Peptide Health Lab

Rx hormone track

Anastrozole

Also known as: Arimidex, Non-steroidal aromatase inhibitor

Regulatory status
FDA approved
Evidence grade
Human RCT evidence

Last reviewed September 1, 2026 · 14 sources

What anastrozole is and how it works

Anastrozole is a small synthetic molecule — not a peptide — classified as a selective non-steroidal aromatase inhibitor. Aromatase is the enzyme that converts androgens into estrogens, and the approved US labeling describes the mechanism in exactly those terms: the enzyme converts adrenal androgens, primarily androstenedione and testosterone, into estrone and estradiol, and inhibiting it lowers serum estradiol with no detectable effect on the formation of adrenal corticosteroids or aldosterone. That is a regulatory document describing pharmacology, and it is stated here without a citation for that reason.

The same inhibition produces two different downstream stories in two different bodies, and keeping them apart is the whole discipline of this page. In postmenopausal women, peripheral aromatization is the main remaining source of estrogen, so blocking the enzyme drives estrogen close to its floor — the point of the drug in hormone-receptor-positive breast cancer, and what the registrational trials tested. In men, estradiol is also the signal that restrains the hypothalamus and pituitary; lowering it releases that restraint, luteinizing hormone rises, and the testes make more testosterone. Randomized trials in older men measured precisely this: over 12 weeks on 1 mg by mouth daily, total testosterone rose from 343 to 572 ng/dL, estradiol fell from 26 to 17 pg/mL, and luteinizing hormone rose, all against placebo.[6] Over 12 months in a larger trial, testosterone rose from 11.2 to 18.2 nmol/L by month 3 and then declined by month 12.[5] That effect is the entire mechanistic argument for the off-label use, and it is real.

Two identity boundaries matter before any evidence below is read. Anastrozole is not letrozole and not exemestane; letrozole is a different non-steroidal molecule and exemestane is a steroidal inactivator with a different mechanism, so a statement about the aromatase-inhibitor class is not a statement about this molecule. And aromatase inhibitors are not selective estrogen receptor modulators — tamoxifen, raloxifene, enclomiphene — which act at the estrogen receptor rather than at the enzyme, and which appear in the same conversations without being the same evidence. Where a source on this page is class-level rather than anastrozole-specific, the sentence says so.[13]

What the research actually shows

The evidence divides into two pools that never touch. Pool A is the evidence behind the approval: trials in postmenopausal women with breast cancer. Pool B is the evidence for the off-label use in men. On 1 September 2026, a PubMed search for anastrozole AND "breast neoplasms"[MeSH Terms] AND randomized controlled trial[pt] returned 267 records, and a search for anastrozole AND hypogonadism AND male[mh] AND randomized controlled trial[pt] returned 15 — roughly eighteen to one in favour of the indication most readers of this page are not here for. Reading those 15 makes the gap wider still: several are mechanistic studies in which anastrozole is a research tool rather than a treatment, and several are separate publications from the same small cohorts.

Pool A, in both halves. In 9,366 postmenopausal women randomized to anastrozole, tamoxifen or the combination, disease-free survival at three years was 89.4% against 87.4% for tamoxifen (hazard ratio 0.83, 95% CI 0.71-0.96, p=0.013) — and the same report states that tamoxifen was significantly better tolerated with respect to musculoskeletal disorders and fractures (p<0.0001 for both), closing that longer follow-up was required before a final benefit-to-risk assessment could be made.[1] At 10 years the disease-free survival advantage held (HR 0.91, 95% CI 0.83-0.99, p=0.04), but there was little difference in overall mortality (0.95, 95% CI 0.84-1.06, p=0.4).[2] In advanced disease, a 668-woman first-line comparison found median time to progression of 8.2 months against 8.3 on tamoxifen — reported as at least equivalence, not superiority.[3] Bone density lost during treatment was partially reversible in the two years after stopping.[4] No man was enrolled in any of these trials.

