous administration of finasteride to pregnant monkeys at doses as high as 800 ng/day (estimated maximal blood concentration of 1.86 ng/mL or about 930 times the highest estimated exposure of pregnant women to finasteride from semen of men taking 1 mg/day) resulted in no abnormalities in male fetuses. In confirmation of the relevance of the rhesus model for human fetal development, oral administration of a dose of finasteride (2 mg/kg/day or approximately 120,000 times the highest estimated blood levels of finasteride from semen of men taking 1 mg/day) to pregnant  monkeys resulted in external genital abnormalities in male fetuses. No other abnormalities were observed in male fetuses and no finasteride- related abnormalities were observed in female fetuses at any dose.

8.3 Nursing Mothers


Finasteride tablets is not indicated  for use in women.

It is not known whether finast eride is excreted in human milk.

8.4 Pediatric Use


Finasteride tablets is not indicated  f or use in pediatric patients.

Safety and effectiveness in pediatric patients have not been established.

8.5 Geriatric Use


Clinical  efficacy  studies with finasteride tablets did not include subjects aged 65 and over. Based on the pharmacokinetics  of  finasteride 5 mg, no dosage adjustment is necessary in the elderly for finasteride tablets  [ see    Clinical    Phar macology   ( 12.3)].   However  the  efficacy  of  finasteride tablets  in  the  elderly  has  not been established.

8.6 Hepatic Impairment


Caution  should  be  exercised  in  the  administration  of  finasteride tablets  in  those  patients  with  liver  function abnormalities,  as finasteride is me tabolized  extensively  in the liver  [ see  Clinical  Phar macology  (12.3) ].

8.7 Renal Impairment

No  dosage  adjustment  is  necessary  in   patients  with  renal  impairment   [ see  Clinical  Phar macology  ( 12.3) ].

10 OVERDOSAGE

In clinical studies, single doses of finasteride up to 400 mg and multiple doses of finasteride up to 80 mg/day for three months did not result in adverse reactions. Until further experience is obtained, no specific treatment for an overdose with finasteride can be recommended.


Significant lethality was observed in male and female mice at single oral doses of 1500 mg/ m2 (500 mg/kg) and in female and male rats at single oral doses of 2360 mg/ m2(400 mg/kg) and 5900 mg/m2 (1000 mg/kg), respectively.

11 DESCRIPTION


Finasteride Tablets, USP contain  finasteride  as  the  active  ingredient.  Finasteride,  a  synthetic 4-azasteroid  compound,  is  a  spe cific  inhibitor  of  steroid  Type  II  5α-reductase,  an  intracellular  enzyme that converts the androgen  testosterone into 5α-dihydrotestosterone (DHT).


The chemical name of finasteride is N-ter t-But yl-3-o xo-4-aza-5 α-androst-1-ene-17β-carboxamide. The empirical formula of finasteride is C23H36N2O2 and its molecular weight is 372.55. Its structural formula is:


finasteride-structure


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.


Finasteride Tablets, USP is   film-coated  tablets  for  oral  administra tion.  Each  tablet  contains  1 mg of  finasteride  and  the  following  inactive  ingredients: lactose  monohydrate,  microcrystalline cellulose, pregelatinized  starch,  sodium  starch  glycolate, lauroylmacrogol 32 glycerides, magnesium stearate, Hypromellose, Titanium Dioxide,  polyethylene glycol, Iron Oxide Red, and Iron Oxide Yellow.


12 CLINICAL PHARMACOLOGY

12.1 Mechanism of Action

Finasteride is a competitive and specific inhibitor of Type II 5α-reductase, an intracellular enzyme that converts the androgen testosterone into DHT. Two disti nct isozymes are found in mice, rats, monkeys, and humans: Type I and II. Each of these isozymes is diff erentially expressed in tissues and developmental stages. In humans, Type I 5 α-reductase is predominant in the sebaceous glands of most regions of skin, including scalp, and liver. Type I 5 α-reductase is responsible for approximately one-third of circulating DHT. The Type II 5 α-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 5 α-reductase over Type I isozyme (IC50=500 and 4.2 nM for Type I and II, respectively). For both isozymes, the inhibition by finasteride is accompanied by reduct ion of the inhibitor to dihydrofinasteride and adduct formation with NADP+. The turnover for the enzyme complex is slow (t1/2 approximately 30 days for the Type II enzyme complex and 14 days for the Type I complex). Inhibition of Type II 5 α-reductase blocks the peripheral conversion of testosterone to DHT, res ulting in significant decreases in serum and tissue DHT concentrations.


In men with male pattern hair loss (androgenetic alopecia), the balding scalp contains miniaturized hair follicles and increased amounts of DHT compared with hairy scalp. Administration of finasteride decreases scalp and serum DHT concentrations in these men. The relative contributions of these reductions to the treatment effect of finasteride have not been defined. By this mechanism, finasteride appears to interrupt a key factor in the development of androgenetic alopecia in those patients genetically predisposed.

