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MedKoo Cat#: 100340 | Name: Exemestane
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Description:

WARNING: This product is for research use only, not for human or veterinary use.

Exemestane is a synthetic androgen analogue. Exemestane binds irreversibly to and inhibits the enzyme aromatase, thereby blocking the conversion of cholesterol to pregnenolone and the peripheral aromatization of androgenic precursors into estrogens.

Chemical Structure

Exemestane
Exemestane
CAS#107868-30-4

Theoretical Analysis

MedKoo Cat#: 100340

Name: Exemestane

CAS#: 107868-30-4

Chemical Formula: C20H24O2

Exact Mass: 296.1776

Molecular Weight: 296.40

Elemental Analysis: C, 81.04; H, 8.16; O, 10.80

Price and Availability

Size Price Availability Quantity
200mg USD 150.00 Ready to ship
500mg USD 350.00 Ready to ship
1g USD 550.00 Ready to ship
2g USD 950.00 Ready to ship
5g USD 1,650.00 Ready to ship
10g USD 2,950.00 Ready to ship
20g USD 5,250.00 Ready to ship
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Related CAS #
No Data
Synonym
PNU155971; PNU-155971; PNU 155971; FCE24304; FCE-24304; FCE 24304; Exemestane; US brand name: Aromasin.
IUPAC/Chemical Name
(8R,9S,10R,13S,14S)-10,13-dimethyl-6-methylene-7,8,9,10,11,12,13,14,15,16-decahydro-3H-cyclopenta[a]phenanthrene-3,17(6H)-dione.
InChi Key
BFYIZQONLCFLEV-DAELLWKTSA-N
InChi Code
InChI=1S/C20H24O2/c1-12-10-14-15-4-5-18(22)20(15,3)9-7-16(14)19(2)8-6-13(21)11-17(12)19/h6,8,11,14-16H,1,4-5,7,9-10H2,2-3H3/t14-,15-,16-,19+,20-/m0/s1
SMILES Code
O=C(C=C1C(C[C@@]2([H])[C@]3([H])CC4)=C)C=C[C@]1(C)[C@@]2([H])CC[C@]3(C)C4=O
Appearance
white solid powder
Purity
>98% (or refer to the Certificate of Analysis)
Shipping Condition
Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.
Storage Condition
Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).
Solubility
Soluble in DMSO, not in water
Shelf Life
>2 years if stored properly
Drug Formulation
This drug may be formulated in DMSO
Stock Solution Storage
0 - 4 C for short term (days to weeks), or -20 C for long term (months).
HS Tariff Code
2934.99.9001
More Info
DRUG DESCRIPTION AROMASIN® Tablets for oral administration contain 25 mg of exemestane, an irreversible, steroidal aromatase inactivator. Exemestane is chemically described as 6-methylenandrosta-1,4-diene-3,17-dione. Its molecular formula is C20H24O2. The active ingredient is a white to slightly yellow crystalline powder with a molecular weight of 296.41. Exemestane is freely soluble in N, N-dimethylformamide, soluble in methanol, and practically insoluble in water. Each AROMASIN Tablet contains the following inactive ingredients: mannitol, crospovidone, polysorbate 80, hypromellose, colloidal silicon dioxide, microcrystalline cellulose, sodium starch glycolate, magnesium stearate, simethicone, polyethylene glycol 6000, sucrose, magnesium carbonate, titanium dioxide, methylparaben, and polyvinyl alcohol.     Mechanism of Action Mechanism of Action Breast cancer cell growth may be estrogen-dependent. Aromatase is the principal enzyme that converts androgens to estrogens both in pre- and postmenopausal women. While the main source of estrogen (primarily estradiol) is the ovary in premenopausal women, the principal source of circulating estrogens in postmenopausal women is from conversion of adrenal and ovarian androgens (androstenedione and testosterone) to estrogens (estrone and estradiol) by the aromatase enzyme in peripheral tissues. Estrogen deprivation through aromatase inhibition is an effective and selective treatment for some postmenopausal patients with hormone-dependent breast cancer. Exemestane is an irreversible, steroidal aromatase inactivator, structurally related to the natural substrate androstenedione. It acts as a false substrate for the aromatase enzyme, and is processed to an intermediate that binds irreversibly to the active site of the enzyme causing its inactivation, an effect also known as “suicide inhibition.” Exemestane significantly lowers circulating estrogen concentrations in postmenopausal women, but has no detectable effect on adrenal biosynthesis of corticosteroids or aldosterone. Exemestane has no effect on other enzymes involved in the steroidogenic pathway up to a concentration at least 600 times higher than that inhibiting the aromatase