Pool B has one reproducible result and a long list of non-results. The hormonal change happens everywhere.[6][5] What it does not do is move what was measured downstream. Across the male trials — 88 men over a year, 37 men over 12 weeks, 26 hypogonadal infertile men over 12 weeks, 23 severely obese men over six months — body composition, strength, quality-of-life scores, erectile-function scores, urinary symptom scores and semen parameters came out no different from placebo, and the largest trial's own summary sentence is that the hormonal alterations did not improve body composition or strength.[5][6][12][10]

Where Pool B does show a consistent non-hormonal effect, it is on bone and it runs against the reader. In 69 men over one year, spine bone mineral density decreased relative to placebo (P = 0.0014), and the authors state that aromatase inhibition does not improve skeletal health in aging men with low or low-normal testosterone.[7] In a 43-man three-arm trial whose primary outcome was lumbar spine density, transdermal testosterone improved it at 12 months and anastrozole did not.[8] The registry results posted for the 23-man obesity trial record percent change in bone failure load at the radius of -4.63 on anastrozole against -2.16 on placebo — less reassuring than the published title reads, and reported here for that reason.[10] Against that, a companion analysis from the same 43-man cohort found prostate volume rose only in the testosterone arm and concluded that 12 months of an aromatase inhibitor was not detrimental to the prostate, which is the clearest genuinely reassuring finding in the male literature.[9]

On gynecomastia, the reason many readers arrive, the randomized answer is negative twice over. In 114 men on bicalutamide, gynecomastia developed in 51% on anastrozole against 73% on placebo and 10% on tamoxifen, and the authors state that anastrozole did not significantly reduce the incidence while tamoxifen was effective.[11] In 80 boys aged 11 to 18 with pubertal gynecomastia — a different population, named here because the finding does not transfer to adults — the response rate was 38.5% against 31.4% on placebo (P = 0.47) while the testosterone-to-estradiol ratio moved 166% against 39%. The hormone changed and the breast tissue did not.[14]

Where the evidence is weak

The badge on this page is earned by the male trials, not by the breast-cancer programme. That is the deliberate grading choice: the compound-level grade is Human RCT evidence because placebo-controlled randomized trials in men exist and have been run, and grading it lower would contradict the trials described above. It is not because those trials found benefit. Most of them found the opposite, and the grade should be read as this has been tested, not as this works.

The male literature is small, short and repetitive. No randomized trial of anastrozole in adult men located for this page enrolled more than 114 men or ran longer than 12 months, and every one is single-centre or a small multicentre programme. Two of the trials cited here report different outcomes from the same 43-man cohort.[8][9] The record count of 15 overstates how many distinct trials exist.

The endpoints are surrogates. A serum estradiol is not a symptom and a testosterone level is not an outcome. Where the male trials measured something a man would notice — strength, walking speed, erectile function, hypogonadal symptom scores, breast tissue, semen parameters — the result was mostly no difference from placebo.[5][6][12]

Clinical outcomes have never been measured in men. A PubMed search on 1 September 2026 for anastrozole AND male[mh] AND randomized controlled trial[pt] AND (mortality OR fracture OR "cardiovascular outcome") returned seven records: four adjuvant breast-cancer trials of a different drug combination, one pulmonary arterial hypertension trial, and two of the male trials already cited here, neither of which reports fracture or mortality outcomes. The one consistent skeletal finding in the male trials is a fall in spine bone mineral density.[7] That is what makes the missing fracture endpoint the specific gap worth naming rather than a routine one.

Industry authorship is present and is disclosed consistently here. The pubertal gynecomastia trial's first author's stated affiliation is the manufacturer, so it is the manufacturer's own randomized trial of the drug for a male indication, and it did not meet its primary endpoint.[14] The prevention bone substudy carries a declared manufacturer grant in its conflict-of-interest statement.[4] Affiliations here were read from each record's own author entries rather than matched by surname, because surname matching sweeps in different people and PubMed reverses given and family order on some records; but PubMed carries per-author affiliation strings only from roughly 2014 onward, so on the older adjuvant and first-line publications the affiliations of authors beyond the first are simply absent. That is a data gap, not evidence of independence, so no trial on this page is described as independent.