12.2 Pharmacodynamics

Finasteride produces a rapid reduction in serum DHT concentration, reaching 65% suppression within 24 hours of oral dosing with a 1-mg tablet. Mean cir culating levels of testosterone and estradiol were increased by approximately 15% as compared to bas eline, but these remained within the physiologic range.


Finasteride has no affinity for the androgen receptor and has no androgenic, antiandrogenic, estrogenic, antiestrogenic, or progestational effects. In studies with finasteride, no clinically meaningful changes in luteinizing hormone (LH), follicle-stimulating hormone (FSH) or prolactin were detected. In healthy volunteers, treatment with finasteride did not alt er the response of LH and FSH to gonadotropin-releasing hormone indicating that the hypothalamic-pituitary-testicular axis was not affected. Finasteride had no effect on circulating levels of cortisol, thyroid-sti mulating hormone, or thyroxine, nor did it affect the plasma lipid profile (e.g., total cholesterol, low-density lipoproteins, h igh-density lipoproteins and triglycerides) or bone mineral density.

12.3 Pharmacokinetics


Absorption

In a study in 15 healthy young male subjects, the mean bioavailability of finasteride 1-mg tablets was 65% (range 26 to 170%), based on the ratio of area under the curve (AUC) relative to an intravenous (IV) reference dose. At steady state following dosing with 1 mg/day (n=12), maximum finasteride plasma concentration averaged 9.2 ng/mL (range, 4.9 to 13.7 ng/mL) and was reached 1 to 2 hours postdose; AUC(0-24 hr) was 53 ng•hr/mL (range, 20 to 154 ng•hr/mL). Bioav ailability of finasteride was not affected by food.


Distribution

Mean steady-state volume of distribution was 76 liters (range, 44 to 96 liters; n=15). Approximately 90% of circulating finasteride is bound to plasma proteins. There is a slow accumulation phase for finasteride after multiple dosing.


Finasteride has been found to cross the blood-brain barrier.


Semen levels have been measured in 35 men taking finast eride 1 mg/day for 6 weeks. In 60% (21 of 35) of the samples, finasteride levels were undetectab le (<0.2 ng/mL). The mean finasteride level was 0.26 ng/mL and the highest level measured was 1.52 ng /mL. Using the highest semen level measured and assuming 100% absorption from a 5-mL ejaculate per day, human exposure through vaginal absorption would be up to 7.6 ng per day, which is 650-fold less than the dose of finasteride (5 µg) that had no effect on circulating DHT levels in men. [See Use in Specific Populations (8.1 ) .]

Metabolism

Finasteride is extensively metabolized in the live r, primarily via the cytochrome P450 3A4 enzyme subfamily. Two metabolites, the t-butyl side chain monohydroxylated and monocarboxylic acid metabolites, have been identified that possess no more than 20% of the 5α-reductase inhibitory activity of finasteride.


Excre tion

Following intravenous infusion in healthy young subje cts (n=15), mean plasma clearance of finasteride was 165 mL/min (range, 70 to 279 mL/min). Mean terminal half-life in plasma was 4.5 hours (range, 3.3 to 13.4 hours; n=12). Following an oral dose of 14C-finasteride in man (n=6), a mean of 39% (range, 32 to 46%) of the dose was excreted in the urine in the form of metabolites; 57% (range, 51 to 64%) was excreted in the fe ce s.


Mean terminal half-life is approximately 5 to 6 hours in men 18 to 60 years of age and 8 hours in men more than 70 years of age.


TABLE 3: Mean (SD) Pharmacokinetic Parameters in Healthy Men (ages 18 to 26) 
 
Mean (±SD)
n=15
Bioavailability
65% (26 to 170%)*
Clearance (mL/min)
165 (55)
Volume of Distribution (L)
76 (14)

*Range



TABLE 4: Mean (SD) Noncompartmental Pharmacokinetic Parameters After Multiple Doses of 1 mg/day in Healthy Men (ages 19 to 42)
 
Mean (±SD) (n=12)
AUC (ng.hr/mL)
53 (33.8)
Peak Concentration (ng/mL)
9.2 (2.6)
Time to Peak (hours)
1.3 (0.5)
Half-Life (hours)*
4.5 (1.6)

*First-dose values; all other parameters are last-dose values


Renal I mpair ment

No dosage adjustment is necessary in patients with renal impairment. In patients with chronic renal impairment, with creatinine clearances ranging f rom 9.0 to 55 mL/min, AUC, maximum plasma concentration, half-life, and protein binding after a single dose of 14C-finasteride were similar to those obtained in healthy volunteers. Urinary excretion of metabolites was decreased in patients with renal impairment. This decrease was associated with an increase in fecal excretion of metabolites. Plasma concentrations of metabolites were significantly higher in patients w ith renal impairment (based on a 60% increase in total radioactivity AUC). However, ifnasteride has been tolerated in men with normal renal function receiving up to 80 mg/day for 12 weeks where exposure of these patien ts to metabolites would presumably be much greater.


