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All about: Femara

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Generic Name: letrozole
Dosage Form: Tablets




      (letrozole tablets)

      2.5 mg Tablets

      Rx only

Prescribing Information

Femara Description

Femara® (letrozole tablets) for oral administration contains 2.5 mg of letrozole, a nonsteroidal aromatase inhibitor (inhibitor of estrogen synthesis). It is chemically described as 4,4'-(1H-1,2,4-Triazol-1-ylmethylene)dibenzonitrile, and its structural formula is


      Letrozole is a white to yellowish crystalline powder, practically odorless, freely soluble in dichloromethane, slightly soluble in ethanol, and practically insoluble in water. It has a molecular weight of 285.31, empirical formula C17H11N5, and a melting range of 184°C-185°C.

      Femara® (letrozole tablets) is available as 2.5 mg tablets for oral administration.

     Inactive Ingredients. Colloidal silicon dioxide, ferric oxide, hydroxypropyl methylcellulose, lactose monohydrate, magnesium stearate, maize starch, microcrystalline cellulose, polyethylene glycol, sodium starch glycolate, talc, and titanium dioxide.

Femara - Clinical Pharmacology

Mechanism of Action

The growth of some cancers of the breast is stimulated or maintained by estrogens. Treatment of breast cancer thought to be hormonally responsive (i.e., estrogen and/or progesterone receptor positive or receptor unknown) has included a variety of efforts to decrease estrogen levels (ovariectomy, adrenalectomy, hypophysectomy) or inhibit estrogen effects (antiestrogens and progestational agents). These interventions lead to decreased tumor mass or delayed progression of tumor growth in some women.

      In postmenopausal women, estrogens are mainly derived from the action of the aromatase enzyme, which converts adrenal androgens (primarily androstenedione and testosterone) to estrone and estradiol. The suppression of estrogen biosynthesis in peripheral tissues and in the cancer tissue itself can therefore be achieved by specifically inhibiting the aromatase enzyme.

      Letrozole is a nonsteroidal competitive inhibitor of the aromatase enzyme system; it inhibits the conversion of androgens to estrogens. In adult nontumor- and tumor-bearing female animals, letrozole is as effective as ovariectomy in reducing uterine weight, elevating serum LH, and causing the regression of estrogen-dependent tumors. In contrast to ovariectomy, treatment with letrozole does not lead to an increase in serum FSH. Letrozole selectively inhibits gonadal steroidogenesis but has no significant effect on adrenal mineralocorticoid or glucocorticoid synthesis.

      Letrozole inhibits the aromatase enzyme by competitively binding to the heme of the cytochrome P450 subunit of the enzyme, resulting in a reduction of estrogen biosynthesis in all tissues. Treatment of women with letrozole significantly lowers serum estrone, estradiol and estrone sulfate and has not been shown to significantly affect adrenal corticosteroid synthesis, aldosterone synthesis, or synthesis of thyroid hormones.


Letrozole is rapidly and completely absorbed from the gastrointestinal tract and absorption is not affected by food. It is metabolized slowly to an inactive metabolite whose glucuronide conjugate is excreted renally, representing the major clearance pathway. About 90% of radiolabeled letrozole is recovered in urine. Letrozole’s terminal elimination half-life is about 2 days and steady-state plasma concentration after daily 2.5 mg dosing is reached in 2-6 weeks. Plasma concentrations at steady state are 1.5 to 2 times higher than predicted from the concentrations measured after a single dose, indicating a slight non-linearity in the pharmacokinetics of letrozole upon daily administration of 2.5 mg. These steady-state levels are maintained over extended periods, however, and continuous accumulation of letrozole does not occur. Letrozole is weakly protein bound and has a large volume of distribution (approximately 1.9 L/kg).

Metabolism and Excretion

Metabolism to a pharmacologically-inactive carbinol metabolite (4,4'-methanol-bisbenzonitrile) and renal excretion of the glucuronide conjugate of this metabolite is the major pathway of letrozole clearance. Of the radiolabel recovered in urine, at least 75% was the glucuronide of the carbinol metabolite, about 9% was two unidentified metabolites, and 6% was unchanged letrozole.