Nothing here speaks to years of exposure. The male trials ran 12 weeks to 12 months. There is no published randomized evidence about what sustained estrogen suppression does to a man's skeleton, lipids or cardiovascular risk over the timeframes the off-label use actually spans.

Legal and regulatory status

Anastrozole is FDA-approved, and the approval is narrow in indication, in route and — decisively for this page — in population.

A Drugs@FDA query on the products.active_ingredients.name field for "ANASTROZOLE" on 1 September 2026 returned 21 applications: two NDAs (NDA 020541, original approval 27 December 1995, and NDA 022214, original approval 5 December 2008) and 19 ANDAs. Every product under all 21 is a 1 mg tablet by the oral route in prescription marketing status, and enumerating the ingredient names inside the result set returns exactly one distinct value, ANASTROZOLE, on all 21 — so this count is not inflated by a longer ingredient name that merely contains the word.

The field the query runs on changes the answer, and here it changes it badly. The same database on the same date, queried on openfda.generic_name for "anastrozole", returned 7 applications — a strict subset of the 21, with nothing in the smaller set absent from the larger. The 14 missing records list ANASTROZOLE 1MG correctly; they simply carry no openFDA annotation block at all. The consequence is that the generic-name field drops NDA 022214 entirely, so an author querying only that field would have reported seven approved applications and silently lost a brand-name NDA. A same-session control on the same two fields for metformin hydrochloride returned 211 against 82, reproducing the same directional gap on an unrelated compound — which is what establishes this as an openFDA annotation-coverage artifact rather than an anastrozole-specific data error.

The approved indications, from current labeling, are three, and every one of them names postmenopausal women: adjuvant treatment of postmenopausal women with hormone-receptor-positive early breast cancer; first-line treatment of postmenopausal women with hormone-receptor-positive or hormone-receptor-unknown locally advanced or metastatic breast cancer; and treatment of advanced breast cancer in postmenopausal women with disease progression following tamoxifen therapy. There is no approved indication in men, at any dose, for any purpose. Not one of the three can be reached by a man. Every use of anastrozole in men — estrogen management alongside testosterone therapy, gynecomastia, male infertility — is off-label, and none of it is supported by the trials that produced the approval.

The labeled dose is one 1 mg tablet once a day, by mouth, with or without food. That is a regulatory fact about a breast-cancer indication in postmenopausal women. It is not a protocol range and it does not appear in the protocol block on this page.

What the approved status changes for a reader is the shape of the evidence underneath it, and the two halves of this page are not comparable on that measure: the indications rest on randomized trials enrolling thousands of postmenopausal women with adjudicated disease endpoints,[2] while the off-label use in men rests on trials enrolling tens of men for a year at most.[5]

There is no boxed warning on this drug, and that was verified rather than assumed. The brand SPL read for this page — effective 2 March 2026, filed under NDA 020541 — carries no boxed_warning key at all, checked by testing for the key rather than by searching the text. Across all 40 anastrozole labels returned by the openFDA labeling endpoint on openfda.generic_name on 1 September 2026, zero populate that field, and none carries an all-capitals boxed-warning heading inside its indications or warnings sections either — which matters, because a label can carry boxed-warning text in another section without populating the coded field. A same-session control on tamoxifen citrate returned 14 labels, all 14 with the field populated and carrying warning text, so the null result is a fact about anastrozole rather than about a malformed query. One route note: an earlier form of that same control query, differing only in how the phrase was URL-encoded, returned HTTP 404 for tamoxifen — an HTTP status is a fact about a route, never a fact about a register.