Hepatic I mpair ment

The effect of hepatic impairment on finasteride pharmacokinetics has not been studied. Caution should be used in the administration of finasteride tablets in patien ts with liver function abnormalities, as finasteride is metabolized extensively in the liver.

13 NONCLINICAL TOXICOLOGY

13.1 Carcinogenesis & Mutagenesis & Impairment Of Fertility

No evidence of a tumorigenic effect was observed in a 24-month study in Sprague-Dawley rats receiving doses of finasteride up to 160 mg/kg/day in males and 320 mg/kg/day in females. These doses produced respective systemic exposure in rats of 888 and 2192 times those observed in man receiving the recommended human dose of 1 mg/day. All exposure calculations were based on calculated AU C(0-24 hr)for animals and mean AU C(0-24 hr)  for man (0.05 µg•hr/mL).


In a 19-month carcinogenicity study in CD-1 mice, a statistically significant (p<0.05) increase in the incidence of testicular Leydig cell adenomas w as observed at 1824 times the human exposure (250 mg/kg/day). In mice at 184 times the human exposure, estimated (25 mg/kg/day) and in rats at 312 times the human exposure (>40 mg/kg/day) an increase in the incidence of Leydig cell hyperplasia was observed. A positive correlation between the proliferative changes in the Leydig cells and an increase in serum LH levels (2- to 3-fold above control) has been demonstrated in both rodent species treated with high doses of finasteride. No drug-related Leydig cell changes were seen in either rats or dogs treated with finasteride for 1 year at 240 and 2800 times (20 mg/kg/day and 45 mg/kg/day, respectively), or in mice treated for 19 months at 18.4 times the human exposure, estimated (2.5 mg/kg/day).


No evidence of mutagenicity was observed in an in vi tro bacterial mutagenesis assay, a mammalian cell mutagenesis assay, or in an in vi tro alkaline elution assay. In an in vi tro chromosome aberration assay, using Chinese hamster ovary cells, there was a slight increase in chromosome aberrations. In an in vivo chromosome aberration assay in mice, no treatment-related increase in chromosome aberration was observed with finasteride at the maximum tol erated dose of 250 mg/kg/day (1824 times the human exposure) as determined in the carcinogenicity studies. In sexually mature male rabbits treated with finasteride at 4344 times the human exposure (80 mg/kg/day) for up to 12 weeks, no effect on fertility, sperm count, or ejaculate volume was seen. In sexually mature male rats treated with 488 times the human exposure (80 mg/kg/day), there were no significant effects on fertility after 6 or 12 weeks of treatment; however, when treatment was continued for up to 24 or 30 weeks, there was an apparent decrease in fertility, fecundity, and an associated significant decrease in the weights of the seminal vesicles and p rostate. All these effects were reversible within 6 weeks of discontinuation of treatment. No drug-rel ated effect on testes or on mating performance has been seen in rats or rabbits. This de crease in fertility in finasteride-treated rats is secondary to its effect on accessory sex organs (prostate and seminal vesicles) resulting in failure to form a seminal plug. The seminal plug is essential for normal fertility in rats but is not relevant in man.

14 CLINICAL STUDIES

14.1 Studies in Men

The  efficacy  of  finasteride tablets  was  demonstrated  in men  (88%  Caucasian) with  mild  to  moderate androgenetic  alopecia  (male  pattern  hair  loss)  between  18  and  41 years of  age. In  order to  prevent seborrheic  dermatitis  which  might  confound  the  assess ment  of  hair growth in these studies, all men, whether  treated  with finasteride or placebo, were i nstructed  to  use a  specified, medicated, tar-based shampoo (Neutrogena T/Gel® Shampoo) during  the first 2 years of the studies.


There  were  three  double-blind,  randomized,  placebo- controlled  studies  of  12-month  duration.  The two primary endpoints were hair count and patient self-assessment; the two secondary endpoints were investigator  assessment  and  ratings  of  photographs.  In addition, information was collected regarding sexual  function  (based  on  a self-administered que stionnaire) and non-scalp body hair growth. The three studies  were  conducted  in  1879  men  with  mild  to   moderate,  but  not  complete,  hair  loss.  Two  of  the studies  enrolled  men  with  predominantly  mild  to  moderate  vertex  hair  loss  (n=1553). The third enrolled men  having  mild  to  moderate  hair  loss  in  the  anterior  mid-scalp  area with or without vertex balding (n=326).