      In human microsomes with specific CYP isozyme activity, CYP3A4 metabolized letrozole to the carbinol metabolite while CYP2A6 formed both this metabolite and its ketone analog. In human liver microsomes, letrozole strongly inhibited CYP2A6 and moderately inhibited CYP2C19.

Special Populations

Pediatric, Geriatric and Race

In the study populations (adults ranging in age from 35 to >80 years), no change in pharmacokinetic parameters was observed with increasing age. Differences in letrozole pharmacokinetics between adult and pediatric populations have not been studied. Differences in letrozole pharmacokinetics due to race have not been studied.

Renal Insufficiency

In a study of volunteers with varying renal function (24-hour creatinine clearance: 9-116 mL/min), no effect of renal function on the pharmacokinetics of single doses of 2.5 mg of Femara® (letrozole tablets) was found. In addition, in a study of 347 patients with advanced breast cancer, about half of whom received 2.5 mg Femara and half 0.5 mg Femara, renal impairment (calculated creatinine clearance: 20-50 mL/min) did not affect steady-state plasma letrozole concentration.

Hepatic Insufficiency

In a study of subjects with mild to moderate non-metastatic hepatic dysfunction (e.g., cirrhosis, Child-Pugh classification A and B), the mean AUC values of the volunteers with moderate hepatic impairment were 37% higher than in normal subjects, but still within the range seen in subjects without impaired function. In a pharmacokinetics study, subjects with liver cirrhosis and severe hepatic impairment (Child-Pugh classification C, which included bilirubins about 2-11 times ULN with minimal to severe ascites) had two-fold increase in exposure (AUC) and 47% reduction in systemic clearance. Breast cancer patients with severe hepatic impairment are thus expected to be exposed to higher levels of letrozole than patients with normal liver function receiving similar doses of this drug. (See DOSAGE AND ADMINISTRATION, Hepatic Impairment.)

Drug/Drug Interactions

A pharmacokinetic interaction study with cimetidine showed no clinically significant effect on letrozole pharmacokinetics. An interaction study with warfarin showed no clinically significant effect of letrozole on warfarin pharmacokinetics. In in-vitro experiments, letrozole showed no significant inhibition in the metabolism of diazepam. Similarly, no significant inhibition of letrozole metabolism by diazepam was observed.

      Coadministration of Femara and tamoxifen 20 mg daily resulted in a reduction of letrozole plasma levels of 38% on average. Clinical experience in the second-line breast cancer pivotal trials indicates that the therapeutic effect of Femara therapy is not impaired if Femara is administered immediately after tamoxifen.

      There is no clinical experience to date on the use of Femara in combination with other anticancer agents.


In postmenopausal patients with advanced breast cancer, daily doses of 0.1 mg to 5 mg Femara suppress plasma concentrations of estradiol, estrone, and estrone sulfate by 75%-95% from baseline with maximal suppression achieved within two-three days. Suppression is dose-related, with doses of 0.5 mg and higher giving many values of estrone and estrone sulfate that were below the limit of detection in the assays. Estrogen suppression was maintained throughout treatment in all patients treated at 0.5 mg or higher.

      Letrozole is highly specific in inhibiting aromatase activity. There is no impairment of adrenal steroidogenesis. No clinically-relevant changes were found in the plasma concentrations of cortisol, aldosterone, 11-deoxycortisol, 17-hydroxy-progesterone, ACTH or in plasma renin activity among postmenopausal patients treated with a daily dose of Femara 0.1 mg to 5 mg. The ACTH stimulation test performed after 6 and 12 weeks of treatment with daily doses of 0.1, 0.25, 0.5, 1, 2.5, and 5 mg did not indicate any attenuation of aldosterone or cortisol production. Glucocorticoid or mineralocorticoid supplementation is, therefore, not necessary.