The labeling carries Warnings and Precautions items instead: an increased incidence of ischemic cardiovascular events in women with pre-existing ischemic heart disease compared with tamoxifen; possible decreases in bone mineral density with a recommendation to consider density monitoring; possible increases in total cholesterol with a recommendation to consider cholesterol monitoring; and embryo-fetal toxicity. Its pediatric section states directly that efficacy in the treatment of pubertal gynecomastia in adolescent boys has not been demonstrated, and summarizes the 80-boy trial that failed to demonstrate it. All of that is labeling and is stated here uncited.

Anastrozole is a prescription drug in the United States. It is not a controlled substance and it is not a dietary supplement. Prescription status, laboratory monitoring and any change in treatment are matters for the licensed prescriber managing the case.

In competitive sport, anastrozole is named on the 2026 Prohibited List. Retrieved on 1 September 2026 through the United States Anti-Doping Agency's prohibited-list page to the WADA-hosted PDF of the World Anti-Doping Code International Standard Prohibited List 2026, which states that it comes into effect on 1 January 2026: the section heading reads "S4 HORMONE AND METABOLIC MODULATORS — PROHIBITED AT ALL TIMES (IN- AND OUT-OF-COMPETITION)", with the scope sentences "Prohibited substances in classes S4.1 and S4.2 are Specified Substances." and "The following hormone and metabolic modulators are prohibited." The subsection reads "S4.1. AROMATASE INHIBITORS" followed by "Including, but not limited to:" and a bulleted list in which Anastrozole appears alongside exemestane, formestane, letrozole, testolactone and aminoglutethimide; the document's index confirms the entry as "Anastrozole, 10." Anastrozole is therefore a Specified Substance prohibited at all times, in and out of competition. It does not appear anywhere on the 2026 Monitoring Program, retrieved by the same route on the same date. A tested athlete's therapeutic-use question is one to settle with the relevant sport body before treatment begins, not after a test.

Questions to bring to a provider

Everything below turns on one prior question: which of the two evidence bases the proposal is being made from.

  • Is this being considered for an approved indication or off-label? The three approved indications all name postmenopausal women with breast cancer, and every use in a man sits outside them.
  • If the goal is a laboratory number, what clinical change is expected to follow from moving it, and over what timeframe would that change be judged? The randomized trials in men moved the numbers reliably and did not move strength, body composition or symptom scores.[5][6]
  • What is the baseline bone assessment and the monitoring plan, given that the one consistent non-hormonal finding in men is a fall in spine bone mineral density?[7][8]
  • Is there existing osteopenia, osteoporosis, a previous fragility fracture, or long-term corticosteroid use, and how does that change the calculation?
  • If the concern is breast tissue, what does the randomized comparison against a selective estrogen receptor modulator imply for the choice, given that anastrozole did not significantly reduce the endpoint in that trial and tamoxifen did?[11]
  • If fertility is the reason, what did the randomized comparison actually measure, and what did it find about semen parameters?[12]
  • What lipid and prostate-specific antigen monitoring is planned, and what result would prompt stopping?[9]
  • What is the agreed stopping rule? None of the male trials ran beyond 12 months, so there is no published evidence describing what indefinite use looks like.
  • Does an S4.1 Specified Substance prohibited at all times create a problem for any sport, testing pool or employment screen this applies to?

A clinician who wants a bone-density measurement and a second confirmatory hormone panel before writing anything is reading the same evidence this page describes.

Evidence by claim

Grades describe how strong the evidence is; the line under each grade describes what kind of studies it is. How we grade evidence.