enzyme. Breast cancer cell growth may be estrogen-dependent. Aromatase is the principal enzyme that converts androgens to estrogens both in pre- and postmenopausal women. While the main source of estrogen (primarily estradiol) is the ovary in premenopausal women, the principal source of circulating estrogens in postmenopausal women is from conversion of adrenal and ovarian androgens (androstenedione and testosterone) to estrogens (estrone and estradiol) by the aromatase enzyme in peripheral tissues. Estrogen deprivation through aromatase inhibition is an effective and selective treatment for some postmenopausal patients with hormone-dependent breast cancer. Exemestane is an irreversible, steroidal aromatase inactivator, structurally related to the natural substrate androstenedione. It acts as a false substrate for the aromatase enzyme, and is processed to an intermediate that binds irreversibly to the active site of the enzyme causing its inactivation, an effect also known as “suicide inhibition.” Exemestane significantly lowers circulating estrogen concentrations in postmenopausal women, but has no detectable effect on adrenal biosynthesis of corticosteroids or aldosterone. Exemestane has no effect on other enzymes involved in the steroidogenic pathway up to a concentration at least 600 times higher than that inhibiting the aromatase enzyme.
Biological target:
Exemestane (FCE24304, PNU155971) is an aromatase inhibitor, inhibits human placental and rat ovarian aromatase with IC50 of 30 nM and 40 nM, respectively.
In vitro activity:
As shown in Fig. 4B, exemestane inhibited aromatase in MCF-7aro cells in a time-dependent manner. Based on previous knowledge and findings from this study, as shown in Scheme 1 , the interaction between exemestane and aromatase can be divided into three steps. Step 1 is the reversible step when exemestane binds to aromatase with a Ki of 26 nmol/L. At step 2, exemestane is converted into an intermediate, through a yet unknown process, and results in an irreversible inactivation of the enzyme. The t1/2 of this process is ∼13.9 minutes. At step 3, a degradation of aromatase by proteasome occurs after the irreversible inactivation step. We have found that in vitro incubation of exemestane with purified aromatase had no effect on aromatase protein stability. Following the exemestane treatment of MCF-7aro cells, the t1/2 of aromatase protein is reduced by 50% or more. We have determined that exemestane, at 200 nmol/L, decreases aromatase t1/2 to 12.5 hours from 28.2 hours in untreated cells. In addition, exemestane treatment did not cause significant changes of aromatase mRNA levels. Therefore, exemestane is a unique AI that can also destabilize aromatase protein. Reference: Cancer Res. 2006 Nov 1;66(21):10281-6. https://cancerres.aacrjournals.org/content/66/21/10281.long
In vivo activity:
The effect of EXE on liver injury and fibrosis were assessed in two hepatic fibrosis rat models, which were induced by either carbon tetrachloride (CCl4) or bile duct ligation (BDL). The influence of EXE treatment on activation and proliferation of primary rat hepatic stellate cells (HSCs) was observed in vitro. The results showed that EXE attenuated the liver fibrosis by decreasing the collagen deposition and α-SMA expression in vivo and inhibited the activation and proliferation of primary rat HSCs in vitro. Additionally, EXE promoted the secretion of antifibrotic and anti-inflammatory cytokine IL-10 in vivo and in HSC-T6 culture media. In conclusion, our findings reveal a new function of EXE on hepatic fibrosis and prompted its latent application in liver fibrotic-related disease. Reference: J Immunol Res. 2017;2017:3072745. https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/29464186/
Solvent mg/mL mM
Solubility
DMSO 54.0 182.19
Ethanol 21.0 70.85
Note: There can be variations in solubility for the same chemical from different vendors or different batches from the same vendor. The following factors can affect the solubility of the same chemical: solvent used for crystallization, residual solvent content, polymorphism, salt versus free form, degree of hydration, solvent temperature. Please use the solubility data as a reference only. Warming and sonication will facilitate dissolving. Still have questions? Please contact our Technical Support scientists.