Studies in Men with Vertex Baldness 

Of  the  men  who  completed  the  first  12  months  of  the  two  vertex  baldness  trials,  1215  elected  to  continue in double-blind, placebo-controlled, 12-month e xtension studies. There were 547 men receiving finasteride tablets for  both  the  initial  study  and  first  extension  periods  (up  to  2  years  of treatment) and 60 men receiving  placebo  for  the  same  periods.  The  extension  studies  were  continued  for  3  additional  years,  with 323 men on finasteride tablets and 23 on placebo ente ring  the fifth year of the study.


In  order  to  evaluate  the  effect  of  discontinuation  of therapy, there  were 65 men who received finasteride tablets for  the  initial  12  months  followed  by  placebo  in  the first 12-month extension period. Some of these men continued  in  additional  extension  studies  and  were  s witched  back to treatment with finasteride tablets with 32 men  entering  the  fifth  year  of  the  study.  Lastly, there were 543 men who received placebo for the initial 12 months  followed  by  finasteride tablets  in the first 12-month extension period. Some of these men continued in additional  extension  studies  receiving  finasteride tablets  with  290  men  entering  the  fifth  year  of the study (see Figure 1 below).


Hair counts were assessed by photog raphic enlargements of a representati ve area of active hair loss. In these two studies in men with vertex baldness, signif icant increases in hair count were demonstrated at 6 and  12  months in men  treated  with finasteride tablets, while significant hair loss from  baseline  was demonstrated  in  those  treated  with placebo. At 12 months there was a 107-hair difference from placebo (p<0.001,  finasteride tablets  [n=679]  vs  placebo  [n=672])  within  a  1-inch  diameter  circle  (5.1  cm2).  Hair  count was  maintained  in  those  men  taking  finasteride tablets  for  up  to  2  years,  resulting  in  a  138-hair  difference between  treatment  groups  (p<0.001,  finasteride tablets  [n=433]  vs  placebo  [n=47])  within  the  same  area.  In men  treated  with  finasteride tablets  the  maximum  impro vement  in  hair  count  compared  to  baseline was achieved  during  the  first 2 years. Although the initial improvement was followed by a slow decline, hair count  was  maintained  above  baseline  throughout the 5 years of the studies. Furthermore, because the decline  in  the  placebo  group  was  more  rapid,  the  difference  between  treatment  groups  also  continued  to increase  throughout  the  studies,  resulting  in  a  277 -hair  difference  (p<0.001,  finasteride tablets [n=219] vs placebo [n=15]) at 5 years (see Figure 1 below).


Patients  who  switched  from  placebo  to  finasteride tablets  (n =425)  had a decrease in hair count at the end of the initial  12-month  placebo period, followed by an increase in hair count after 1 year of treatment with finasteride tablets.  This  increase  in hair count was less (56 hairs above original baseline) than the increase (91 hairs above original baseline) observed after  1 year of treatment in men initially randomized to finasteride tablets.  Although  the  increase  in  hair  count,  relative  to  when therapy was initiated, was comparable between  these  two  groups,  a  higher  absolute hair count  was achieved in patients who were started on treatment  with  finasteride tablets in the initial study.  This advantage was maintained through the remaining 3 years  of  the  studies.  A  change  of  treatment  from  finasteride tablets  to  placebo  (n=48) at the end of the initial 12 months  resulted  in  reversal  of  the  increase  in  hair  count  12  months  later,  at  24  months (see Figure 1 below).


At  12  months,  58%  of  men in the placebo group had f urther hair loss (defined as any decrease in hair count  from  baseline),  compared  with  14%  of  men  treated  with  finasteride tablets.  In  men  treated  for  up  to  2 years,  72%  of  men in the pla cebo group demonstrated hair loss, compa red with 17% of men treated with finasteride tablets.  At  5  years,  100%  of  men  in  the  p lacebo  group  demonstrated  hair  loss,  compared  with  35% of men treated with finasteride tablets.


 

Figure 1


finasteride-figure1


Patient  self-assessment  was  obtained  at  each  clinic  visit  from  a  self-administered questionnaire, which included  questions on  their  perception of  hair growth,  hair loss,  and appearance. This  self-assessment demonstrated  an  increase  in  amount  of  hair,  a  dec rease  in  hair loss,  and  improvement in  appearance in men  treated  with  finasteride tablets.  Overall  improvement  compared  with  placebo  was  seen  as  early  as  3 months (p<0.05), with improve ment maintained  over 5 years.


Investigator  assessment  was  based  on  a 7-point scale e valuating increases or decreases in scalp hair at each  patient  visit.  This  assessment  showed  significantly  greater  increases  in hair growth in men treated with  finasteride tablets  compared  with placebo as early as 3 months (p<0.001). At 12 months, the investigators rated  65%  of  men  treated  with finasteride tablets as having increased hair growth compared with 37% in the placebo  group.  At  2 years, the investigators rated 80% of men treated with finasteride tablets as having increased  hair  growth  compared  with  47%  of  men  treated  with  placebo.  At  5  years,  the investigators rated 77%  of  men  treated  with  finasteride tablets  as having inc reased hair growth, compared with 15% of men treated with placebo.