Adjuvant and first-line treatment of hormone-receptor-positive breast cancer in postmenopausal women
Human RCT evidence human RCT

This is the approved indication and it carries the strongest evidence on this page. In 9,366 postmenopausal women randomized to anastrozole, tamoxifen or both, disease-free survival at three years was 89.4% against 87.4% for tamoxifen (hazard ratio 0.83, 95% CI 0.71-0.96, p=0.013), and the authors' own closing sentence was that longer follow-up was required before a final benefit-to-risk assessment could be made. At 10 years the disease-free survival advantage held (HR 0.91, 95% CI 0.83-0.99, p=0.04) and time to recurrence improved (HR 0.84), but there was little difference in overall mortality (0.95, 95% CI 0.84-1.06, p=0.4) — a recurrence benefit that did not convert into a survival benefit. In advanced disease, a 668-woman first-line trial found median time to progression of 8.2 months on anastrozole against 8.3 on tamoxifen, which the investigators report as at least equivalence rather than superiority. Every participant in all three trials was a postmenopausal woman; none of this evidence bears on any use in men.

[1] [2] [3]

Bone mineral density and fractures in postmenopausal women taking anastrozole
Human RCT evidence human RCT · human observational

Reported in both directions by the same trial programme. Fractures and musculoskeletal disorders were significantly more common on anastrozole than on tamoxifen (p<0.0001 for both) in the 9,366-woman adjuvant trial, and the 10-year analysis put the excess at 451 against 351 fractures during active treatment (OR 1.33, p<0.0001) with no excess afterwards (110 against 112, OR 0.98, p=0.9). A bone substudy of a separate prevention trial found that in 528 women who stopped anastrozole after five years, lumbar spine density rose 1.25% over the following two years, and concluded the negative effects on density in the preventive setting are partially reversible. That substudy is an analysis within a randomized trial but is not itself indexed by PubMed as a randomized controlled trial, and it is declared here as observational for that reason.

[1] [2] [4]

Raising testosterone and lowering estradiol in men with low testosterone
Human RCT evidence human RCT

Established, and it is the only thing in the male literature that is. In 37 elderly men, total testosterone rose from 343 to 572 ng/dL on 1 mg daily over 12 weeks while estradiol fell from 26 to 17 pg/mL and luteinizing hormone rose (P < 0.001 against placebo). In 88 older hypogonadal men, testosterone rose from 11.2 to 18.2 nmol/L by month 3 and then declined by month 12. In 26 hypogonadal infertile men randomized against clomiphene citrate for 12 weeks, testosterone rose in both arms while estradiol fell only on anastrozole. In the same trials, the measured clinical endpoints — body composition, strength, quality-of-life scores, erectile-function scores, urinary symptom scores and semen parameters — did not change. The hormonal effect is real, reproducible, and on its own is not an outcome.

[6] [5] [12]

Symptoms, strength and body composition in men with low testosterone
Human RCT evidence human RCT

Randomized evidence exists and it is largely null, which is why this claim is graded on the male trials rather than on the approval. In 88 men over 12 months, body composition and strength did not change, and the authors state that the hormonal alterations did not improve body composition or strength. In 37 men over 12 weeks, quality-of-life, erectile-function and urinary symptom scores did not change. In 23 severely obese men, changes in symptom scores and muscle strength did not differ from the weight-loss-only arm, although fat mass fell more on anastrozole (p = 0.04); the trial's posted registry results record percent change in knee extension of 3.7 on anastrozole against 12.8 on placebo, which is less favourable than the published title reads. In a 43-man three-arm trial, lean body mass increased on anastrozole while fast gait speed improved only with transdermal testosterone.

[5] [6] [10] [8]

Bone health in men taking an aromatase inhibitor
Human RCT evidence human RCT

Adverse, and this is the mandatory counterweight to any statement that the drug raises testosterone in men. In 69 men aged 60 and older over one year, posterior-anterior spine bone mineral density decreased on anastrozole relative to placebo (P = 0.0014), and the authors conclude that aromatase inhibition does not improve skeletal health in aging men with low or low-normal testosterone. In a 43-man three-arm trial whose primary outcome was lumbar spine density, transdermal testosterone improved it at 12 months and anastrozole did not. The posted registry results of the 23-man obesity trial record percent change in bone failure load at the radius of -4.63 on anastrozole against -2.16 on placebo, and bone stiffness at the radius of -4.02 against -2.09, which are less reassuring than the published abstract's tibial trabecular finding on its own would suggest; both are reported here.

