Antioestrogens

Written by Megan Boucher

Last updated: 24th July 2026
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Hormonal, or endocrine, therapy is an important treatment option for oestrogen-receptor positive breast cancer. This article discusses the mechanisms of action, clinical uses, pharmacokinetics, adverse effects, contraindications and clinically relevant drug interactions associated with tamoxifen and the aromatase inhibitors anastrozole and letrozole. It also compares the use of tamoxifen and aromatase inhibitors according to menopausal status and highlights important considerations for the prevention and treatment of breast cancer. 

Indications for Use

Hormonal therapies are used in oestrogen-receptor positive breast cancer, either as neoadjuvant therapy, adjuvant therapy or to slow progression of advanced disease. 

When hormonal therapies are indicated in the treatment of breast cancer, tamoxifen is commonly used first line in premenopausal women and men, whereas aromatase inhibitors are used first line in postmenopausal women because they are more effective than tamoxifen in this population. In premenopausal women, an aromatase inhibitor may only be used when ovarian function is adequately suppressed or ablated. 

Treatment of breast cancer with tamoxifen or aromatase inhibitors generally continues for at least 5 years, although treatment may be extended to up to 10 years in selected patients depending on individual risk and treatment strategy. Tamoxifen and anastrozole are also licensed for primary prevention of breast cancer in women at moderate-high risk. 

Mechanism of Action

Oestrogen receptors are found in a substantial proportion of breast cancers and activation of these receptors leads to cell proliferation, therefore antagonism of oestrogen suppresses cell growth in ER positive breast cancers. 

Tamoxifen

Tamoxifen is a selective oestrogen receptor modulator (SERM). It acts as an oestrogen receptor antagonist in breast tissue, preventing oestrogen-mediated receptor activation and reducing oestrogen-dependent tumour cell proliferation. 

Tamoxifen also acts as a partial agonist at oestrogen receptors in plasma lipid, endometrium and bone. This activity possibly contributes to an increased risk of endometrial cancers and the bone-sparing effects in post menopausal women. 

Tamoxifen also reduces total cholesterol and low density lipoproteins by 10-20% leading to a cardioprotective effect. However, this potential favourable effect on lipid profiles does not eliminate the need to consider the overall cardiovascular and thromboembolic risk associated with treatment. 

Aromatase Inhibitors

Anastrozole and letrozole are aromatase inhibitors which interfere with oestrogen synthesis outside of the ovaries, in peripheral tissues. 

As they have little effect on oestrogen production in the ovaries, aromatase inhibitors are only effective in postmenopausal women, unless ovarian function has been suppressed or ablated such as post oophorectomy (removal of ovaries). 

Aromatase converts adrenal androgens (androstenedione and testosterone) to oestrogens (oestrone and oestradiol), aromatase inhibitors competitively bind and inhibit the aromatase enzyme leading to a reduction in oestrogen production.

 

Fig 1
Mechanism of Action of Aromatase Inhibitors

 

Pharmacokinetics

The following table describes the key pharmacokinetic parameters for antioestrogens:

Absorption Distribution Metabolism Excretion
Tamoxifen Tmax = 4-7 hours Plasma protein binding >99%  Metabolised by CYP2D6 and CYP3A4 to active metabolites with similar activity to tamoxifen 

Poor CYP2D6 metabolisers may lead to a reduced response 

Primarily excreted in faeces. Half-life (t½) is approximately 5-7 days for tamoxifen and approximately 14 days for the active metabolite N-desmethyltamoxifen.  
Letrozole  F = 99.9%

Tmax = 1-2 hours

Steady state plasma levels reached within 2-6 weeks 

Plasma protein binding = 60%

Volume of distribution = 1.87L/kg 

Small fraction metabolised by CYP2A6 and CYP3A4 to inactive metabolites  T½ = 2-4 days

 

Primarily excreted renally – no dose adjustment required in renal impairment (however limited evidence if CrCl <10ml/min)

