INTRODUCTION:

Based on the expression of the tumor's receptors, especially whether the tumor expresses the Human Epidermal Growth Factor receptor-2 (HER2) gene, the Progesterone receptor (PR), the Estrogen receptor (ER), or both, breast cancer is categorized into subgroups.¹

Most patients with breast cancer are classified as having ER+ disease. Because this disease segment depends on ER, most treatment efforts focus on inhibiting distinct portions of this route.²

Figure 1. Representation of HER2-Positive Cancer Cell ⁴

In reality, the standard of care for patients with ER-positive breast cancer still involves either regulating the activity of the ER pathway (such as with tamoxifen) or inhibiting the production of estrogen (such as with aromatase inhibitors [AI]).³

Because of this ongoing reliance on ER, novel selective estrogen receptor degraders, or SERDs, have received a lot of interest as a potential means of improving progression-free survival and providing longer-lasting benefits.⁵

Selective estrogen receptor modulators (SERMs), such as tamoxifen, block estrogen receptor (ER) function. examples of available endocrine drugs are selective estrogen receptor blocking agents (SERDs), such as fulvestrant, and aromatase inhibitors. The only SERD approved for hormone receptor-positive postmenopausal women with advanced breast cancer is fulvestrant. Compared with anastrozole, fulvestrant showed significant therapeutic benefit and longer progression-free survival (PFS).⁶Fulvestrant has limitations due to its intramuscular route of administration and pharmacokinetic (PK) properties, highlighting the need for new potent ER antagonists with better PK profiles.^5,7The investigational non-steroidal oral SERD is an elastic band. Elacestrant showed dose-dependent degradation of ER in ER+ breast cancer cell lines and reduced estradiol-dependent stimulation of ER target gene transcription and cell proliferation.^5,7,8Elacestrant inhibited estradiol-activated tumor growth in ER+ MCF-7 breast cancer. Cells lineal xenograft models and patient-derived xenograft models from patients who have undergone extensive pre-treatment.^5,7,8In addition to resistance to CDK4/6 inhibitors, Elacestrant has also shown antitumor activity in breast cancer animals with resistance-causing mutations. in the estrogen receptor alpha gene (ESR1), such as Y537S and D538G.^5,9,10 In a phase 1 study (RAD1901-005) in heavily pretreated postmenopausal women with ER+/human epidermal growth factor receptor (HER)2 advanced/metastatic breast cancer (ABC/mBC), 400 mg Elacestrant daily had an objective response rate (ORR) of 19.4% and a median PFS of 4.5 months.¹¹ The current phase 1b study (RAD1901-106) was initiated while the RAD1901-005 phase 1 study was still ongoing to investigate how elacestrant treatment affected ER availability in lesions of ABC patients using low-dose FES-PET computed tomography (FES-PET/CT) to measure ER level regulation. Trial and objectives also included evaluation of PK, safety, initial efficacy, correlation of ER availability and response, and initial efficacy of Elacestrant in postmenopausal women with ER + ABC.¹²

Description^13,14,15:

Table 1. Brief description of the drug

Name	Elacestrant dihydrochloride
Molecular Weight	531.6 g/mol
Molecular Formula	C₃₀H₄₀Cl₂N₂O₂
Synonyms	⁎ 1349723-93-8 ⁎ 8NZT0PRAL ⁎ RAD1901 ⁎ Q27270799 ⁎ C171898
Structure
3D Structure
IUPAC Name	(6R)-6-[2-[ethyl-[[4-[2-(ethylamino)ethyl]phenyl]methyl]amino]-4-methoxyphenyl]-5,6,7,8-tetrahydronaphthalen-2-ol; dihydrochloride
Type	Small molecule
Brand Name	ORSERDU
Generic Name	Elacestrant
Appearance	White to off-white to grey
State	Solid
Solubility (25°C)	In- vitro soluble in DMSO, Water and Ethanol and freely soluble in 0.01N HCl
Storage (From the date of receipt)	3 years -20°C powder 1 years -80°C in solvent 68℉ to 77℉ (20℃ to 25℃) RT

Patents of Elacestrant^16-22:

