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Arimidex

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Arimidex

Arimidex

CLINICAL PHARMACOLOGY

Mechanism of Action

The growth of many cancers of the breast is stimulated or maintained by estrogens.

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.

Anastrozole is a selective non-steroidal aromatase inhibitor. It significantly lowers serum estradiol concentrations and has no detectable effect on formation of adrenal corticosteroids or aldosterone.

Pharmacodynamics

Effect on Estradiol

Mean serum concentrations of estradiol were evaluated in multiple daily dosing trials with 0.5, 1, 3, 5, and 10 mg of ARIMIDEX in postmenopausal women with advanced breast cancer. Clinically significant suppression of serum estradiol was seen with all doses. Doses of 1 mg and higher resulted in suppression of mean serum concentrations of estradiol to the lower limit of detection (3.7 pmol/L). The recommended daily dose, ARIMIDEX 1 mg, reduced estradiol by approximately 70% within 24 hours and by approximately 80% after 14 days of daily dosing. Suppression of serum estradiol was maintained for up to 6 days after cessation of daily dosing with ARIMIDEX 1 mg.

The effect of ARIMIDEX in premenopausal women with early or advanced breast cancer has not been studied. Because aromatization of adrenal androgens is not a significant source of estradiol in premenopausal women, ARIMIDEX would not be expected to lower estradiol levels in premenopausal women.

Effect on Corticosteroids

In multiple daily dosing trials with 3, 5, and 10 mg, the selectivity of anastrozole was assessed by examining effects on corticosteroid synthesis. For all doses, anastrozole did not affect cortisol or aldosterone secretion at baseline or in response to ACTH. No glucocorticoid or mineralocorticoid replacement therapy is necessary with anastrozole.

Other Endocrine Effects

In multiple daily dosing trials with 5 and 10 mg, thyroid stimulating hormone (TSH) was measured; there was no increase in TSH during the administration of ARIMIDEX. ARIMIDEX does not possess direct progestogenic, androgenic, or estrogenic activity in animals, but does perturb the circulating levels of progesterone, androgens, and estrogens.

Pharmacokinetics

Absorption

Inhibition of aromatase activity is primarily due to anastrozole, the parent drug. Absorption of anastrozole is rapid and maximum plasma concentrations typically occur within 2 hours of dosing under fasted conditions. Studies with radiolabeled drug have demonstrated that orally administered anastrozole is well absorbed into the systemic circulation. Food reduces the rate but not the overall extent of anastrozole absorption. The mean Cmax of anastrozole decreased by 16% and the median Tmax was delayed from 2 to 5 hours when anastrozole was administered 30 minutes after food. The pharmacokinetics of anastrozole are linear over the dose range of 1 to 20 mg, and do not change with repeated dosing. The pharmacokinetics of anastrozole were similar in patients and healthy volunteers.

Distribution

Steady-state plasma levels are approximately 3- to 4-fold higher than levels observed after a single dose of ARIMIDEX. Plasma concentrations approach steady-state levels at about 7 days of once daily dosing. Anastrozole is 40% bound to plasma proteins in the therapeutic range.

Metabolism

Metabolism of anastrozole occurs by N-dealkylation, hydroxylation and glucuronidation. Three metabolites of anastrozole (triazole, a glucuronide conjugate of hydroxy-anastrozole, and a glucuronide conjugate of anastrozole itself) have been identified in human plasma and urine. The major circulating metabolite of anastrozole, triazole, lacks pharmacologic activity.

Anastrozole inhibited reactions catalyzed by cytochrome P450 1A2, 2C8/9, and 3A4 in vitro with Ki values which were approximately 30 times higher than the mean steady-state Cmax values observed following a 1 mg daily dose. Anastrozole had no inhibitory effect on reactions catalyzed by cytochrome P450 2A6 or 2D6 in vitro. Administration of a single 30 mg/kg or multiple 10 mg/kg doses of anastrozole to healthy subjects had no effect on the clearance of antipyrine or urinary recovery of antipyrine metabolites.

Excretion

Eighty-five percent of radiolabeled anastrozole was recovered in feces and urine. Hepatic metabolism accounts for approximately 85% of anastrozole elimination. Renal elimination accounts for approximately 10% of total clearance. The mean elimination half-life of anastrozole is 50 hours.

