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54965-24-1 Usage


Tamoxifen citrate, also known as Nolvadex, is a selective estrogen response modifier (SERM) that functions as an estrogen receptor antagonist/partial agonist. It is used to prevent and treat breast cancer in both women and men, and has additional applications in cardiovascular health and bone cancer treatment. Tamoxifen is metabolized into active metabolites, including 4-hydroxytamoxifen (4-OHT) and endoxifen, by cytochrome P450 isoforms CYP2D6 and CYP3A4. It is a white to off-white powder and has been a benchmark in endocrine therapy for over 40 years.


Used in Oncology:
Tamoxifen citrate is used as an estrogen antagonist and antineoplastic agent for the treatment of estrogen receptor-positive breast cancer in both women and men. It is particularly effective in treating early and advanced breast carcinoma in postmenopausal women and has been shown to reduce the occurrence of contralateral breast cancer in patients receiving adjuvant therapy.
Used in Cardiovascular Applications:
Tamoxifen citrate is used as an anti-estrogen with beneficial cardiovascular effects, potentially reducing the risk of heart-related complications in patients undergoing treatment for breast cancer.
Used in Bone Cancer Treatment:
Tamoxifen citrate is used as a treatment for bone cancer, as it has been shown to induce DNA adduct formation, which may help in the treatment of certain types of bone cancer.
Used in Protein Kinase C Inhibition:
Tamoxifen citrate is used as a protein kinase C inhibitor, which may have implications for the treatment of various cancers and other diseases.
Used in Anti-angiogenesis:
Tamoxifen citrate is used as an anti-angiogenetic factor, inhibiting the formation of new blood vessels that supply tumors with nutrients, thereby potentially slowing tumor growth.
Used in Prophylaxis:
Tamoxifen citrate is used as a long-term prophylactic treatment to reduce the recurrence rate of breast cancer, with the risk-lowering effect persisting for at least 10 years.
Used in Adjuvant Therapy:
Tamoxifen citrate is used as an adjuvant therapy for postmenopausal women with node-positive or node-negative, estrogen or progesterone receptor-positive breast cancer, often administered for a period of 2 to 5 years.
Used in Ovulation Stimulation:
Tamoxifen citrate is occasionally used to stimulate ovulation in women undergoing fertility treatments.

Mode of action

Tamoxifen is being frequently prescribed as hormonal therapy of estrogen positive breast cancer in the clinics of Pakistan. There is a competitive binding of tamoxifen to estrogen receptors in cancer cells and other tissue targets, and this in turn produces a nuclear complex that decreases DNA synthesis and inhibits estrogen action. It is a non-steroidal agent with potential anti estrogenic abilities which occupies estrogen binding sites in breast tissue and metabolized by the liver enzyme Cyp2D6 (cytochrome P450, family 2, subfamily D, polypeptide 6), rendering active metabolites of Tamoxifen includes N-desmethyl tamoxifen, endoxifen and 4 hydroxy tamoxifen[2]. Tamoxifen is known as a classic pro-drug requiring metabolic activation to start its pharmacological activity. Mainly 2D6 of cytochrome 450 appears to be the rate-limiting enzyme converting the pharmacologically inactive metabolites (Tamoxifen and NDM) to endoxifen, and further contributes to the formation of 4-OH-Tam from Tamoxifen. The findings depict that both genetic and environmental (drug-induced) factors that change CYP2D6 enzyme activity affect Tamoxifen treatment results[2]. Research was done to check the breast density after use of Tamoxifen in patients. MRI of breast was performed after Tamoxifen use. It was concluded that with the use of Tamoxifen breast cancer is reduced hence the breast density came out to be less[3].