Anastrazole Tmax <2 hours  Plasma protein binding = 40% Extensively metabolised – major metabolite is not active  T ½ = 40-50 hours

Primarily renally excreted – no dose adjustment required in renal impairment (caution in severe renal impairment) 

 

Fig 2
Metabolism of Tamoxifen to Active Metabolites

Adverse Effects

Oestrogen Depletion Related Adverse Effects

Both tamoxifen and aromatase inhibitors can cause symptoms associated with reduced oestrogen activity, including: 

  • Vaginal dryness
  • Hot flushes
  • Reduced bone mineral density, particularly with aromatase inhibitors and tamoxifen in premenopausal women  
  • Menstrual abnormalities

Tamoxifen

Important adverse effects associated with tamoxifen include: 

  • Severe cutaneous adverse reactions (SCARs) including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) 
  • Increased risk of endometrial cancer 
  • 2-3 fold increased risk of venous thromboembolism (VTE)
  • Rare prolongation of QTc interval

Aromatase Inhibitors

Aromatase inhibitors may be associated with: 

  • Abnormal liver function tests 
  • Tendonitis 
  • Increased risk of hypercholestrolaemia and hypertension; cardiovascular risks should be considered when starting either agent

Contraindications

Letrozole and anastrozole are contraindicated in pregnancy and breastfeeding, tamoxifen is also contraindicated during pregnancy. Aromatase inhibitors are contraindicated in women with premenopausal endocrine status. 

When tamoxifen is used for primary prevention of breast cancer, it should not be used in patients with history of a venous thromboembolism or in patients who require treatment with warfarin. 

Aromatase inhibitors should not be used as monotherapy in women who remain premenopausal because ovarian oestrogen production continues, unless ovarian function has been adequately suppressed or ablated.

Interactions

Tamoxifen

Tamoxifen is metabolised to active metabolites by CYP2D6, therefore when given alongside CYP2D6 inhibitors such as paroxetine, fluoxetine, quinidine, cinacalcet or bupropion, hepatic activation may be inhibited leading to reduced effectiveness of tamoxifen. Manufacturers recommend concomitant administration should be avoided where possible.

Furthermore, tamoxifen inhibits CYP2C9, therefore can increase levels of drugs that are substrates such as warfarin. 

In addition to this, tamoxifen can prolong the QT interval therefore administration alongside other agents that can cause this effect should be with caution. 

If tamoxifen is given alongside aromatase inhibitors, it may reduce the pharmacological action of the aromatase inhibitor. If given in combination with cytotoxic drugs in the treatment of breast cancer, there is an increased risk of developing VTE. 

Aromatase Inhibitors

Anastrozole inhibits CYP1A2, 2C8/9 and 3A4 in vitro however clinical studies found no significant interactions with substrates for these enzymes, such as amitriptyline and warfarin. Therefore, clinically significant CYP-mediated interactions are considered unlikely at the recommended dose.  

References

  1. Breast cancer | Treatment summaries | BNF | NICE Accesed 23/7/26
  2. Ritter JM, Flower RJ, Henderson G, Loke YK, MacEwan DJ. Rang & Dale’s Pharmacology. 9th ed. London: Elsevier; 2019.
  3. Hitchings BSc, M., Lonsdale, D., Burrage, D., Baker, E. (2022). The Top 100 Drugs – E-Book. Netherlands: Elsevier.
  4. Letrozole 2.5 mg film-coated tablets – Summary of Product Characteristics (SmPC) – (emc) | 9957  Accessed 23/07/26
  5. Tamoxifen 20mg Film-Coated Tablets – Summary of Product Characteristics (SmPC) – (emc) | 2248  Accessed 23/07/26
  6. Anastrozole 1 mg, film-coated tablets – Summary of Product Characteristics (SmPC) – (emc) | 13573 Accessed 23/07/26

 

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