Effect of Gender and Age

Anastrozole pharmacokinetics have been investigated in postmenopausal female volunteers and patients with breast cancer. No age-related effects were seen over the range < 50 to > 80 years.

Effect of Race

Estradiol and estrone sulfate serum levels were similar between Japanese and Caucasian postmenopausal women who received 1 mg of anastrozole daily for 16 days. Anastrozole mean steady-state minimum plasma concentrations in Caucasian and Japanese postmenopausal women were 25.7 and 30.4 ng/mL, respectively.

Effect of Renal Impairment

Anastrozole pharmacokinetics have been investigated in subjects with renal impairment. Anastrozole renal clearance decreased proportionally with creatinine clearance and was approximately 50% lower in volunteers with severe renal impairment (creatinine clearance < 30 mL/min/1.73m²) compared to controls. Total clearance was only reduced 10%. No dosage adjustment is needed for renal impairment [see DOSAGE AND ADMINISTRATION and Use In Specific Populations].

Effect of Hepatic Impairment

Anastrozole pharmacokinetics have been investigated in subjects with hepatic cirrhosis related to alcohol abuse. The apparent oral clearance (CL/F) of anastrozole was approximately 30% lower in subjects with stable hepatic cirrhosis than in control subjects with normal liver function. However, these plasma concentrations were still with the range of values observed in normal subjects. The effect of severe hepatic impairment was not studied. No dose adjustment is necessary for stable hepatic cirrhosis [see DOSAGE AND ADMINISTRATION and Use In Specific Populations].

Animal Toxicology and/or Pharmacology

Reproductive Toxicology

Anastrozole has been found to cross the placenta following oral administration of 0.1 mg/kg in rats and rabbits (about 1 and 1.9 times the recommended human dose, respectively, on a mg/m² basis). Studies in both rats and rabbits at doses equal to or greater than 0.1 and 0.02 mg/kg/day, respectively (about 1 and 1/3, respectively, the recommended human dose on a mg/m² basis), administered during the period of organogenesis showed that anastrozole increased pregnancy loss (increased pre- and/or post-implantation loss, increased resorption, and decreased numbers of live fetuses); effects were dose related in rats. Placental weights were significantly increased in rats at doses of 0.1 mg/kg/day or more.

Evidence of fetotoxicity, including delayed fetal development (i.e., incomplete ossification and depressed fetal body weights), was observed in rats administered doses of 1 mg/kg/day (which produced plasma anastrozole Cssmax and AUC0-24 hr that were 19 times and 9 times higher than the respective values found in postmenopausal volunteers at the recommended dose). There was no evidence of teratogenicity in rats administered doses up to 1.0 mg/kg/day. In rabbits, anastrozole caused pregnancy failure at doses equal to or greater than 1.0 mg/kg/day (about 16 times the recommended human dose on a mg/m² basis); there was no evidence of teratogenicity in rabbits administered 0.2 mg/kg/day (about 3 times the recommended human dose on a mg/m² basis).

Clinical Studies

Adjuvant Treatment of Breast Cancer in Postmenopausal Women

A multicenter, double-blind trial (ATAC) randomized 9,366 postmenopausal women with operable breast cancer to adjuvant treatment with ARIMIDEX 1 mg daily, tamoxifen 20 mg daily, or a combination of the two treatments for five years or until recurrence of the disease.

The primary endpoint of the trial was disease-free survival (i.e., time to occurrence of a distant or local recurrence, or contralateral breast cancer or death from any cause). Secondary endpoints of the trial included distant disease-free survival, the incidence of contralateral breast cancer and overall survival. At a median follow-up of 33 months, the combination of ARIMIDEX and tamoxifen did not demonstrate any efficacy benefit when compared with tamoxifen in all patients as well as in the hormone receptor positive subpopulation. This treatment arm was discontinued from the trial. Based on clinical and pharmacokinetic results from the ATAC trial, tamoxifen should not be administered with anastrozole [see DRUG INTERACTIONS].

Demographic and other baseline characteristics were similar among the three treatment groups (see Table 7).