The excretory fate of Tamoxifen and its metabolites has not been well characterized. Following oral administration of 20 mg dose of radio labeled Tamoxifen in women, normally 65% of the administered dose was excreted in feces for a 2-week time period, mainly as polar conjugates; unchanged tamoxifen and unconjugated metabolites accounted for less than 30% of the fecal radioactivity. Unchanged tamoxifen and N-desmethyl tamoxifen have been detected in urine in small amounts. In animals, Tamoxifen and/or its metabolites appear to undergo extensive enterohepatic circulation and are excreted in feces and urine as glucuronides, other conjugates, and unidentified polar metabolites[6]. In a study involving six healthy male volunteers, Tamoxifen tablets were shown to be as bioavailable as a solution of Tamoxifen citrate. After administration of a single dose of 20 mg, peak serum levels of Tamoxifen were 42 ng/ml; those of the metabolite were 12 ng/ml. The half-lives of the drug and metabolite were approximately 4 and 9 days, respectively, after a single dose. After three widely separated single doses, a reversible increase in elimination half-life occurred[7]. Tamoxifen is extensively metabolised after oral administration. N-desmethyl Tamoxifen, the major metabolite found in patients’ plasma, undergoes secondary metabolism to 4-hydroxy-N-desmethyl Tamoxifen (endoxifen). The enzyme involved in this conversion is cytochrome P450 2D6 (CYP2D6), which also converts Tamoxifen to 4-hydroxy Tamoxifen. This metabolite undergoes secondary metabolism to endoxifen. It is widely accepted that the majority of the anti-proliferative effect of Tamoxifen occurs via its active metabolites. 4-hydroxy Tamoxifen has at least 100-fold greater affinity for the ER than Tamoxifen, and has a similarly increased potency in anti-proliferative action. Endoxifen has an equivalent anti-proliferative potency and ER binding ability to 4-hydroxy Tamoxifen but is present in higher concentrations in the plasma. Any factor that diminishes production of these metabolites could impact on Tamoxifen efficacy. Several enzymes are involved in these metabolic pathways, with CYP2D6 playing a pivotal role. CYP2D6 is a polymorphic gene with over 90 documented alleles[8]. Peak concentrations occur 4-7 h after oral dosing. Peak concentrations after single oral doses of 20mg are about 40μg/l. There is no information on absolute bioavailability[10-12]. The elimination is biphasic, with an initial half-life of around 7 h and a terminal half-life of 7-11 days[8-10]. Tamoxifen is more than 99% protein-bound in serum, predominantly to albumin. In patients with breast cancer, concentrations of Tamoxifen and its metabolites in pleural, pericardial and peritoneal effusion fluid are between 20 and 100% of those in serum, but only trace amounts enter the cerebrospinal fluid. Concentrations in breast cancer tissue exceed those in serum. The volume of distribution is 50-60 l/kg[11,12].

Side effects

Most common side effects caused by tamoxifen are nausea, hot flashes, vaginal dryness, loss of sexual desire. It is notable that tamoxifen is not an antagonist at all tissues like in breast tissue. It therefore has agonist effect in bones and ovaries. In addition, it does not have a cardioprotective effect on heart and causes thromboembolism and fatty liver. It shows a reduction in libido and evidences of decreased cognition have been reported. The side effect of tamoxifen at mitochondrial level lies in an increased reactive oxygen species pathway due to tamoxifen within mitochondria of a cell leading to apoptosis[13]. Whilst it may also prove that the tamoxifen may leads to aging process as it is being used by breast cancer patients for more than 5 years. Less common side effects include anxiety, blistering, peeling, or loosening of the skin and mucous membranes, blurred vision, cataracts in the eyes or other eye problems, change in vaginal discharge, chest pain, chills, confusion, cough, dizziness, fainting, fast heartbeat, fever, hoarseness, lightheadedness, lower back or side pain, pain or feeling of pressure in the pelvis, pain or swelling in the legs, pain, redness, or swelling in your arm or leg, painful or difficult urination, rapid shallow breathing, shortness of breath or trouble with breathing, skin rash or itching over the entire body, sweating, weakness or sleepiness, wheezing, vaginal bleeding and yellow eyes or skin. More common side effects are absent, missed, or irregular periods and decrease in the amount of urine. There seems to be correlation between long-term Tamoxifen administration and endometrial proliferation[14]. Mild-moderate gastrointestinal toxicity (diarrhea, anorexia) and reversible neurotoxicity were observed in dogs receiving chemotherapy plus high-dose Tamoxifen given for seven days[15]. Nausea and vomiting can occur. Dizziness, lethargy, depression, irritability and cerebellar dysfunction have been described.