Table 2. Patents of Elacestrant

Patent No.	Title	Filing date	Publication date
US-2020361853-A1 US20210269389-A1 US11643385-B2	Polymorphic forms of RAD1901-2HCl	06-07-2020 03-07-2019 03-07-2019	19-11-2020 02-09-2021 09-05-2023
US20220117963A1 PH-12021551235-A1	Elacestrant in combination with Abemaciclib in women with breast cancer	26-11-2019 28-05-2021	21-04-2022 13-12-2021
WO-2023064519-A1	Solid state forms of Elacestrant and processes for preparation thereof	14-10-2022	20-04-2023
CA2984195-A15A1	Use of rad1901 in the treatment of cancer	29-04-2016	03-11-2016

Other Similar Drugs²³:

Toremifeme Idoxifene Bazedoxifene

Pipindoxifene Raloxifene

Arzoxifene Lasofoxifene

Acolbifene

Mechanism of Action:

SERDs favor and oppose ER transcriptional exertion. These agents bind to the ER, incapacitate and destabilize the ER- SERD complex, promoting ER declination via the ubiquitin-proteasome pathway.²⁴Recent studies indicate that SERDs reduce ER nuclear translocation, thereby adding ER development due to limited intracellular mobility. In addition, SERD- related conformational changes in the ER reduce the recap of ER- modulated genes. In the clinical setting of Estrogen Receptor 1(ESR1) mutation- convinced ET resistance, SERDs are also useful.²⁵

The estrogen receptor nascence (ERα) binding emulsion Elacestrant is an estrogen receptor antagonist. In ER-positive (ER), HER2-negative (HER2-) breast cancer cells, elacestrant reduced 17-estradiol-intermediated cell proliferation at attention that convinced ER protein declination via the proteasomal pathway.²⁶ Breast cancer models with ER HER2 status resistant to fulvestrant and cyclin-dependent kinase4/6 impediments and models with estrogen receptor 1 gene (ESR1) mutations showed antitumor efficacy when Elacestrant was used in both in vitro and in vivo studies.¹⁵

Figure 2. General mechanism of action of SERD: Selective Estrogen Receptor Degrader ²³

Figure 3. Mechanism of Elacestrant²⁶

ER: Estrogen receptor; SERD: Selective estrogen receptor degrader; SERM: Selective estrogen receptor modulator.

Comparison of MOA of Different Class:

Figure 4. Mechanism of Action of Various Classesof Drugs²³

Pharmacological Properties:

· Absorption:^14,15,27

The Peak plasma concentration (t_max) might be reached in anywhere between one and four hours. About 10% of Elacestrant is bioavailable when taken orally.

Effect of Food:

When compared to fasted administration, the C_max and AUC of Elacestrant 345mg were enhanced by 42% and 22%, respectively, when given with a high-fat meal (800–1000 calories, 50% fat).

· Distribution: 5800L is the estimated apparent volume of distribution. Elacestrant has a >99%, concentration-independent plasma protein binding rate.

· Metabolism:^14,15,28 CYP3A4 is predominantly responsible for Elacestrant's metabolism, with CYP2A6 and CYP2C9 having a minor role.

· Elimination:^14,15Elacestrant has a 30 to 50hour half-life in the body. The renal clearance of Elacestrant is predicted to be 0.14L/hr, while the mean (% CV) clearance is 186L/hr (43.5%).

· Excretion:^14,15 A single dose of 345mg radio labeled oral medication resulted in 82% recovery in the faeces (34% unaltered), 7.5% recovery in the urine (< 1% unchanged), and the remaining 1% in both tissues.

Most common Side effects¹⁵:

· Muscle and joint (musculoskeletal) pain

· Nausea

· Increased cholesterol and triglyceride levels in your blood

· Increased liver function tests

· Tiredness

· Decreased red blood cell counts

· Vomiting

· Decreased salt (sodium) levels in your blood

· Increased kidney function test

· Decreased appetite

· Diarrhea

· Headache

· Constipation

· Stomach-area (abdominal) pain

· Hot flush

· Indigestion or heartburn*

Recommended Dosage^15,29,30:

Until illness progression or intolerable toxicity occurs, a daily dose of 345mg of Elacestrant given orally with food is advised.

Take Elacestrant around the same time every day. Reduce nausea and vomiting by taking with food.