Table 7 : Demographic and Baseline Characteristics for ATAC Trial

Demographic Characteristic ARIMIDEX 1 mg
(N*=3125)
Tamoxifen 20 mg
(N*=3116)
ARIMIDEX 1 mg plus Tamoxifen1, 20 mg
(N*=3125)
Mean age (yrs.) 64.1 64.1 64.3
Age Range (yrs.) 38.1 - 92.8 32.8 - 94.9 37.0 - 92.2
Age Distribution (%)
< 45 yrs. 0.7 0.4 0.5
45-60 yrs. 34.6 35.0 34.5
> 60 < 70 yrs. 38.0 37.1 37.7
> 70 yrs. 26.7 27.4 27.3
Mean Weight (kg) 70.8 71.1 71.3
Receptor Status (%)
Positive† 83.5 83.1 84.0
Negative§ 7.4 8.0 7.0
Other¶ 8.8 8.6 9.0
Other Treatment (%) prior to Randomization
Mastectomy 47.8 47.3 48.1
Breast conservation# 52.3 52.8 51.9
Axillary surgery 95.5 95.7 95.2
Radiotherapy 63.3 62.5 61.9
Chemotherapy 22.3 20.8 20.8
Neoadjuvant Tamoxifen 1.6 1.6 1.7
Primary Tumor Size (%)
T1 ( ≤ 2 cm) 63.9 62.9 64.1
T2 ( > 2 cm and ≤ 5 cm) 32.6 34.2 32.9
T3 ( > 5 cm) 2.7 2.2 2.3
Nodal Status (%)
Node positive 34.9 33.6 33.5
1-3 (# of nodes) 24.4 24.4 24.3
4-9 7.5 6.4 6.8
> 9 2.9 2.7 2.3
Tumor Grade (%)
Well-differentiated 20.8 20.5 21.2
Moderately differentiated 46.8 47.8 46.5
Poorly/undifferentiated 23.7 23.3 23.7
Not assessed/recorded 8.7 8.4 8.5
* N=Number of patients randomized to the treatment
† The combination arm was discontinued due to lack of efficacy benefit at 33 months of follow-up
‡ Includes patients who were estrogen receptor (ER) positive or progesterone receptor (PgR) positive, or both positive
§Includes patients with both ER negative and PgR negative receptor status
¶ Includes all other combinations of ER and PgR receptor status unknown
#Among the patients who had breast conservation, radiotherapy was administered to 95.0% of patients in the ARIMIDEX arm, 94.1% in the tamoxifen arm and 94.5% in the ARIMIDEX plus tamoxifen arm.

Patients in the two monotherapy arms of the ATAC trial were treated for a median of 60 months (5 years) and followed for a median of 68 months. Disease-free survival in the intent-totreat population was statistically significantly improved [Hazard Ratio (HR) = 0.87, 95% CI: 0.78, 0.97, p=0.0127] in the ARIMIDEX arm compared to the tamoxifen arm. In the hormone receptor-positive subpopulation representing about 84% of the trial patients, disease-free survival was also statistically significantly improved (HR = 0.83, 95% CI: 0.73, 0.94, p=0.0049) in the ARIMIDEX arm compared to the tamoxifen arm.

Figure 1 : Disease-Free Survival Kaplan Meier Survival Curve for all Patients Randomized to ARIMIDEX or Tamoxifen Monotherapy in the ATAC trial (Intent-to-Treat)

Disease-Free Survival Kaplan Meier Survival Curve for all Patients Randomized to ARIMIDEX or Tamoxifen Monotherapy in the ATAC trial - Illustration

Figure 2 : Disease-free Survival for Hormone Receptor-Positive Subpopulation of Patients Randomized to ARIMIDEX or Tamoxifen Monotherapy in the ATAC Trial

Disease-free Survival for Hormone Receptor-Positive Subpopulation of Patients Randomized to ARIMIDEX or Tamoxifen Monotherapy in the ATAC Trial - Illustration

The survival data with 68 months follow-up is presented in Table 9.

In the group of patients who had previous adjuvant chemotherapy (N=698 for ARIMIDEX and N=647 for tamoxifen), the hazard ratio for disease-free survival was 0.91 (95% CI: 0.73 to 1.13) in the ARIMIDEX arm compared to the tamoxifen arm.