Shahbaz K, Mehfooz A, Khadam W, Din MU, Shahbaz K, et al. (2014) Breast Cancer Vaccination- An Envisioned Future. IAJPR 4(3): 1580-1585. Fuchs WS, Leary WP, van der MMJ, Gay S, Witschital K, et al. (1996) Pharmacokinetics and Bioavailability of Tamoxifen in Postmenopausal healthy women. Arzneimittelforschung 46(4): 418-422. Chen JH, Yeun CC, Daniel C, Yi TW, Ke N, et al. (2011) Reduction of breast density using tamoxifen treatment evaluated by 3D MRI. Magon reson imaging 29(1): 91-98. Cuzick J, Forbes JF, Sestak I, Cawthorn S, Hamed H, et al. (2007) Long-Term Results of Tamoxifen Prophylaxis for Breast Cancer 96-Month Follow-up of the Randomized IBIS-I Trial. J Natl Cancer Inst 99(4): 272-282. Guelen P, Stevenson D, Briggs R, De Vos D (1987) The bioavailability of Tamoplex (tamoxifen). Part 2. A single dose cross-over study in healthy male volunteers. Methods Find Exp Clin Pharmacol 9(10): 685-90. De Santana DP, Rossana MCB, Ruth S, Miracy MA, César GB, et al. (2008) Reversed phase HPLC determination of Tamoxifen in dog plasma and its pharmacokinetic after a single oral dose administration. Quim Nova 31(1): 47-52. 21. Adam HK, Patterson JS, Kemp JV (1980) Studies in the metabolism and pharmacokinetics of Tamoxifen in normal volunteers. Cancer Treat Rep 64(6-7): 761-764. Golander Y, Sternson LA (1980) Paired-ion chromatographic analysis of Tamoxifen and two major metabolites in plasma. J Chromatogr 181(1): 41-49. Carter SJ, Li XF, Mackey JR, Modi S, Hanson J et al. (2001) Biomonitoring of Urinary Tamoxifen and its metabolites from breast cancer patients using non-aqueous capillary electrophoresis with electrospray mass spectrometry. Electrophoresis 22(13): 2730-2706. Martindale (1999) The Complete Drug Reference (33rd edn), Pharmaceutical Press, London, pp: 2315. Buckley MMT, Goa KL (1989) Tamoxifen. Drugs 37(4): 451-490. Lien EA, E Solheim, OA Lea, S Lundgren, S Kvinnsland, PM Ueland (1989) Distribution of 4-hydroxy-N-desmethylTamoxifen and other Tamoxifen metabolites in human biological fluids during Tamoxifen treatment. Cancer Res 49(8): 2175-2183. Nazarewicz RR, Zenebe WJ, Parihar A, Larson SK, Alidema E, et al. (2007) Tamoxifen Induces Oxidative Stress and Mitochondrial Apoptosis via Stimulating Mitochondrial Nitric Oxide Synthase. Cancer Res 67(3): 1282-1290. Uziely B, Lewin A, Brufman G, Dorembus D, Mor-Yosef S (1993) The effect of tamoxifen on the endometrium. Breast Cancer Res Treat 26(1): 101-105. 15. Waddle J, Fine R, Case B, Trogdon M, Tyczkowska K, et al. (1999) Phase I and pharmacokinetic analysis of high-dose tamoxifen and chemotherapy in normal and tumor-bearing dogs. Cancer Chemother Pharmacol 44(1): 74


1) Ferlini et al. (1999), Tamoxifen induces oxidative stress and apoptosis in oestrogen receptor-negative human cancer cell lines; Br. J. Cancer, 79 257 2) Kimelberg et al. (2003), Neuroprotective activity of tamoxifen in permanent focal ischemia; J. Neurosurg., 99 138 3) Couldwell et al. (1994), Protein kinase C inhibitors induce apoptosis in human malignant glioma cell lines; FEBS Lett., 345 43 4) Thomas et al. (2005), Identity of an estrogen membrane receptor coupled to a G protein in human breast cancer cells; Endocrinology, 146 624 5) Jordan et al. (2006), Tamoxifen (ICI46,474) as a targeted therapy to treat and prevent breast cancer; Br. J. Pharmacol., 147 S269

Therapeutic Function

Antiestrogen, Antineoplastic

Biological Activity

Estrogen receptor antagonist/partial agonist. Selective and potent inhibitor of mammalian sterol isomerase. Neuroprotective in female rats in vivo . Also high affinity agonist at the membrane estrogen receptor GPR30.

Biochem/physiol Actions

Cell permeable: yes

Safety Profile

Confirmed human carcinogen with experimental carcinogenic data. Poison by intraperitoneal route. Moderately toxic by ingestion. Experimental reproductive effects. Human systemic effects: visual field changes, retinal changes. An anti-estrogenic drug. Mutation data reported. When heated to decomposition it emits toxic fumes of NOx.

Check Digit Verification of cas no

The CAS Registry Mumber 54965-24-1 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 5,4,9,6 and 5 respectively; the second part has 2 digits, 2 and 4 respectively.
Calculate Digit Verification of CAS Registry Number 54965-24:
151 % 10 = 1
So 54965-24-1 is a valid CAS Registry Number.