An  independent  panel  rated  standardized  photographs  of  the  head  in  a blinded fashion based on increases  or  decreases  in  scalp  hair  using  the  same  7-point scale as the investigator assessment. At 12 months,  48%  of  men  treated  with  finasteride tablets mg had an increase as compared with 7% of men treated with placebo.  At 2 years, an increase in hair growth was demonstrated in 66% of men treated with finasteride tablets,  compared with 7% of men treated with placebo. At 5 years, 48% of men treated with finasteride tablets  demonstrated  an  increase in hair growth, 42% were rated as having no change (no further visible  progression  of  hair  loss  from  baseline)  and  10% were  rated  as  having  lost  hair  when  compared  to baseline.  In  comparison, 6%  of  men  treated  with  placebo  demonstrated  an  increase  in  hair  growth,  19% were rated as having no change and 75% were rated as  having lost hair when compared to baseline.


A  48-week,  placebo-controlled  study  designed to assess  by phototrichogram the effect of finasteride tablets on total  and  actively  growing  (anagen)  scalp  hairs  in  vertex  baldness  enrolled  212  men  with androgenetic alopecia.  At  baseline  and  48  weeks,  total  and  anagen  hair  counts  were  obtained  in  a  1-cm2 target  area  of the  scalp.  Men  treated  with  finasteride tablets  showed  increases  from  baseline  in  total  and  anagen  hair  counts of  7  hairs  and  18  hairs,  respectively,  whereas  men  treated  with  placebo  had decreases of 10 hairs and 9 hairs,  respectively.  These  changes  in  hair  counts  resulted  in  a  between-group  difference  of  17  hairs  in total  hair count (p<0.001) and 27 hairs in anagen hair count (p<0.001), and an improvement in the proportion of anagen hairs from 62% at basel ine to 68% for men treated with finasteride tablets.


Other Results in Vertex Baldness Studies 

A  sexual function questionnaire was self-administered  by patients participating in the two vertex baldness trials  to  detect  more subtle changes in  sexual function. At Month 12, statistically significant differences in favor of placebo were found in 3 of 4 domains (se xual interest, erections, and perception of sexual problems).  However,  no  significant  difference  was   seen  in  the  question  on  overall  satisfaction  with  sex life.


In  one  of  the  two  vertex  baldness  studies,  patients  were  questioned  on  non-scalp  body  hair growth. finasteride tablets did not appear  to affect non-scalp  body hair.


Study  in Men with Hair Loss in the Anterior Mid-Scalp Area 

A  study  of  12-month  duration,  designed  to  assess  the  efficacy  of  finasteride tablets in men with hair loss in the anterior  mid-scalp  area,  also  demonstrated significant increases in hair count compared with placebo. Increases  in  hair  count  were  accompanied  by  imp rovements  in  patient sel f-assessment, investigator assessment,  and  ratings  based  on standardized photograph s. Hair counts were obtained in the anterior mid-scalp area, and did not include the area of b itemporal recession or the anterior hairline.


Summary  of Clinical Studies in Men 

Clinical  studies  were  conducted  in  men  aged  18  to  41  with  mild  to  moderate  degrees  of  androgenetic alopecia.  All  men  treated  with  finasteride tablets or  placebo  received  a  tar-based  shampoo  (Neutrogena T/Gel® Shampoo)  during  the  first  2  years  of  the  studies. Clini cal improvement was seen as early as 3 months in the  patients  treated  with  finasteride tablets  and  led  to  a  net increase  in  scalp  hair  count  and  hair  regrowth.  In clinical  studies for up to 5 years, treatment with  finasteride tablets slowed the further progression of hair loss observed in the placebo group.  In general, the difference between treatment groups continued to increase throughout the 5 years of the studies.


Ethnic Anal ysis of Clinical Data from Men 

In  a  combined analysis of the two studies on ver tex baldness, mean hair count changes from baseline were  91 vs -19  hairs  (Finasteride tablets  vs  placebo)  among  Caucasians  (n=1185),  49 vs -27  hairs  among Blacks  (n=84),  53 vs -38  hairs among Asians ( n=17), 67 vs 5 hairs  among  Hispanics (n=45) and 67 vs -15  hairs  among  other  ethnic  groups  (n=20).  Patient  self-assessment  showed  improvement  across racial  groups  with  finasteride tablets  treatment,  except  for  satisfaction  of  the  frontal  hairline  and  vertex  in Black men, who were satisfied overall.