The frequency of individual events in the intent-to-treat population and the hormone receptor-positive subpopulation are described in Table 8.

Table 8 : All Recurrence and Death Events*

  Intent-To-Treat Population‡ Hormone Receptor-Positive Subpopulation‡
ARIMIDEX 1 mg
(N†=3125)
Tamoxifen 20 mg
(N†=3116)
ARIMIDEX 1 mg
(N†=2618)
Tamoxifen 20 mg
(N†=2598
Median Duration of Therapy (mo) 60 60 60 60
Median Efficacy Follow-up (mo) 68 68 68 68
Loco-regional recurrence 119 (3.8) 149 (4.8) 76 (2.9) 101 (3.9)
Contralateral breast cancer 35 (1.1) 59 (1.9) 26 (1.0) 54 (2.1)
Invasive 27 (0.9) 52 (1.7) 21 (0.8) 48 (1.8)
Ductal carcinoma in situ 8 (0.3) 6 (0.2) 5 (0.2) 5 (0.2)
Unknown 0 1 ( < 0.1) 0 1 ( < 0.1)
Distant recurrence 324 (10.4) 375 (12.0) 226 (8.6) 265 (10.2)
Death from Any Cause 411 (13.2) 420 (13.5) 296 (11.3) 301 (11.6)
Death breast cancer 218 (7.0) 248 (8.0) 138 (5.3) 160 (6.2)
Death other reason (including unknown) 193 (6.2) 172 (5.5) 158 (6.0) 141 (5.4)
* The combination arm was discontinued due to lack of efficacy benefit at 33 months of follow-up.
† N=Number of patients randomized.
‡ Patients may fall into more than one category.

A summary of the study efficacy results is provided in Table 9.

Table 9 : ATAC Efficacy Summary*

  Intent-To-Treat Population Hormone Receptor- Positive Subpopulation
ARIMIDEX 1 mg
(N=3125)
20 mg
(N=3116)
ARIMIDEX 1 mg
(N=2618)
Tamoxifen 20 mg
(N=2598)
Number of Events Number of Events
Disease- free Survival 575 651 424 497
Hazard ratio 0.87 0.83
2-sided 95% CI 0.78 to 0.97 0.73 to 0.94
p-value 0.0127 0.0049
Distant Disease- free Survival 500 530 370 394
Hazard ratio 0.94 0.93
2-sided 95% CI 0.83 to 1.06 0.80 to 1.07
Overall Survival 411 420 296 301
Hazard ratio 0.97 0.97
2-sided 95% CI 0.85 to 1.12 0.83 to 1.14
* The combination arm was discontinued due to lack of efficacy benefit at 33 months of follow-up.

10-year median follow-up Efficacy Results from the ATAC Trial

In a subsequent analysis of the ATAC trial, patients in the two monotherapy arms were followed for a median of 120 months (10 years). Patients received study treatment for a median of 60 months (5 years) (see Table 10).

Table 10 : Efficacy Summary

  Intent-To-Treat Population Hormone Receptor-Positive Subpopulation
ARIMIDEX 1 mg
(N=3125)
Tamoxifen 20 mg
(N=3116)
ARIMIDEX 1 mg
(N=2618)
Tamoxifen 20 mg
(N=2598)
Number of Events Number of Events
Disease- free Survival 953 1022 735 924
Hazard ratio 0.91 0.86
2-sided 95% CI 0.83 to 0.99 0.78 to 0.95
p-value 0.0365 0.0027
Overall Survival 734 747 563 586
Hazard ratio 0.97 0.95
2-sided 95% CI 0.88 to 1.08 0.84 to 1.06

Figure 3 : Disease-Free Survival Kaplan Meier Survival Curve for all Patients Randomized to ARIMIDEX or Tamoxifen Monotherapy in the ATAC Trial (Intent-toTreat)a

Disease-Free Survival Kaplan Meier Survival Curve for all Patients Randomized to ARIMIDEX or Tamoxifen Monotherapy in the ATAC Trial - Illustration

a The proportion of patients with 120 months' follow-up was 29.4%.