      No changes were noted in plasma concentrations of androgens (androstenedione and testosterone) among healthy postmenopausal women after 0.1, 0.5, and 2.5 mg single doses of Femara or in plasma concentrations of androstenedione among postmenopausal patients treated with daily doses of 0.1 mg to 5 mg. This indicates that the blockade of estrogen biosynthesis does not lead to accumulation of androgenic precursors. Plasma levels of LH and FSH were not affected by letrozole in patients, nor was thyroid function as evaluated by TSH levels, T3 uptake, and T4 levels.

Clinical Studies

Adjuvant Treatment of Early Breast Cancer in Postmenopausal Women

A multicenter, double-blind study randomized over 8,000 postmenopausal women with resected, receptor-positive early breast cancer to one of the following arms:

  1. tamoxifen for 5 years
  2. Femara for 5 years
  3. tamoxifen for 2 years followed by Femara for 3 years
  4. Femara for 2 years followed by tamoxifen for 3 years

Median treatment duration was 24 months, median follow-up duration was 26 months, 76% of the patients have been followed for more than 2 years, and 16% of patients for 5 years or longer.

      Data in Table 2 reflect results from non-switching arms (arms A and B) together with data truncated 30 days after the switch in the two switching arms (arms C and D). The analysis of monotherapy vs sequencing of endocrine treatments will be conducted when the necessary number of events has been achieved. Selected baseline characteristics for the study population are shown in Table 1. 

Table 1:      Selected Study Population Demographics for Adjuvant Study (ITT Population)
Baseline Status Femara® tamoxifen
N=4003 N=4007
Age (median, years) 61 61
Age Range (years) 38-89 39-90
Hormone Receptor Status (%)
ER+ and/or PgR+ 99.7 99.7
Both Unknown 0.3 0.3
Nodal Status (%)
Node Negative 52 52
Node Positive 41 41
Nodal Status Unknown 7 7
Prior Adjuvant Chemotherapy (%) 25 25

Table 2: Adjuvant Study Results
Femara® tamoxifen Hazard Ratio P-Value
N=4003 N=4007 (95 % CI)
Disease-Free Survival1 296 369 0.79 (0.68, 0.92) 0.002
Node Positive 0.71 (0.59, 0.86) 0.0005
Node Negative 0.92 (0.70, 1.22) 0.572
Prior Adjuvant Chemotherapy 0.70 (0.53, 0.93) 0.013
No Chemotherapy 0.83 (0.69, 1.00) 0.046
Systemic Disease-Free Survival2 268 321 0.83 (0.70, 0.97) 0.022
Time to Distant Metastasis3  184 249 0.73 (0.60, 0.88) 0.001
Node Positive 0.67 (0.54, 0.84) 0.0005
Node Negative 0.90 (0.60, 1.34) 0.597
Prior Adjuvant Chemotherapy 0.69 (0.50, 0.95) 0.024
No Chemotherapy 0.75; (0.60, 0.95) 0.018
Contralateral Breast Cancer 19 31 0.61 (0.35, 1.08) 0.091
Overall Survival 166 192 0.86 (0.70, 1.06) 0.155
Node Positive 0.81 (0.63, 1.05) 0.113
Node Negative 0.88 (0.59, 1.30) 0.507
Prior Adjuvant Chemotherapy 0.76 (0.51, 1.14) 0.185
No Chemotherapy 0.90 (0.71, 1.15) 0.395
*Definition of
1 Disease-Free Survival: Time from randomization to the earliest occurrence of invasive loco-regional recurrence, distant
metastases, invasive contralateral breast cancer, or death from any cause.
2Systemic Disease-Free Survival: Time from randomization to invasive regional recurrence, distant metastases, or death from
any cause.
3Time to Distant Metastasis: Time from randomization to distant metastases.

Figure 1 shows the Kaplan-Meier curves for Disease-Free Survival.

Extended Adjuvant Treatment of Early Breast Cancer in Postmenopausal Women After Completion of 5 Years of Adjuvant Tamoxifen Therapy

A double-blind, randomized, placebo-controlled trial of Femara® (letrozole tablets) was performed in over 5,100 postmenopausal women with receptor-positive or unknown primary breast cancer who were disease free after 5 years of adjuvant treatment with tamoxifen. Patients had to be within 3 months of completing the 5 years of tamoxifen.