14.2 Study in Women

In  a  study  involving  137  postmenopausal  women  with  androgenetic  alopecia who were treated with finasteride tablets  (n=67)  or  placebo  (n=70)  for  12  month s,  effectiveness  could  not be demonstrated. There was no  improvement  in  hair  counts,  patient  self-assessment,  investigator  assessment,  or ratings of standardized  photographs  in  the  women  treated  with  finasteride tablets  when compared with the placebo group[see Indications and Usage (1)].

16 HOW SUPPLIED/STORAGE AND HANDLING


Finasteride tablets, USP 1 mg are available as  reddish brown colored, 7 mm round, biconvex, film-coated tablets, marked “F1” on one side and plain on other side. They are supplied  as follows:


30’s HDPE Container pack: NDC 67877-455-30

90’s HDPE Container pack: NDC 67877-455-90

500’s HDPE Container pack: NDC 67877-455-05

30 (3 x 10) Unit Dose Tablets (Alu-PVC/PVDC Pack): NDC 67877-455-94


Storage and Handling 

Store at 20º to 25ºC (68º to 77ºF) [See USP Controlled Room Temperature]. Preserve in a tight, light-resistant container


Women  should  not  handle crushed or broken Finasteride Tablets when they are pregnant or may potentially be pregnant  because  of the possibility of absorption of finasteride and the subsequent potential  risk  to  a  male  fetus.  Finasteride Tablets, USP 1 mg are  coated  and  will  prevent  contact  with  the  active ingredient  during normal handling, provided that the tablets are not broken or crushed [ see  Warnings  and  Precautions  (5.1)Use  in  Specific  Populations   (8.1)and Patient  Counseling  Infor mation  (17.1)] .

17 PATIENT COUNSELING INFORMATION


See FDA-approved patient labeling (Patient Information).


17.1 Exposure of Women — Risk to Male Fetus

Physicians  should  inform  patients  that  women  who  are  pregnant  or  may  potentially  be  pregnant  should not  handle  crushed  or  broken  finasteride tablets  because  of  the  possibility  of  absorption  of  finasteride and  the  subsequent  potential  risk  to  a  male  fetus.  Finasteride tablets are coated and will prevent contact with  the  active  ingredient  during  normal  handling,  provided that the table ts  have not  been broken or crushed.  If  a  woman  who  is  pregnant  or  may  potenti ally  be pregnant comes in contact with crushed or broken  finasteride tablets,  the  contact  area   should  be  washed  immediately  with  soap  and  water [see Contraindications (4), Warnings and Precautions (5.1)Use in Specific Populations (8.1) and How Supplied/Storage and Handling (16)].


17.2 Increased Risk of High-Grade Prostate Cancer

Patients should be informed that there was an increase in high-grade prostate cancer in men treated with 5α-reductase inhibitors indicated for BPH treatment, compared to those treated with placebo in studies looking at the use of these drugs to prevent prostate cancer [see Warnings and Precautions (5.3) and Adverse Reactions (6.1)].


17.3 Additional Instructions

Physicians  should  instruct  their  patients  to  promptly  report  any  changes  in  their  breasts  such  as  lumps, pain  or  nipple  discharge.  Breast  changes  including  breast  enlargement,  tenderness  and  neoplasm  have been  reported [see Adverse Reactions (6.1)].


Physicians should instruct their patients to read the patient package insert be fore starting therapy with finasteride tablets and to read it again each time the prescript ion is renewed so that they are aware of current information for patients regarding  finasteride tablets.


The trademarks depicted herein are owned by their respective companies.

Manufactured by:

Alkem Laboratories Ltd.

Mumbai - 400 013, INDIA

Distributed by:

Ascend Laboratories, LLC

Parsippany, NJ 07054

Revised: January 2017


PT 2307-01

Patient Information

Finasteride Tablets, USP
(fin NAH steh ride)


Finasteride tablets, USP is for use by MEN ONLY and should NOT be used by women or children.


Read  this  Patient  Information  before  you  start  taking  finasteride tablets, USP and  each  time  you  get  a  refill.  There may  be  new  information.  This  information  does not take the place of talking with your healthcare provider about your medical condition or treatment.


What is finasteride tablets, USP? 


Finasteride tablets, USP is  a  prescription  medicine  used  for  the  treatment  of  male  pattern  hair  loss  (androgenetic alopecia).


It  is  not  known  if  finasteride tablets, USP works  for  a  reced ing  hairline  on  either  side  of  and  above  your  forehead (temporal area).


Finasteride tablets, USP is not for use by   women and children.

 

Who should not take finasteride tablets, USP? 