Figure 4 : Disease-Free Survival for Hormone Receptor-Positive Subpopulation of Patients Randomized to ARIMIDEX or Tamoxifen Monotherapy in the ATAC Trialb

Disease-Free Survival for Hormone Receptor-Positive Subpopulation of Patients Randomized to ARIMIDEX or Tamoxifen Monotherapy in the ATAC Trial - Illustration

bThe proportion of patients with 120 months' follow-up was 29.8%.

First-Line Therapy in Postmenopausal Women with Advanced Breast Cancer

Two double-blind, controlled clinical studies of similar design (0030, a North American study and 0027, a predominately European study) were conducted to assess the efficacy of ARIMIDEX compared with tamoxifen as first-line therapy for hormone receptor positive or hormone receptor unknown locally advanced or metastatic breast cancer in postmenopausal women. A total of 1021 patients between the ages of 30 and 92 years old were randomized to receive trial treatment. Patients were randomized to receive 1 mg of ARIMIDEX once daily or 20 mg of tamoxifen once daily. The primary endpoints for both trials were time to tumor progression, objective tumor response rate, and safety.

Demographics and other baseline characteristics, including patients who had measurable and no measurable disease, patients who were given previous adjuvant therapy, the site of metastatic disease and ethnic origin were similar for the two treatment groups for both trials. The following table summarizes the hormone receptor status at entry for all randomized patients in trials 0030 and 0027.

Table 11 : Demographic and Other Baseline Characteristics

Receptor status Number (%) of subjects
Trial 0030   Trial 0027
ARIMIDEX 1 mg
(N=171)
Tamoxifen 20 mg
(N=182)
ARIMIDEX 1 mg
(N=340)
Tamoxifen 20 mg
(N=328)
ER* and/or PgR† 151 (88.3) 162 (89.0) 154 (45.3) 144 (43.9)
ER* unknown, PgR†unknown 19 (11.1) 20 (11.0) 185 (54.4) 183 (55.8)
* ER=Estrogen receptor
† PgR=Progesterone receptor

For the primary endpoints, trial 0030 showed that ARIMIDEX had a statistically significant advantage over tamoxifen (p=0.006) for time to tumor progression; objective tumor response rates were similar for ARIMIDEX and tamoxifen. Trial 0027 showed that ARIMIDEX and tamoxifen had similar objective tumor response rates and time to tumor progression (see Table 12 and Figures 5 and 6).

Table 12 below summarizes the results of trial 0030 and trial 0027 for the primary efficacy endpoints.

Table 12 : Efficacy Results of First-line Treatment

Endpoint Trial 0030   Trial 0027  
ARIMIDEX 1 mg
(N=171)
Tamoxifen 20 mg
(N=182)
ARIMIDEX 1 mg (N=340) Tamoxifen 20 mg
(N=328)
Time to progression (TTP)
Median TTP (months) 11.1 5.6 8.2 8.3
Number (%) of subjects who progressed 114 (67%) 138 (76%) 249 (73%) 247 (75%)
Hazard ratio (LCL* )† 1.42 (1.15) 1.01 (0.87)
2-sided 95% CI‡ (1.11, 1.82) (0.85, 1.20)
p-value§ 0.006 0.920
Best objective response rate
Number (%) of subjects With CR¶ + PR# 36 (21.1%) 31 (17.0%) 112 (32.9%) 107 (32.6%)
Odds Ratio (LCL* )♠ 1.30 (0.83) 1.01 (0.77)
* LCL=Lower Confidence Limit
† Tamoxifen:ARIMIDEX
‡ CI=Confidence Interval
§Two-sided Log Rank
¶ CR=Complete Response
#PR=Partial Response
♠ARIMIDEX:Tamoxifen

Figure 5 : Kaplan-Meier probability of time to disease progression for all randomized patients (intent-to-treat) in Trial 0030

Kaplan-Meier probability of time to disease progression for all randomized patients (intent-to-treat) in Trial 0030 - Illustration

Figure 6 : Kaplan-Meier probability of time to progression for all randomized patients (intent-to-treat) in Trial 0027

Kaplan-Meier probability of time to progression for all randomized patients (intent-to-treat) in Trial 0027 - Illustration

Results from the secondary endpoints were supportive of the results of the primary efficacy endpoints. There were too few deaths occurring across treatment groups of both trials to draw conclusions on overall survival differences.