      The planned duration of treatment for patients in the study was 5 years, but the trial was terminated early because of an interim analysis showing a favorable Femara effect on time without recurrence or contralateral breast cancer. At the time of unblinding, women had been followed for a median of 28 months, 30% of patients had completed 3 or more years of follow-up and less than 1% of patients had completed 5 years of follow-up.

      Selected baseline characteristics for the study population are shown in Table 3. 

Table 3: Selected Study Population Demographics (Modified ITT Population)
Baseline Status Femara® Placebo
N=2582 N=2586
Hormone Receptor Status (%)
ER+ and/or PgR+ 98 98
Both Unknown 2 2
Nodal Status (%)
Node Negative 50 50
Node Positive 46 46
Nodal Status Unknown 4 4
Chemotherapy 46 46

      Table 4 shows the study results. Disease-free survival was measured as the time from randomization to the earliest event of loco-regional or distant recurrence of the primary disease or development of contralateral breast cancer or death. Data were premature for an analysis of survival.

Table 4: Extended Adjuvant Study Results
N = 2582
N = 2586
Hazard Ratio
(95% CI)
Disease Free Survival (DFS) 122 (4.7%) 193 (7.5%) 0.62 (0.49, 0.78)1 0.00003
(First event of loco-regional recurrence,
distant relapse, contralateral breast cancer
or death from any cause)
Local Breast Recurrence 9 22
Local Chest Wall Recurrence 2 8
Regional Recurrence 7 4  
Distant Recurrence 55 92 0.61 (0.44 - 0.84) 0.003
Contralateral Breast Cancer 19 29
Deaths Without Recurrence or Contralateral Breast Cancer 30 38
DFS by Stratification    
Receptor Status
-      Positive 117/2527(4.6%) 190/2530(7.5%) 0.60(0.48,0.76)
-      Unknown 5/55(9.1%) 3/56(5.4%) 1.78(0.43,7.5)
Nodal Status
-      Positive 77/1184(6.5%) 123/1187(10.4) 0.61(0.46,0.81)
-      Negative 39/1298(3.0%) 63/1301(4.8%) 0.61(0.41,0.91)
-      Unknown 6/100(6.0%) 7/98(7.1%) 0.81(0.27,2.4)
Adjuvant Chemotherapy
-      Yes 58/1197(4.8%) 88/1199(7.3%) 0.64(0.46,0.90)
-      No 64/1385(4.6%) 105/1387(7.6%) 0.60(0.44,0.81)
CI = confidence interval for hazard ratio. Hazard ratio of less than 1.0 indicates difference in favor of Femara (lesser
risk of recurrence); hazard ratio greater than 1.0 indicates difference in favor of placebo (higher risk of recurrence with
1 Analysis stratified by receptor status, nodal status and prior adjuvant chemotherapy (stratification factors as at
randomization). P-value based on stratified logrank test.

First-Line Breast Cancer

A randomized, double-blinded, multinational trial compared Femara 2.5 mg with tamoxifen 20 mg in 916 postmenopausal patients with locally advanced (Stage IIIB or loco-regional recurrence not amenable to treatment with surgery or radiation) or metastatic breast cancer. Time to progression (TTP) was the primary endpoint of the trial. Selected baseline characteristics for this study are shown in Table 5.

Table 5: Selected Study Population Demographics
Baseline Status Femara® tamoxifen
N=458 N=458
Stage of Disease
      IIIB 6% 7%
      IV 93% 92%
Receptor Status
      ER and PgR Positive 38% 41%
      ER or PgR Positive 26% 26%
      Both Unknown 34% 33%
      ER- or PgR- / Other Unknown <1% 0
Previous Antiestrogen Therapy
      Adjuvant 19% 18%
      None 81% 82%
Dominant Site of Disease
      Soft Tissue 25% 25%
      Bone 32% 29%
      Viscera 43% 46%

Femara was superior to tamoxifen in TTP and rate of objective tumor response (see Table 6).

Table 6 summarizes the results of the trial, with a total median follow-up of approximately 32 months. (All analyses are unadjusted and use 2-sided P-values.)