[7] [8] [10]

Gynecomastia in adult men
Human RCT evidence human RCT

Negative in the one randomized trial in adult men located for this page. In 114 men with prostate cancer on bicalutamide, gynecomastia developed in 73% on placebo, 10% on tamoxifen and 51% on anastrozole, and the authors' conclusion is that anastrozole did not significantly reduce the incidence of bicalutamide-induced gynecomastia and breast pain while tamoxifen was effective. Adverse events were reported in 69% of the anastrozole arm against 37% of the placebo arm (P = .004). This is a trial in men receiving androgen-receptor blockade, not in men on testosterone therapy, and its population is named here for that reason.

[11]

Gynecomastia in pubertal boys
Human RCT evidence human RCT

Negative, and separated from the adult claim above because the trial enrolled a different population. In 80 boys aged 11 to 18 with pubertal gynecomastia, six months of anastrozole 1 mg daily produced a response rate of 38.5% against 31.4% on placebo (odds ratio 1.513, 95% CI 0.496-4.844, P = 0.47) while the median testosterone-to-estradiol ratio moved 166% against 39%. The hormone changed and the breast tissue did not. The trial's first author's stated affiliation is the manufacturer, so this is the manufacturer's own randomized trial of the drug for a male indication, and it did not meet its primary endpoint.

[14]

Semen parameters and male infertility
Human RCT evidence human RCT · review

Weak, and weaker for anastrozole specifically than for the class. In 26 hypogonadal infertile men randomized to anastrozole 1 mg daily or clomiphene citrate 25 mg daily for 12 weeks, neither group showed significant changes in seminal parameters or patient-reported outcomes, and clomiphene produced significantly higher testosterone than anastrozole while anastrozole produced the larger testosterone-to-estradiol ratio. A separate systematic review of randomized trials of aromatase inhibitors as a class — a class-level source supporting only a class-level statement — included three studies with 100 participants and could analyse data from only 54, concluding that there is only low-quality evidence regarding the effectiveness of aromatase inhibitor therapy in infertile men and that further trials are needed. Within that review, anastrozole appears only in a single comparison against letrozole, which favoured letrozole.

[12] [13]

Long-term outcomes in men — fractures, mortality, cardiovascular events
Anecdotal reports only human RCT

Graded down deliberately, because no randomized trial has measured them. The longest randomized trials of anastrozole in adult men located for this page ran 12 months and measured surrogate endpoints — bone mineral density, body composition, hormone levels and symptom scores — rather than clinical events. A PubMed search on 1 September 2026 for anastrozole AND male[mh] AND randomized controlled trial[pt] AND (mortality OR fracture OR "cardiovascular outcome") returned seven records: four adjuvant breast-cancer trials of a different drug combination, one pulmonary arterial hypertension trial, and two trials in men that are cited elsewhere on this page, neither of which reports fracture or mortality outcomes. What exists for this claim area is inference from surrogate measurements, which is what this grade records.

[5] [8]

Typical protocol range in the research

  • The largest and longest published randomized trial of anastrozole in adult men: 88 men aged 60 and older with low or borderline-low testosterone and hypogonadal symptoms, randomized double-blind against placebo for one year

    Anastrozole 1 mg by mouth once daily, or matching placebo, for 12 months. This is the amount the trial administered; it is not a recommendation and the trial reported no improvement in body composition or strength on it. [5]

  • A three-arm randomized double-blind trial in 37 elderly men aged 62 to 74 with screening testosterone below 350 ng/dL, testing two different administration frequencies against placebo over 12 weeks