Second-Line Therapy in Postmenopausal Women with Advanced Breast Cancer who had Disease Progression following Tamoxifen Therapy

Anastrozole was studied in two controlled clinical trials (0004, a North American study; 0005, a predominately European study) in postmenopausal women with advanced breast cancer who had disease progression following tamoxifen therapy for either advanced or early breast cancer. Some of the patients had also received previous cytotoxic treatment. Most patients were ER-positive; a smaller fraction were ER-unknown or ER-negative; the ER-negative patients were eligible only if they had had a positive response to tamoxifen. Eligible patients with measurable and non-measurable disease were randomized to receive either a single daily dose of 1 mg or 10 mg of ARIMIDEX or megestrol acetate 40 mg four times a day. The studies were double-blinded with respect to ARIMIDEX. Time to progression and objective response (only patients with measurable disease could be considered partial responders) rates were the primary efficacy variables. Objective response rates were calculated based on the Union Internationale Contre le Cancer (UICC) criteria. The rate of prolonged (more than 24 weeks) stable disease, the rate of progression, and survival were also calculated.

Both trials included over 375 patients; demographics and other baseline characteristics were similar for the three treatment groups in each trial. Patients in the 0005 trial had responded better to prior tamoxifen treatment. Of the patients entered who had prior tamoxifen therapy for advanced disease (58% in Trial 0004; 57% in Trial 0005), 18% of these patients in Trial 0004 and 42% in Trial 0005 were reported by the primary investigator to have responded. In Trial 0004, 81% of patients were ER-positive, 13% were ER-unknown, and 6% were ER-negative. In Trial 0005, 58% of patients were ER-positive, 37% were ER-unknown, and 5% were ER-negative. In Trial 0004, 62% of patients had measurable disease compared to 79% in Trial 0005. The sites of metastatic disease were similar among treatment groups for each trial. On average, 40% of the patients had soft tissue metastases; 60% had bone metastases; and 40% had visceral (15% liver) metastases.

Efficacy results from the two studies were similar as presented in Table 13. In both studies there were no significant differences between treatment arms with respect to any of the efficacy parameters listed in the table below.

Table 13 : Efficacy Results of Second-line Treatment

  ARIMIDEX 1 mg ARIMIDEX 10 mg Megestrol Acetate 160 mg
Trial 0004
(N. America) (N=128) (N=130) (N=128)
Median Follow-up (months)* 31.3 30.9 32.9
Median Time to Death (months) 29.6 25.7 26.7
2 Year Survival Probability (%) 62.0 58.0 53.1
Median Time to Progression (months) 5.7 5.3 5.1
Objective Response (all patients) (%) 12.5 10.0 10.2
Stable Disease for > 24 weeks (%) 35.2 29.2 32.8
Progression (%) 86.7 85.4 90.6
Trial 0005
(Europe, Australia, S. Africa) (N=135) (N=118) (N=125)
Median Follow-up (months)* 31.0 30.9 31.5
Median Time to Death (months) 24.3 24.8 19.8
2 Year Survival Probability (%) 50.5 50.9 39.1
Median Time to Progression (months) 4.4 5.3 3.9
Objective Response 12.6 15.3 14.4
(all patients) (%)
Stable Disease for > 24 weeks (%) 24.4 25.4 23.2
Progression (%) 91.9 89.8 92.0
* Surviving Patients

When data from the two controlled trials are pooled, the objective response rates and median times to progression and death were similar for patients randomized to ARIMIDEX 1 mg and megestrol acetate. There is, in this data, no indication that ARIMIDEX 10 mg is superior to ARIMIDEX 1 mg.

Table 14 : Pooled Efficacy Results of Second-line Treatment

Trials 0004 & 0005 (Pooled Data) ARIMIDEX 1 mg
N=263
ARIMIDEX 10 mg
N=248
Megestrol Acetate 160 mg
N=253
Median Time to Death (months) 26.7 25.5 22.5
2 Year Survival Probability (%) 56.1 54.6 46.3
Median Time to Progression 4.8 5.3 4.6
Objective Response (all patients) (%) 12.5 12.5 12.3

Last reviewed on RxList: 5/31/2013
This monograph has been modified to include the generic and brand name in many instances.

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