Do not take finasteride tablets, USP if you: 

·                are pregnant or may become pregnant. Finasteride Tablets, USP 1 mg may harm your unborn baby.

o      Finasteride tablets, USP are coated and will prevent  contact with the medicine during handling, as  long  as  the  tablets  are  not  broken  or crushed. Females who are pregnant or who may become pregnant should not come in contact with broken or crushed finasteride tablets, USP. If  a  pregnant  woman  comes  in  contact  with c rushed or broken finasteride tablets, USP, wash the  contact  area  right  away  with  soap  and  w ater.  If  a  woman who is pregnant comes into contact  with the active ingredient in  finasteride tablets, USP, a healthcare provider should be consulted.

o      If  a  woman  who  is  pregnant  with  a  male  baby  swallows  or  comes  in  contact  with  the medicine in finasteride tablets, USP, the male baby may be  born with sex organs that are not normal.

·                are  allergic  to  any  of  the  ingredients  in  finasteride tablets, USP.  See  the  end  of  this  leaflet  for  a  complete  list of ingredients in finasteride tablets, USP.


What should I tell my  healthcare pro vider before taking finasteride tablets, USP?

Before taking finasteride tablets, USP,  tell your healthcare provider if you:


·                have any other medical conditions, including  problems with your prostate or liver


Tell   your  healthcare  pro vider  about  all  the  medicines   you  take,  including  prescription  and  non- prescription medicines, vitamins, and herbal supplements.


Know  the  medicines  you  take.  Keep  a  list  of  them  to  show  your  healthcare  provider  and  pharmacist  when you get a new medicine.


How  should I take finasteride tablets, USP? 

·                Take finasteride tablets, USP exactly as your healt hcare provider tells you to take it.

·                You may take finasteride tablets, USP with or without food.

·                If you forget to ta ke finasteride tablets, USP, do not take an extra tablet. Just take the next tablet as usual. 


Finasteride tablets, USP will not  work faster or better if you take it more than once a day.


What are the possible side effects of Finasteride tablets, USP? 


·                decrease  in   your  blood  Prostate  Specific  Antigen  (PSA)  le vels.  Finasteride tablets, USP  can  affect  a  blood test  called  PSA  (Prostate-Specific  Antigen)  for  the  screening  of  prostate  cancer.  If  you  have  a PSA  test  done  you  should  tell  your  healthcare  pro vider  that you are taking finasteride tablets, USP because finasteride tablets, USP decreases  PSA  level s.  Changes  in PSA levels will need to be evaluated by your healthcare  provider.  Any  increase  in  follow-up  PSA  l evels  from  their lowest point may signal the presence of prostate cancer and should be evaluated, even if the test results are still within the normal  range  for  men  not  taking  finasteride tablets, USP.  You  should  also  tell your healthcare provider if you have  not  been  taking  finasteride tablets, USP  as  prescribed  because  this  may  affect  the  PSA  test  results. For more information, talk to your healthcare provider.

·                There may be an increased  risk  of a  more  serious form  of  prostate  cancer  in  men taking finasteride at 5 times the dose of finasteride tablets, USP.


The most common side effects of finasteride tablets, USP include:

·                decrease in sex drive

·                trouble getting or keeping an erection

·                a decrease in the amount of semen


The following have been reported in general use with finasteride tablets, USP:


·                breast  tenderness  and  enlargement.  Tell  your  healt hcare  provider  about  any  changes  in  your breasts such as lumps, pain or nipple discharge.

·                depression;

·                decrease in sex drive that con tinued after stopping the medication;

·                allergic reactions including rash, itching, hiv es and swelling of the lips, tongue, throat, and face;

·                problems with ejaculation that continued after stopping medication;

·                testicular pain;

·                difficulty in achieving an erection that continued after stopping the medication;

·                male infertility and/or poor quality of semen.

·                in rare cases, male breast cancer.


Tell your healthcare provider if you have any side  effect that bothers you or that does not go away.


These  are  not  all  the  possible  side  effects  of  finasteride tablets, USP.  For  more  information,  ask  your  healthcare provider or pharmacist.


Call  your  doctor  for  medical  advice  about  side  effects.  You  may  report  side  effects  to  FDA  at  1-800-FDA-1088.


How  should I store Finasteride Tablets, USP 1 mg? 


·                Store finasteride tablets, USP at room temperature between 68˚F to 77˚F (20˚C to 25˚C).

·                Keep Finasteride Tablets, USP 1 mg  in a  closed container  and  keep finasteride tablets, USP  dry (protect from moisture).


Keep finasteride tablets, USP and all medici nes out of the reach of children.

 

General information about the safe and effecti ve use of finasteride tablets, USP. 


Medicines  are  sometimes  prescribed  for  purposes  other  than  those  listed  in  this  Patient  Information leaflet.  Do  not  use finasteride tablets, USP for a condition for which it was not prescribed. Do not give finasteride tablets, USP to other people, even if they have the same  symptoms you have. It may harm them.


This  Patient  Information  leaflet  summarizes  the  most  important  information  about  finasteride tablets, USP.  If  you would like more information, talk with your  healthcare  provider. You  can ask  your pharmacist or healthcare  provider  for  information  about  finasteride tablets, USP that  is  written  for  health  professionals. For more information go to http://www.ascendlaboratories.com or call 1-877-ASC-RX01 (877-272-7901).