    Anastrozole 1 mg by mouth once daily in one arm (12 men) and anastrozole 1 mg by mouth twice weekly in a second arm (11 men), against daily placebo in a third arm (14 men), for 12 weeks [6]

  • A randomized double-blind placebo-controlled pilot trial in 23 severely obese men aged 35 to 65 with hypogonadotropic hypogonadism, in which every participant also followed a supervised diet-and-exercise weight-loss programme

    Anastrozole 1 mg by mouth once daily (12 men) or matching placebo (11 men) for six months, both arms alongside the weight-loss programme [10]

Every figure above is an amount administered to adult men in a published randomized trial, by mouth, with the arm and the population named. None of them is merged with an oncology figure, and none is a recommendation. The 1 mg daily amount that appears on the approved US label is a regulatory fact about a breast-cancer indication in postmenopausal women, and it is described in the Legal and regulatory status section rather than here. In the trials cited on this page the longest treatment period in adult men is 12 months, and a PubMed search on 1 September 2026 for anastrozole AND male[mh] AND randomized controlled trial[pt] AND (mortality OR fracture OR "cardiovascular outcome") returned seven records — four adjuvant breast-cancer trials of a different drug combination, one pulmonary arterial hypertension trial, and the bone-density and gynecomastia trials already cited here — none of which reports fracture or mortality outcomes for anastrozole in men.

Ranges are what published research reports, not a recommendation. PHL does not prescribe, and nothing here is personalized to you.

Side effects & safety signals

  • Loss of bone mineral density in men

    Reported in every randomized trial in men that measured it. In a one-year placebo-controlled trial in 69 men aged 60 and older, posterior-anterior spine bone mineral density decreased in the anastrozole group relative to placebo (P = 0.0014) · This is the one consistent non-hormonal direction of effect in the male literature, and it runs against the reader rather than for them. In the 69-man trial, spine density fell from 1.121 to 1.102 g/cm2 on anastrozole while rising from 1.180 to 1.189 g/cm2 on placebo, and the authors' own conclusion is that aromatase inhibition does not improve skeletal health in aging men with low or low-normal testosterone. A separate 43-man three-arm trial found that transdermal testosterone improved lumbar spine density — its primary outcome — at 12 months while anastrozole did not, and concluded that aromatization of testosterone is required to maintain bone density in older men with low testosterone. Existing osteopenia, osteoporosis, a fracture history or long-term corticosteroid use are reasons to raise this with a clinician before anything is considered.

    [7] [8]

  • Bone loss and fractures in postmenopausal women

    In the 9,366-woman adjuvant trial, tamoxifen was significantly better tolerated than anastrozole with respect to musculoskeletal disorders and fractures (p<0.0001 for both); at 10 years, fractures during active treatment numbered 451 on anastrozole against 351 on tamoxifen (OR 1.33, 95% CI 1.15-1.55, p<0.0001) · This entry is scoped to postmenopausal women because that is who those trials enrolled, and it is not transferable to men. Two features of it are worth stating in full. In the same 10-year analysis, fracture counts were similar in the post-treatment follow-up period (110 against 112, OR 0.98, p=0.9), so the excess tracked active treatment rather than persisting. And in a bone substudy of a separate prevention trial, 528 women who had completed five years of anastrozole without a bisphosphonate showed a lumbar spine density increase of 1.25% (95% CI 0.73 to 1.77, P=0.0004) in the two years after stopping, larger than on placebo, which the authors describe as the negative effects on density in the preventive setting being partially reversible.

    [1] [2] [4]

  • Higher overall adverse-event rate in men in the one trial that counted them against placebo

    Adverse events were reported in 69% of men in the anastrozole arm against 37% in the placebo arm of a 114-man randomized trial (P = .004) · That trial studied men with prostate cancer receiving bicalutamide, so the background rate is not a healthy-population rate and the figure should not be read as a general incidence. It is reported here because it is the only randomized head-to-head adverse-event count against placebo in adult men located for this page, and because the same trial found that anastrozole did not significantly reduce the breast symptoms it was given to prevent. Both halves belong together.