Table 6: Results
Femara® tamoxifen Hazard or Odds
2.5 mg 20 mg Ratio (95% CI)
N=453 N=454 P-Value (2-Sided)
Median Time to Progression 9.4 months 6.0 months 0.72 (0.62, 0.83)1
Objective Response Rate
      (CR + PR) 145 (32%) 95 (21%) 1.77 (1.31, 2.39)2
      (CR) 42 (9%) 15 (3%) 2.99 (1.63, 5.47)2
Duration of Objective Response
      Median 18 months 16 months
(N=145) (N=95)
Overall Survival 35 months 32 months
(N=458) (N=458) P=0.51363

1 Hazard ratio

2 Odds ratio

3 Overall logrank test

      Figure 2 shows the Kaplan-Meier curves for TTP.

      Table 7 shows results in the subgroup of women who had received prior antiestrogen adjuvant therapy, Table 8, results by disease site and Table 9, the results by receptor status.

Table 7: Efficacy in Patients Who Received PriorAntiestrogen Therapy
Variable Femara ® tamoxifen
2.5 mg 20 mg
N=84 N=83
Median Time to
Progression (95% CI)
8.9 months (6.2, 12.5) 5.9 months (3.2, 6.2)
Hazard Ratio for
TTP (95% CI)
0.60 (0.43, 0.84)
Objective Response Rate
      (CR + PR) 22 (26%) 7 (8%)
      Odds Ratio for
Response (95% CI)
3.85 (1.50, 9.60)

Hazard ratio less than 1 or odds ratio greater than 1 favors Femara; hazard ratio greater than 1 or odds ratio less than 1 favors tamoxifen.

Table 8: Efficacy by Disease Site
Femara® tamoxifen
2.5 mg 20 mg
Dominant Disease Site
      Soft Tissue: N=113 N=115
           Median TTP 12.1 months 6.4 months
           Objective Response Rate 50% 34%
     Bone: N=145 N=131
           Median TTP 9.5 months 6.3 months
           Objective Response Rate 23% 15%
     Viscera: N=195 N=208
           Median TTP 8.3 months 4.6 months
           Objective Response Rate 28% 17%

Table 9: Efficacy by Receptor Status
Variable Femara® tamoxifen
2.5 mg 20 mg
Receptor Positive N=294 N=305
Median Time to
Progression (95% CI)
9.4 months (8.9, 11.8) 6.0 months (5.1, 8.5)
Hazard Ratio for
TTP (95% CI)
0.69 (0.58, 0.83)
Objective Response
Rate (CR+PR)
97 (33%) 66 (22%)
Odds Ratio for Response
95% CI)
1.78 (1.20, 2.60)
Receptor Unknown N=159 N=149
Median Time to
Progression (95% CI)
9.2 months (6.1, 12.3) 6.0 months (4.1, 6.4)
Hazard Ratio for
TTP (95% CI)
0.77 (0.60, 0.99)
Objective Response
Rate (CR+PR)
48 (30%) 29 (20%)
Odds Ratio for Response
(95% CI)
1.79 (1.10, 3.00)

Hazard ratio less than 1 or odds ratio greater than 1 favors Femara; hazard ratio greater than 1 or odds ratio less than 1 favors tamoxifen.

Figure 3 shows the Kaplan-Meier curves for survival.


Legend: Randomized Femara: n=458, events 57%, median overall survival 35 months (95% CI 32 to 38 months)

Randomized tamoxifen: n=458, events 57%, median overall survival 32 months (95% CI 28 to 37 months)

Overall logrank P=0.5136 (i.e., there was no significant difference between treatment arms in overall survival).

      The median overall survival was 35 months for the Femara group and 32 months for the tamoxifen group, with a P-value 0.5136.

      Study design allowed patients to cross over upon progression to the other therapy. Approximately 50% of patients crossed over to the opposite treatment arm and almost all patients who crossed over had done so by 36 months. The median time to cross over was 17 months (Femara to tamoxifen) and 13 months (tamoxifen to Femara). In patients who did not cross over to the opposite treatment arm, median survival was 35 months with Femara (n=219, 95% Cl 29 to 43 months) vs 20 months with tamoxifen (n=229, 95% Cl 16 to 26 months).