54965-24-1 Well-known Company Product Price

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  • (T0014000)  Tamoxifen citrate  European Pharmacopoeia (EP) Reference Standard

  • 54965-24-1

  • T0014000

  • 1,880.19CNY

  • Detail
  • Sigma-Aldrich

  • (T0015000)  Tamoxifen citrate for performance test  European Pharmacopoeia (EP) Reference Standard

  • 54965-24-1

  • T0015000

  • 1,880.19CNY

  • Detail
  • Sigma

  • (T9262)  Tamoxifencitratesalt  ≥99%

  • 54965-24-1

  • T9262-1G

  • 3,591.90CNY

  • Detail
  • Sigma

  • (T9262)  Tamoxifencitratesalt  ≥99%

  • 54965-24-1

  • T9262-5G

  • 12,577.50CNY

  • Detail



According to Globally Harmonized System of Classification and Labelling of Chemicals (GHS) - Sixth revised edition

Version: 1.0

Creation Date: Aug 13, 2017

Revision Date: Aug 13, 2017


1.1 GHS Product identifier

Product name tamoxifen citrate

1.2 Other means of identification

Product number -
Other names Tamoxifen citrate salt

1.3 Recommended use of the chemical and restrictions on use

Identified uses For industry use only.
Uses advised against no data available

1.4 Supplier's details

1.5 Emergency phone number

Emergency phone number -
Service hours Monday to Friday, 9am-5pm (Standard time zone: UTC/GMT +8 hours).

More Details:54965-24-1 SDS

54965-24-1Synthetic route



citric acid

citric acid

tamoxifen citrate

tamoxifen citrate

In acetonitrile


citric acid

citric acid


tamoxifen citrate

tamoxifen citrate


(Z)-2-(4-(1,2-diphenylbut-1-enyl)phenoxy)-N,N-dimethylethylamine citrate

(Z)-2-(4-(1,2-diphenylbut-1-enyl)phenoxy)-N,N-dimethylethylamine citrate

Stage #1: 1-(4-(2-(dimethylamino)ethoxy)phenyl)-1,2-diphenylbutan-1-ol With hydrogenchloride In water; isopropyl alcohol for 5h; Reflux;
Stage #2: citric acid In acetone at -5 - 10℃; for 10h;
A n/a
B 7.5 g

54965-24-1Downstream Products

54965-24-1Relevant articles and documents

Crystalline form information from multiwell plate salt screening by use of raman microscopy

Kojima, Takashi,Onoue, Satomi,Murase, Noriaki,Katoh, Fumie,Mano, Takashi,Matsuda, Yoshihisa

, p. 806 - 812 (2006)

Purpose. The purpose of this study was to establish a useful methodology, possibly providing information on the stoichiometry of pharmaceutical drug salts obtained from salt screening by using a multiwell plate and a Raman microscope. Methods. Tamoxifen salt screening was conducted with monobasic and polybasic acids on 96-well quartz plates with a Raman microscope. Appearance and crystalline forms of salts prepared on 96-well plates were observed by polarizing light microscope and Raman microscope, respectively. Based on the results of the salt screening, tamoxifen citrate and fumarate salts were prepared on a large scale. The salts prepared were characterized by powder X-ray diffractometry (PXRD) and ion chromatography. Results. The results of the multiwell salt screening indicated that tamoxifen has a tendency toward the formation of mono salt as opposed to hemi salt with polybasic acid, and that most of tamoxifen salts gave several potential polymorphic forms. PXRD patterns of scaled-up tamoxifen citrate and fumarate salts suggested that the same crystalline form was obtained from the binary mixture regardless of molar ratios of 2:1 or 1:1 (tamoxifen/acid). The crystalline forms obtained were tamoxifen monocitrate and monofumarate salts as measured by ion chromatography. Conclusions. Salt screening on multiwell plates with a Raman microscope provided novel insight into the characteristics prediction of the stoichiometrical salts in addition to potential polymorph information. Based on the stoichiometrical information of salts, the amount of compound and time required for crystalline form selection of drug candidates would be significantly reduced.

Method of treating nausea and vomiting with certain substituted-phenylalkylamino (and aminoacid) derivatives and other serotonin depleting agents


, (2008/06/13)

A method for the treatment of emesis in a mammal, which method comprises administering to said mammal an emesis inhibiting amount of a compound which depletes serotonin in the brain of mammals; among which are compounds having the formula: STR1 wherein, R is selected from hydrogen, loweralkyl, trifluoromethyl, carboxyl, or loweralkoxycarbonyl; R1 and R2 are hydrogen or loweralkyl; Z is trifluoromethyl or halogen; the optical isomers and pharmaceutically acceptable salts thereof; two of the preferred compounds of the invention are fenfluramine and norfenfluramine.

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