What are the ingredients in finasteride tablets, USP? 

Active ingredient: Finasteride, USP

Inactive ingredients: lactose  monohydrate,  microcrystalline cellulose, pregelatinized  starch,  sodium  starch  glycolate, lauroylmacrogol 32 glycerides, magnesium stearate, hypromellose, titanium dioxide,  polyethylene glycol, iron oxide red, and iron oxide yellow.


This Patient Information has been approved by the U.S. Food and Drug Administration. 

 

Manufactured by:

Alkem Laboratories Ltd.

Mumbai - 400 013, INDIA


Distributed by:

Ascend Laboratories, LLC

Parsippany, NJ 07054


Revised: January 2017

PT 2328-01

PACKAGE LABEL.PRINCIPAL DISPLAY PANEL



FINASTERIDE TABLETS, USP 1 MG

Warning: Finasteride Tablets, USP 1 mg should not be used by women or children. Women who are or may potentially be pregnant must not use Finasteride Tablets, USP 1 mg. They should also not handle crushed or broken tablets of Finasteride Tablets, USP 1 mg. (See Package Insert.)
Rx only
30 Tablets


finasteride-1mg-30s

FINASTERIDE TABLETS, USP 1 MG
Warning: Finasteride Tablets, USP 1 mg should not be used by women or children. Women who are or may potentially be pregnant must not use Finasteride Tablets, USP 1 mg. They should also not handle crushed or broken tablets of Finasteride Tablets, USP 1 mg. (See Package Insert.)
Rx only
90 Tablets
finasteride-1mg-90s
FINASTERIDE TABLETS, USP 1 MG

Warning: Finasteride Tablets, USP 1 mg should not be used by women or children. Women who are or may potentially be pregnant must not use Finasteride Tablets, USP 1 mg. They should also not handle crushed or broken tablets of Finasteride Tablets, USP 1 mg. (See Package Insert.)
Rx only
500 Tablets


finasteride-1mg-500s

FINASTERIDE 
finasteride tablet, coated
Product Information
Product Type HUMAN PRESCRIPTION DRUG Item Code (Source) NDC:67877-455
Route of Administration ORAL
Active Ingredient/Active Moiety
Ingredient Name Basis of Strength Strength
FINASTERIDE (UNII: 57GNO57U7G) (FINASTERIDE - UNII:57GNO57U7G) FINASTERIDE 1 mg
Inactive Ingredients
Ingredient Name Strength
LACTOSE MONOHYDRATE (UNII: EWQ57Q8I5X)  
MICROCRYSTALLINE CELLULOSE (UNII: OP1R32D61U)  
STARCH, CORN (UNII: O8232NY3SJ)  
SODIUM STARCH GLYCOLATE TYPE A POTATO (UNII: 5856J3G2A2)  
MAGNESIUM STEARATE (UNII: 70097M6I30)  
LAUROYL PEG-32 GLYCERIDES (UNII: H5ZC52369M)  
HYPROMELLOSE 2910 (6 MPA.S) (UNII: 0WZ8WG20P6)  
TITANIUM DIOXIDE (UNII: 15FIX9V2JP)  
POLYETHYLENE GLYCOL 6000 (UNII: 30IQX730WE)  
FERRIC OXIDE RED (UNII: 1K09F3G675)  
FERRIC OXIDE YELLOW (UNII: EX438O2MRT)  
Product Characteristics
Color RED (REDDISH BROWN) Score no score
Shape ROUND (biconvex) Size 7mm
Flavor Imprint Code F1
Contains     
Packaging
# Item Code Package Description Marketing Start Date Marketing End Date
1 NDC:67877-455-30 30 in 1 BOTTLE; Type 0: Not a Combination Product 01/06/2017
2 NDC:67877-455-90 90 in 1 BOTTLE; Type 0: Not a Combination Product 01/06/2017
3 NDC:67877-455-05 500 in 1 BOTTLE; Type 0: Not a Combination Product 01/06/2017
4 NDC:67877-455-94 3 in 1 CARTON 01/06/2017
4 NDC:67877-455-34 10 in 1 BLISTER PACK; Type 0: Not a Combination Product
Marketing Information
Marketing Category Application Number or Monograph Citation Marketing Start Date Marketing End Date
ANDA ANDA207750 01/06/2017
Labeler - Ascend Laboratories, LLC (141250469)
Establishment
Name Address ID/FEI Business Operations
Alkem Laboratories Limited 677605851 MANUFACTURE(67877-455)

Revised: 3/2019
Document Id: da6af33e-f661-436c-b5ed-8e35e1c01050
Set id: ecd2fbb2-a4bd-44f2-831d-179e7dbf0741
Version: 7
Effective Time: 20190301
 
Ascend Laboratories, LLC