As a whole, swallow the Elacestrant tablet(s). Before swallowing, do not split, chew, or crush the pill. Any Elacestrant tablets that are damaged, cracked, or appear broken should not be taken. Take the next dose at the regularly scheduled time the next day if a dose is missed for longer than 6 hours or if vomiting develops.

DOSAGE FORMS AND STRENGTHS¹⁵:

Tablets: Elacestrant 345mg, which is equivalent to 400 mg of Elacestrant dihydrochloride, and 86mg, which is equivalent to 100mg of Elacestrant dihydrochloride.

· 345mg: light blue, unscored, oval film-coated biconvex tablet, imprinted with “MH” on one side and plain on the other side.

· 86mg: light blue, unscored, round film-coated biconvex tablet, imprinted with “ME” on one side and plain on the other side

WARNINGS AND PRECAUTIONS¹⁵:

1) Dyslipidemia: -

Patients on Elacestrant experienced an incidence of 30% and 27%, respectively, of hypercholesterolemia and hypertriglyceridemia. Hypercholesterolemia and hypertriglyceridemia in Grades 3 and 4 occurred 0.9% and 2.2%, respectively.

Lipid profile before starting elacestrant and on a regular basis.

2) MonitorEmbryo-Fetal Toxicity:

According to animal research, Elacestrant can be harmful to a fetus when administered to a pregnant mother. When elacestrant was given to pregnant rats, poor developmental results, such as embryo-fetal mortality and morphological abnormalities, resulted. Women who are or may become pregnant should be warned about the risk and urged to use effective contraception both throughout treatment with Elacestrant and for one week following the last dose. Patients who are men should utilize reliable contraception.

Drug-Drug Interactions³¹:

It is known that Elacestrant interacts with 220 different medications. 142 medications interact altogether, 78 of which are mild and 142 are significant.

Table 3. Drug-Drug Interactions

A	Adagrasib, afatinib, aliskiren, alpelisib, alvimopan, ambrisentan, aminoglutethimide, amobarbital, amprenavir, apalutamide, apixaban, apremilast, aprepitant, armodafinil, artesunate, atazanavir, atorvastatin
B	Belinostat, belzutifan, berotralstat, betrixaban, bexarotene, boceprevir, bosentan, bosutinib, brentuximab, brigatinib, butabarbital, butalbital
C	Cabazitaxel, carbamazepine, cenobamate, ceritinib, chloramphenicol, ciprofloxacin, cladribine, clarithromycin, cobicistat, cobimetinib, colchicine, conivaptan, crizotinib, cyclosporine
D	Dabigatran, dabrafenib, daclatasvir, dactinomycin, darolutamide, darunavir, deferasirox, delafloxacin, delavirdine, dexamethasone, digoxin, diltiazem, docetaxel, doxorubicin, doxorubicin liposomal, dronedarone, duvelisib
E	Edoxaban, efavirenz, elagolix, eliglustat, eltrombopag, empagliflozin, enzalutamide, erythromycin, eslicarbazepine, etoposide, etravirine, everolimus
F	Fedratinib, felbamate, fexinidazole, fexofenadine, fidaxomicin, fluconazole, fosamprenavir, fosaprepitant, fosphenytoin
G	Gilteritinib, glycerol phenylbutyrate, griseofulvin
H	hydrocortisone
I	Idarubicin, idelalisib, imatinib, indacaterol, indinavir, irinotecan, irinotecan liposomal, isavuconazonium, itraconazole, ivermectin, ivosidenib, ixabepilone
K	Ketoconazole
L	Lapatinib, larotrectinib, lemborexant, lenacapavir, lenalidomide, lesinurad, letermovir, levoketoconazole, linagliptin, lonafarnib, lonapegsomatropin, loperamide, loratadine, lorlatinib, lurasidone, lusutrombopag
M	Maraviroc, mephobarbital, methotrexate, metreleptin, mibefradil, mifepristone, mirabegron, mitapivat, mitomycin, mitotane, mitoxantrone, modafinil, morphine
N	Nafcillin, naldemedine, naloxegol, nefazodone, nelfinavir, nevirapine, nicardipine, nilotinib, nintedanib, niraparib
O	Olaparib, oritavancin, osimertinib, oxcarbazepine, ozanimod
P	Paclitaxel, pazopanib, pentobarbital, pexidartinib, phenobarbital, phenylbutazone, phenytoin, pitolisant, ponatinib, posaconazole, pralsetinib, primidone, prucalopride
Q	Quinidine
R	Ranolazine, relugolix, ribociclib, rifabutin, rifampin, rifapentine, rifaximin, rimegepant, riociguat, ritonavir, rivaroxaban, romidepsin, rosuvastatin, rucaparib, rufinamide
S	Saquinavir, saxagliptin, secobarbital, selexipag, silodosin, sirolimus, sirolimus protein-bound, sirolimus topical, sitagliptin, sofosbuvir, somapacitan-beco, somatrem, somatropin, sotorasib, st. john's wort, stiripentol, sulfasalazine, sulfinpyrazone
T	Tacrolimus, talazoparib, tazemetostat, tecovirimat, telaprevir, telithromycin, telotristat, teniposide, tenofovir, tenofovir alafenamide, teriflunomide, ticagrelor, tipranavir, tolvaptan, topotecan, trametinib, troglitazone, troleandomycin, tucatinib
U	Ubrogepant
V	Vemurafenib, venetoclax, verapamil, vibegron, vinblastine, vincristine, vincristine liposome, vinorelbine, voriconazole, voxelotor
Z	Zanubrutinib