Second-Line Breast Cancer

Femara was initially studied at doses of 0.1 mg to 5.0 mg daily in six non-comparative Phase I/II trials in 181 postmenopausal estrogen/progesterone receptor positive or unknown advanced breast cancer patients previously treated with at least antiestrogen therapy. Patients had received other hormonal therapies and also may have received cytotoxic therapy. Eight (20%) of forty patients treated with Femara 2.5 mg daily in Phase I/II trials achieved an objective tumor response (complete or partial response).

      Two large randomized, controlled, multinational (predominantly European) trials were conducted in patients with advanced breast cancer who had progressed despite antiestrogen therapy. Patients were randomized to Femara 0.5 mg daily, Femara 2.5 mg daily, or a comparator (megestrol acetate 160 mg daily in one study; and aminoglutethimide 250 mg b.i.d. with corticosteroid supplementation in the other study). In each study over 60% of the patients had received therapeutic antiestrogens, and about one-fifth of these patients had had an objective response. The megestrol acetate controlled study was double-blind; the other study was open label. Selected baseline characteristics for each study are shown in Table 10.

Table 10: Selected Study Population Demographics
Parameter megestrol acetate aminoglutethimide
study study
No. of Participants 552 557
Receptor Status
      ER/PR Positive 57% 56%
      ER/PR Unknown 43% 44%
Previous Therapy
      Adjuvant Only 33% 38%
      Therapeutic +/- Adj. 66% 62%
Sites of Disease
      Soft Tissue 56% 50%
      Bone 50% 55%
      Viscera 40% 44%

      Confirmed objective tumor response (complete response plus partial response) was the primary endpoint of the trials. Responses were measured according to the Union Internationale Contre le Cancer (UICC) criteria and verified by independent, blinded review. All responses were confirmed by a second evaluation 4-12 weeks after the documentation of the initial response.

      Table 11 shows the results for the first trial, with a minimum follow-up of 15 months, that compared Femara 0.5 mg, Femara 2.5 mg, and megestrol acetate 160 mg daily. (All analyses are unadjusted.)

Table 11: Megestrol Acetate Study Results
Femara®  Femara®  megestrol
0.5 mg 2.5 mg acetate
N=188 N=174 N=190
Objective Response (CR + PR) 22 (11.7%) 41 (23.6%) 31 (16.3%)
Median Duration of Response 552 days (Not reached) 561 days
Median Time to Progression 154 days 170 days 168 days
Median Survival 633 days 730 days 659 days
Odds Ratio for Response Femara 2.5: Femara 0.5=2.33 Femara 2.5: megestrol=1.58
(95% CI: 1.32, 4.17); P=0.004* (95% CI: 0.94, 2.66); P=0.08*
Relative Risk of Progression Femara 2.5: Femara 0.5=0.81 Femara 2.5: megestrol=0.77
(95% CI: 0.63, 1.03); P=0.09* (95% CI: 0.60, 0.98), P=0.03*

* two-sided P-value

      The Kaplan-Meier curves for progression for the megestrol acetate study is shown in Figure 4.

      The results for the study comparing Femara to aminoglutethimide, with a minimum follow-up of 9 months, are shown in Table 12. (Unadjusted analyses are used.)

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Table 12: Aminoglutethimide Study Results
Femara®  Femara® 
0.5 mg 2.5 mg aminoglutethimide
N=193 N=185 N=179
Objective Response
(CR + PR)
34 (17.6%) 34 (18.4%) 22 (12.3%)
Median Duration of
619 days 706 days 450 days
Median Time To
103 days 123 days 112 days
Median Survival 636 days 792 days 592 days
Odds Ratio for
Femara 2.5: Femara 2.5:
Femara 0.5=1.05 aminoglutethimide=1.61
(95% CI: 0.62, 1.79); P=0.85* (95% CI: 0.90, 2.87); P=0.11*
Relative Risk of
Femara 2.5: Femara 2.5:
Femara 0.5=0.86 aminoglutethimide=0.74