Preparing Stock Solutions

The following data is based on the product molecular weight 296.40 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Recalculate based on batch purity %
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 1.15 mL 5.76 mL 11.51 mL
5 mM 0.23 mL 1.15 mL 2.3 mL
10 mM 0.12 mL 0.58 mL 1.15 mL
50 mM 0.02 mL 0.12 mL 0.23 mL
Formulation protocol:
1. Wang X, Chen S. Aromatase destabilizer: novel action of exemestane, a food and drug administration-approved aromatase inhibitor. Cancer Res. 2006 Nov 1;66(21):10281-6. doi: 10.1158/0008-5472.CAN-06-2134. PMID: 17079446. 2. Jayapal JJ, Dhanaraj S. Exemestane loaded alginate nanoparticles for cancer treatment: Formulation and in vitro evaluation. Int J Biol Macromol. 2017 Dec;105(Pt 1):416-421. doi: 10.1016/j.ijbiomac.2017.07.064. Epub 2017 Jul 13. PMID: 28711612. 3. Wang YH, Li RK, Fu Y, Li J, Yang XM, Zhang YL, Zhu L, Yang Q, Gu JR, Xing X, Zhang ZG. Exemestane Attenuates Hepatic Fibrosis in Rats by Inhibiting Activation of Hepatic Stellate Cells and Promoting the Secretion of Interleukin 10. J Immunol Res. 2017;2017:3072745. doi: 10.1155/2017/3072745. Epub 2017 Dec 10. PMID: 29464186; PMCID: PMC5804406.
In vitro protocol:
1. Wang X, Chen S. Aromatase destabilizer: novel action of exemestane, a food and drug administration-approved aromatase inhibitor. Cancer Res. 2006 Nov 1;66(21):10281-6. doi: 10.1158/0008-5472.CAN-06-2134. PMID: 17079446. 2. Jayapal JJ, Dhanaraj S. Exemestane loaded alginate nanoparticles for cancer treatment: Formulation and in vitro evaluation. Int J Biol Macromol. 2017 Dec;105(Pt 1):416-421. doi: 10.1016/j.ijbiomac.2017.07.064. Epub 2017 Jul 13. PMID: 28711612.
In vivo protocol:
1. Wang YH, Li RK, Fu Y, Li J, Yang XM, Zhang YL, Zhu L, Yang Q, Gu JR, Xing X, Zhang ZG. Exemestane Attenuates Hepatic Fibrosis in Rats by Inhibiting Activation of Hepatic Stellate Cells and Promoting the Secretion of Interleukin 10. J Immunol Res. 2017;2017:3072745. doi: 10.1155/2017/3072745. Epub 2017 Dec 10. PMID: 29464186; PMCID: PMC5804406.
1: Scott LJ, Wiseman LR. Exemestane. Drugs. 1999 Oct;58(4):675-80; discussion 681-2. doi: 10.2165/00003495-199958040-00007. PMID: 10551437. 2: Turner NC, Swift C, Kilburn L, Fribbens C, Beaney M, Garcia-Murillas I, Budzar AU, Robertson JFR, Gradishar W, Piccart M, Schiavon G, Bliss JM, Dowsett M, Johnston SRD, Chia SK. ESR1 Mutations and Overall Survival on Fulvestrant versus Exemestane in Advanced Hormone Receptor-Positive Breast Cancer: A Combined Analysis of the Phase III SoFEA and EFECT Trials. Clin Cancer Res. 2020 Oct 1;26(19):5172-5177. doi: 10.1158/1078-0432.CCR-20-0224. Epub 2020 Jun 16. PMID: 32546646. 3: Wang Y, Jing F, Wang H. Role of Exemestane in the Treatment of Estrogen- Receptor-Positive Breast Cancer: A Narrative Review of Recent Evidence. Adv Ther. 2022 Feb;39(2):862-891. doi: 10.1007/s12325-021-01924-2. Epub 2022 Jan 6. PMID: 34989983. 4: Sobral AF, Amaral C, Correia-da-Silva G, Teixeira N. Unravelling exemestane: From biology to clinical prospects. J Steroid Biochem Mol Biol. 2016 Oct;163:1-11. doi: 10.1016/j.jsbmb.2016.03.019. Epub 2016 Mar 15. PMID: 26992705. 5: Buzdar A. Exemestane in advanced breast cancer. Anticancer Drugs. 2000 Sep;11(8):609-16. doi: 10.1097/00001813-200009000-00002. PMID: 11081451. 