Note: Bold lettered drugs are Major drugs;

Highly clinically significant.

Avoid combinations; the risk of the interaction outweighs the benefit.

ADVERSE EFFECTS³²

Of the individuals who got Elacestrant, 12% experienced major adverse effects. Musculoskeletal discomfort (1.7% of patients who took elacestrant experienced severe side effects) and nausea (1.3%) were the most common. In 1.7% of individuals, adverse events that were fatal occurred got elacestrant, as well as diverticulitis, septic shock, and unidentified symptoms cause (per individual).

USE IN SPECIFIC POPULATIONS¹⁵:

Patients with this type of conditions should not take this drug, as it may cause severe adverse effects to the patients

NONCLINICAL TOXICOLOGY¹⁵:

· Carcinogenesis, Mutagenesis, Impairment of Fertility:

Elacestrant has not been studied for malignancy, and it has not been found to be mutagenic or clastogenic in in-vitro or in vivo tests. However, at doses below 10 mg/kg/day in rats and cynomolgus monkeys, negative effects were observed in female reproductive organs, including atrophy of the vagina, cervix, uterus, and follicular cysts. Male rats were also affected by decreased cellularity of Leydig cells and atrophy/degeneration of the seminiferous epithelium in the testis.

· Methods of Analysis:^5,9,12,33

Methods
Sr. No	Name of Method
1	ESR1 mutation analysis
2	Pharmacokinetic Analysis
3	Tumor Assessments
4	Safety Assessments
5	Statistical Methods
6	In-vitro Cancer Cell Proliferation
7	Western Blot
8	Quantitative Reverse Transcriptase PCR Analyses
9	MCF-7 Xenografts
10	IHC
11	Uterine Wet Weight Analysis
12	Colony Formation Assay
13	RNA sequencing
14	Patient-derived Xenografts

CONCLUSION:

Elacestrant, an oral non-steroidal SERM/ SERD having an amino basic side chain, has been shown to be effective as a monotherapy as well as in combination with palbociclib or everolimus to suppress ER signaling and exhibit antitumor activity in HR+ BC cell lines and patient-derived xenografts. Additionally, elacestrant was tested in vivo and in vitro models of BC that were resistant to CDK4/6i, and it was found to decrease tumor development even in the presence of ESR1 mutations. Due to its unusual pharmacologic properties, elacestrant functions as a SERD at larger doses and as a SERM at lower ones. The distinct pharmacologic characteristics, in addition to its capacity to traverse the blood-brain barrier and its efficacy against both wild-type (WT) and mutated ER (such as the Y537S and D538G variants, which are typically linked to significant resistance to ET), may be ascribed to the distinct binding mechanism of elacestrant with ER.

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Received on 15.03.2024 Revised on 13.09.2024

Accepted on 02.12.2024 Published on 28.02.2025

Available online from March 04, 2025

Asian Journal of Pharmaceutical Analysis. 2025;15(1):66-72.

DOI: 10.52711/2231-5675.2025.00011

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Creative Commons License.