    [11]

  • Cholesterol and lipid changes

    Direction depends on the trial and the population. In 88 older hypogonadal men over 12 months, lipid levels did not change. In 23 severely obese men on a weight-loss programme, total and LDL cholesterol fell more in the placebo arm than in the anastrozole arm (p = 0.03 for both), which the authors describe as a minimal increase of unlikely meaningful clinical impact · Reported as the sources report it, in both directions. The approved US labeling separately carries a Warnings and Precautions item stating that increases in total cholesterol may occur and that cholesterol monitoring should be considered, which is a labeling fact about the approved population and is stated as such in the regulatory section rather than being read across from these male trials.

    [5] [10]

  • Prostate-specific antigen changes in men

    In a 12-week trial in 37 elderly men, PSA rose in the twice-weekly arm only (1.7 to 2.2 ng/mL, P = 0.031 against placebo). In a 31-man 12-month trial, PSA increased in both active arms at 6 months. In an 88-man 12-month trial, PSA did not change · A monitoring surface rather than a settled harm. The 31-man trial's primary outcome was prostate volume, which increased significantly only in the transdermal-testosterone arm, and its authors concluded that 12 months of an aromatase inhibitor was not detrimental to the prostate. Personal or family prostate history is a provider-discussion flag before anything is considered.

    [6] [9] [5]

  • Hormone effects that do not settle at a stable level

    In the 88-man one-year trial, testosterone rose from 11.2 to 18.2 nmol/L by month 3 and then declined by month 12, while estradiol fell from 55.8 to 42.2 pmol/L by month 3 and then remained stable · Framing rather than a verdict: the hormonal effect that is the entire rationale for off-label use in men was not flat over a year in the longest trial that measured it, and the same trial recorded no change in body composition, strength, PSA, symptoms of benign prostatic hypertrophy, haematocrit or lipids. A hormone level that moves is not the same thing as a clinical effect that lasts.

    [5]

Published lists are never exhaustive, so report anything unexpected to a licensed provider.

Storage, handling & reconstitution

Lyophilized storage
Anastrozole is not supplied as a lyophilized powder. Every US application in Drugs@FDA is a film-coated 1 mg oral tablet in prescription marketing status, dispensed as a finished, lot-tested pharmaceutical. The approved labeling's storage instruction is controlled room temperature, 20 to 25 degrees Celsius (68 to 77 degrees Fahrenheit), and the storage answer therefore comes from the container the tablets arrive in rather than from any research-peptide convention.
Reconstituted storage
Not applicable. There is no solution phase for this compound in any marketed US dosage form, so there is no reconstituted storage window to describe and none is invented here.
Reconstitution
Not applicable. Anastrozole is supplied only as a 1 mg film-coated tablet for oral administration. There is no vial, no diluent, no lyophilized cake and no solution phase anywhere in the marketed US dosage form, so there is nothing to reconstitute and no handling technique to describe.
Handling notes
The drug substance itself is described in the approved labeling as an off-white powder of molecular weight 293.4 with moderate aqueous solubility, but that is a description of the bulk chemical in a manufacturing context, not of anything a person is dispensed. Nothing on this page describes handling of unfinished material.

The how-to guides cover the conventions behind these fields, and what the published stability data does and does not establish: Storage, Reconstitution, Handling.

Working with a licensed provider

This is a prescription therapy. A licensed provider is required — to judge whether it is appropriate at all, to order and interpret the labs that monitor it, and to manage titration over time. Peptide Health Lab does not prescribe.

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Questions for your provider

Bring this page to a licensed provider. A provider can order labs, review your medications and history, and tell you whether anything here is relevant to your situation. This page can't. Peptide Health Lab does not prescribe and does not sell peptides.

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Citations

14 sources · every identifier checked against PubMed

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