6: Yardley DA, Noguchi S, Pritchard KI, Burris HA 3rd, Baselga J, Gnant M, Hortobagyi GN, Campone M, Pistilli B, Piccart M, Melichar B, Petrakova K, Arena FP, Erdkamp F, Harb WA, Feng W, Cahana A, Taran T, Lebwohl D, Rugo HS. Everolimus plus exemestane in postmenopausal patients with HR(+) breast cancer: BOLERO-2 final progression-free survival analysis. Adv Ther. 2013 Oct;30(10):870-84. doi: 10.1007/s12325-013-0060-1. Epub 2013 Oct 25. Erratum in: Adv Ther. 2014 Sep;31(9):1008-9. PMID: 24158787; PMCID: PMC3898123. 7: Shetty YC, Chakkarwar PN, Acharya SS, Rajadhyaksha VD. Exemestane: a milestone against breast cancer. J Postgrad Med. 2007 Apr-Jun;53(2):135-8. doi: 10.4103/0022-3859.32218. PMID: 17495383. 8: Deeks ED, Scott LJ. Exemestane: a review of its use in postmenopausal women with breast cancer. Drugs. 2009;69(7):889-918. doi: 10.2165/00003495-200969070-00007. PMID: 19441873. 9: Decensi A, Dunn BK, Puntoni M, Gennari A, Ford LG. Exemestane for breast cancer prevention: a critical shift? Cancer Discov. 2012 Jan;2(1):25-40. doi: 10.1158/2159-8290.CD-11-0248. PMID: 22585166; PMCID: PMC3354700. 10: Clemett D, Lamb HM. Exemestane: a review of its use in postmenopausal women with advanced breast cancer. Drugs. 2000 Jun;59(6):1279-96. doi: 10.2165/00003495-200059060-00007. PMID: 10882163. 11: Lønning PE. Exemestane in breast cancer: current status and future directions. Clin Breast Cancer. 2000 Sep;1 Suppl 1:S28-33. doi: 10.3816/cbc.2000.s.006. PMID: 11970747. 12: Jones SA, Jones SE. Exemestane: a novel aromatase inactivator for breast cancer. Clin Breast Cancer. 2000 Oct;1(3):211-6. doi: 10.3816/CBC.2000.n.017. PMID: 11899645. 13: Baselga J, Campone M, Piccart M, Burris HA 3rd, Rugo HS, Sahmoud T, Noguchi S, Gnant M, Pritchard KI, Lebrun F, Beck JT, Ito Y, Yardley D, Deleu I, Perez A, Bachelot T, Vittori L, Xu Z, Mukhopadhyay P, Lebwohl D, Hortobagyi GN. Everolimus in postmenopausal hormone-receptor-positive advanced breast cancer. N Engl J Med. 2012 Feb 9;366(6):520-9. doi: 10.1056/NEJMoa1109653. Epub 2011 Dec 7. PMID: 22149876; PMCID: PMC5705195. 14: di Salle E, Ornati G, Giudici D, Lassus M, Evans TR, Coombes RC. Exemestane (FCE 24304), a new steroidal aromatase inhibitor. J Steroid Biochem Mol Biol. 1992 Sep;43(1-3):137-43. doi: 10.1016/0960-0760(92)90198-r. PMID: 1525055. 15: Bertelli G, Gangadhara S. Exemestane in postmenopausal women with early or advanced breast cancer: a review. Expert Opin Pharmacother. 2010 Aug;11(11):1933-42. doi: 10.1517/14656566.2010.495945. PMID: 20569090. 16: Wang J, Cai L, Song Y, Sun T, Tong Z, Teng Y, Li H, Ouyang Q, Chen Q, Cui S, Yin Y, Liao N, Sun Q, Feng J, Wang X, Xu B. Clinical efficacy of fulvestrant versus exemestane as first-line therapies for Chinese postmenopausal oestrogen- receptor positive /human epidermal growth factor receptor 2 -advanced breast cancer (FRIEND study). Eur J Cancer. 2023 May;184:73-82. doi: 10.1016/j.ejca.2023.02.007. Epub 2023 Feb 15. PMID: 36905771. 17: Higa GM. Exemestane: treatment of breast cancer with selective inactivation of aromatase. Am J Health Syst Pharm. 2002 Nov 15;59(22):2194-2201; quiz 2202-4. doi: 10.1093/ajhp/59.22.2202. PMID: 12455303. 18: Lønning PE, Geisler J. Experience with exemestane in the treatment of early and advanced breast cancer. Expert Opin Drug Metab Toxicol. 2008 Jul;4(7):987-97. doi: 10.1517/17425255.4.7.987. PMID: 18624685. 19: Glück S. Exemestane as first-line therapy in postmenopausal women with recurrent or metastatic breast cancer. Am J Clin Oncol. 2010 Jun;33(3):314-9. doi: 10.1097/COC.0b013e31819fdf9b. PMID: 19730353. 20: Dunn BK, Cazzaniga M, DeCensi A. Exemestane: one part of the chemopreventive spectrum for ER-positive breast cancer. Breast. 2013 Jun;22(3):225-37. doi: 10.1016/j.breast.2013.02.015. Epub 2013 Mar 25. PMID: 23535509.